Dutton's orthopaedic examination, evaluation, and intervention [5 ed.] 9781260143874, 1260143872

Table of contents :
Cover
Title Page
Copyright Page
Dedication
Contents
Preface
Acknowledgments
Introduction
SECTION I ANATOMY
1 The Musculoskeletal System
2 Tissue Behavior, Injury, Healing, and Treatment
3 The Nervous System
SECTION II EXAMINATION AND EVALUATION
4 Patient/Client Management
5 Differential Diagnosis
6 Gait and Posture Analysis
7 Imaging Studies in Orthopaedics
SECTION III INTERVENTION
8 The Intervention
9 Pharmacology for the Orthopaedic Physical Therapist
10 Manual Techniques
11 Neurodynamic Mobility and Mobilizations
12 Improving Muscle Performance
13 Improving Mobility
14 Improving Neuromuscular Control
15 Improving Cardiovascular Endurance
SECTION IV THE EXTREMITIES
16 The Shoulder
17 Elbow Complex
18 The Forearm, Wrist, and Hand
19 Hip Joint Complex
20 The Knee Joint Complex
21 Lower Leg, Ankle, and Foot
SECTION V THE SPINE AND TMJ
22 Vertebral Column
23 The Craniovertebral Region
24 Vertebral Artery
25 The Cervical Spine
26 The Temporomandibular Joint
27 The Thoracic Spine
28 Lumbar Spine
29 The Sacroiliac Joint
SECTION VI SPECIAL CONSIDERATIONS
30 Special Populations
Index

Citation preview

DUTTON’S ORTHOPAEDIC EXAMINATION, EVALUATION, AND INTERVENTION

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NOTICE Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The authors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of 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 of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs.

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DUTTON’S ORTHOPAEDIC EXAMINATION, EVALUATION, AND INTERVENTION FIFTH EDITION

Mark Dutton, PT

New York  Chicago  San Francisco  Athens  London  Madrid  Mexico City Milan  New Delhi  Singapore  Sydney  Toronto

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Copyright © 2020, 2017, 2012, 2008, 2004 by McGraw-Hill Education. All rights reserved. Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher. ISBN: 978-1-26-044011-9 MHID: 1-26-044011-7 The material in this eBook also appears in the print version of this title: ISBN: 978-1-26-014387-4, MHID: 1-26-014387-2. eBook conversion by codeMantra Version 1.0 All trademarks are trademarks of their respective owners. Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefit of the trademark owner, with no intention of infringement of the trademark. Where such designations appear in this book, they have been printed with initial caps. McGraw-Hill Education eBooks are available at special quantity discounts to use as premiums and sales promotions or for use in corporate training programs. To contact a representative, please visit the Contact Us page at www.mhprofessional.com. TERMS OF USE This is a copyrighted work and McGraw-Hill Education and its licensors reserve all rights in and to the work. Use of this work is subject to these terms. Except as permitted under the Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill Education’s prior consent. You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited. Your right to use the work may be terminated if you fail to comply with these terms. THE WORK IS PROVIDED “AS IS.” McGRAW-HILL EDUCATION AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HYPERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. McGraw-Hill Education and its licensors do not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free. Neither McGraw-Hill Education nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom. McGraw-Hill Education has no responsibility for the content of any information accessed through the work. Under no circumstances shall McGraw-Hill Education and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages. This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise.

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.

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Your Legacy Will you have earned the respect of your peers and the admiration of your critics? Will you have acted humbly during success and gracefully in the face of adversity? Will you be remembered for how often you brought smiles to the hearts of others? Will you have looked for the very best, and done your utmost to build worth, in others? Will you have left this world a better place by the life you have lived?

Modified from The Legacy You Leave ©2000 by Rick Beneteau

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Contents

Preface ix Acknowledgments xi Introduction xiii

SECTION I ANATOMY 1 The Musculoskeletal System 2 Tissue Behavior, Injury, Healing, and Treatment 3 The Nervous System

3 28 61

SECTION IV THE EXTREMITIES 16 17 18 19 20 21

The Shoulder Elbow Complex The Forearm, Wrist, and Hand Hip Joint Complex The Knee Joint Complex Lower Leg, Ankle, and Foot

555 676 739 824 922 1024

SECTION V SECTION II

THE SPINE AND TMJ

EXAMINATION AND EVALUATION 4 5 6 7

Patient/Client Management Differential Diagnosis Gait and Posture Analysis Imaging Studies in Orthopaedics

163 214 279 329

SECTION III

22 23 24 25 26 27 28 29

Vertebral Column The Craniovertebral Region Vertebral Artery The Cervical Spine The Temporomandibular Joint The Thoracic Spine Lumbar Spine The Sacroiliac Joint

1123 1141 1175 1183 1259 1295 1335 1417

INTERVENTION 8 The Intervention 9 Pharmacology for the Orthopaedic Physical Therapist 10 Manual Techniques 11 Neurodynamic Mobility and Mobilizations 12 Improving Muscle Performance 13 Improving Mobility 14 Improving Neuromuscular Control 15 Improving Cardiovascular Endurance

353

SECTION VI

380 398 423 440 498 533 544

SPECIAL CONSIDERATIONS 30

Special Populations

1453

Index 1501

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Preface

The fifth edition of this book is an update of information and bibliography provided in the previous versions together with a reorganization of various chapters. The 2017 Global Burden of Disease study revealed that musculoskeletal disorders are the second biggest contributor to disability worldwide.1 The United States currently spends more money on healthcare per person than any other country in the world, with current projections indicating that the United States will spend 20% of the gross domestic product on healthcare by the year 2019.1 As the population continues to age, the treatment of musculoskeletal conditions, and their subsequent expenses, will also increase. This financial burden will place an increasing pressure on the orthopaedic clinician to provide value for money—the achievement of 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, the emphasis must now be placed on outcomes such as patient satisfaction and accurate measures of clinical outcomes, for it is the consistent measurement and reporting of clinical outcomes that are the most powerful tools in moving toward a value-based system.2 The APTA’s current vision statement, “Transforming society by optimizing movement to improve the human experience,”

highlights the fact that the “physical therapy profession will define and promote the movement system as the foundation for optimizing movement to improve the health of society.”2 To that end, this book aims to provide the reader with a systematic and evidence-based approach to the examination and intervention of the orthopaedic patient from the viewpoint of an expert on the movement system. Such an approach must be eclectic because no single method works all of the time. Thus, this book attempts to incorporate the most reliable concepts currently available. I hope that this book will be the best available textbook, guide, review, and reference for healthcare students and clinicians involved in the care of the orthopaedic population. Mark Dutton, PT

REFERENCES 1. Disease GBD, Injury I, Prevalence C. Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet. 2017;390:1211–1259. 2. Sahrmann SA. The human movement system: our professional identity. Phys Ther. 2014;94:1034–1042.

Comments about this book may be sent to me at [email protected].

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Acknowledgments

From inception to completion, the various editions span almost 15 years. Such an endeavor cannot be completed without the help of many. I would like to take this opportunity to thank the following: ▶▶ The faculty of the North American Institute of Manual and Manipulative Therapy (NAIOMT)—especially, Jim Meadows, Erl Pettman, Cliff Fowler, Diane Lee, and the late Dave Lamb. ▶▶

The exceptional team at McGraw-Hill, for their superb guidance throughout this object. Thank you especially

to Michael Weitz for his advice and support and to other members of the team. ▶▶ To the production crew at Cenveo, especially the project manager, Radhika Jolly. ▶▶ Bob Davis for his creative eye and the excellent photography. ▶▶ ▶▶

Leah for agreeing to be the photographic model. To the countless clinicians throughout the world who continually strive to improve their knowledge and clinical skills.

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Introduction

“The very first step towards success in any occupation is to become interested in it.” —Sir William Osler (1849–1919) Until the beginning of the last century, knowledge about the mechanism of healing and the methods to decrease pain and suffering were extremely limited. Although we may scoff at many of the interventions used in the distant past, many of the interventions we use today, albeit less radical, have still to demonstrate much more in the way of effectiveness. That may soon change with the recent emphasis within many healthcare professions on evidence-based clinical practice. The process of evidence-based practice is outlined in Table I-1. When

TABLE I-1

The Process of Evidence-Based Practice

1.  Identify the patient problem. Derive a specific question. 2.  Search the literature. 3.  Appraise the literature. 4.  Integrate the appraisal of literature with your clinical expertise, experience, patient values, and unique circumstances. 5.  Implement the findings. 6.  Assess outcome and reappraise. Data from Sackett DL, Strauss SE, Richardson WS, et al. Evidence Based Medicine: How to Practice and Teach EBM. 2nd ed. Edinburgh, Scotland: Churchill Livingstone; 2000.

combining clinical expertise with the best available external clinical evidence, clinicians can make informed decisions regarding patient management, including the selection and interpretation of the most appropriate evaluation procedures. Also, intervention strategies based on the best available evidence will have a greater likelihood of success with the least associated risk. The goal of every clinician should be to enhance patient/ client satisfaction, increase efficiency, and decrease unproven treatment approaches. The management of the patient/client is a complex process involving an intricate blend of 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 of the time. For any intervention to be successful, an accurate diagnosis must be followed by a carefully planned and specific rehabilitation program to both the affected area and its related structures. In this book, great emphasis is placed on the appropriate use of manual techniques and therapeutic exercise based on these considerations. Electrotherapeutic and thermal/cryotherapeutic modalities should be viewed as adjuncts to the rehabilitative process. Please go to www .accessphysiotherapy.com, for numerous video clips of manual techniques and therapeutic exercises, which the reader is encouraged to view. The following icon is used throughout the text to indicate when such clips are available. [VIDEO]

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SECTION I

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ANATOMY

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The Musculoskeletal System

CHAPTER 1

CHAPTER OBJECTIVES At the completion of this chapter, the reader will be able to: 1. Describe the various types of biological tissue of the musculoskeletal system. 2. Describe the tissue mechanics and structural differences and similarities between muscle, tendons, fascia, and ligaments. 3. Describe the different types of joints and their various characteristics. 4. Define the various terminologies used to describe the joint position, movements, and relationships. 5. Give definitions for commonly used biomechanical terms. 6. Describe the different planes of the body. 7. Define the body’s center of gravity and its location. 8. Describe the different axes of the body and the motions that occur around them. 9. Define the terms osteokinematic motion and arthrokinematic motion. 10. Differentiate between the different types of motion that can occur at the joint surfaces. 11. Describe the basic biomechanics of joint motion in terms of their concave–convex relationships. 12. List the different types of levers found within the body and provide examples of each. 13. Describe the difference between a closed kinematic chain and an open kinematic chain and how each can influence an exercise prescription.

OVERVIEW The correct embryonic development of the musculoskeletal system requires a coordinated morphogenesis of the fundamental tissues of the body. Throughout the human body, there are four major types of tissues: Epithelial. Epithelial tissue covers all internal and external body surfaces and includes structures such as the skin and the inner lining of the blood vessels. ▶▶ Connective. Connective tissue (CT) includes four different classes: CT proper, bone, cartilage, and blood tissue. In the embryo, muscle tissue and its fascia form as a differentiation of the paraxial mesoderm that divides into somites on either side of the neural tube and notochord. The cartilage and bone of the vertebral column and ribs develop from the sclerotome, which is the anterior (ventral) part of the somite.1,2 The dermomyotome, which is the posterior (dorsal) part of the somite, gives rise to the overlying dermis of the back and the skeletal muscles of the body and limbs.2 CT provides structural and metabolic support for other tissues and organs of the body. ▶▶ Muscle. Muscles are classified functionally as either voluntary or involuntary, and structurally as either smooth, striated (skeletal), or cardiac. There are approximately 430 skeletal muscles in the body, each of which can be considered anatomically as a separate organ. Of these 430 muscles, about 75 pairs provide the majority of 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). ▶▶

14. Define the terms close-packed and open-packed and the significance of each.

3

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The various types of CT, as they relate to the musculoskeletal system, are described in the following sections.

CONNECTIVE TISSUE CT proper has a loose, flexible matrix, called ground substance. The most common cell within CT proper is the fibroblast. Fibroblasts produce collagen, elastin, and reticular fibers: Collagen is a group of naturally occurring proteins. The collagens are a family of extracellular matrix (ECM) proteins that play a dominant role in maintaining the structural integrity of various tissues and in providing tensile strength to tissues. The ECM is formed from glycosaminoglycan (GAG) subunits that are long polysaccharide chains containing amino sugars and are strongly hydrophilic to allow rapid diffusion of water-soluble molecules and the easy migration of cells. Proteoglycans, which are a major component of the ECM, are macromolecules that consist of a protein backbone to which the GAGs are attached. There are two types of GAGs: chondroitin sulfate and keratin sulfate.2 Glycoproteins, another component of the ECM, consist of fibronectin and thrombospondin and function as adhesive structures for repair and regeneration.2,3 ▶▶ Elastic fibers, as their name suggests, are composed of a protein called elastin, which provides elastic properties to the tissues in which it is situated.4 Elastin fibers can stretch, but they normally return to their original length when the tension is released. Thus, the elastic fibers of elastin determine the patterns of distention and recoil in most organs, including the skin and lungs, blood vessels, and CT. Bundles of collagen and elastin combine to form a matrix of CT fascicles. This matrix is organized within the primary collagen bundles as well as between the bundles that surround them.2 ▶▶ Reticular fibers are composed of a type of collagen that is secreted by reticular cells. These fibers crosslink to form a fine meshwork, called reticulin, which acts as a supporting mesh in bone marrow, the tissues and organs of the lymphatic system, and the liver. ▶▶

ANATOMY

The various characteristics of collagen differ depending on whether it is loose or dense collagen. The anatomic and functional characteristics of loose and dense collagen are summarized in Table 1-1. Collagenous and elastic fibers are sparse and irregularly arranged in loose CT but are tightly packed in dense CT.



TABLE 1-1

Fascia Fascia, for example, the thoracolumbar fascia and the plantar fascia, is viewed as a loose CT that provides support and protection to a joint, and acts as an interconnection between tendons, aponeuroses, ligaments, capsules, nerves, and the intrinsic components of muscle.2 Fascia may be categorized as fibrous or nonfibrous, with the fibrous components consisting mainly of collagen and elastin fibers, and the nonfibrous portion consisting of amorphous ground substance.2 Three different types of fascia have been identified, namely, superficial, deep, and visceral. Various three-dimensional biomechanical models of the human fascial system have been developed, which correlate dysfunctional movement with various interrelated abnormal amounts of tension throughout the network of fascia. In particular, deep fascia has been implicated in being involved with the deep venous return, in having a possible role in proprioception, and responding to mechanical traction induced by muscular activity in different regions.5 However, there is still little evidence to justify such claims. Histological studies of deep fascia in the limbs show that it consists of elastic fibers and undulated collagen fibers arranged in layers.6 Each collagen layer is aligned in a different direction, and this permits a certain degree of stretch as well as a capacity to recoil.

Tendons Tendons are dense, regularly arranged CTs that attach muscle to the bone at each end of the muscle. At first glance, tendons appear to be very simple rope-like structures. However, closer inspection reveals that the structure and material properties of tendons are not universal, and therefore, each tendon cannot be treated in the same manner as another. Medical imaging today allows clinicians and researchers to more precisely characterize the tendon structures that provide the tendon with its physiological capacity. The predominant cell type found in a tendon is the tenocyte, a structure that is sensitive to the mechanical loading environment and is capable of controlling tendon structure.7 The collagen-forming triple helices (tropocollagen) of the tendon pack together to form microfibrils, which interdigitate to form fibrils, which coalesce to form fibers, which combine to form fascicles, which in turn are bundled together to

Loose and Dense Collagen

Joint Type

Anatomic Location

Fiber Orientation

Mechanical Specialization

Dense irregular connective tissue

Composes the external fibrous layer of the joint capsule, forms ligaments, bone, aponeuroses, and tendons

Parallel, tightly aligned fibers

Ligament: binds bones together and restrains unwanted movement at the joints; resists tension in several directions Tendon: attaches muscle to bone

Loose irregular connective tissue

Found in capsules, muscles, nerves, fascia, and skin

Random fiber orientation

Provides structural support

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CLINICAL PEARL Paratenon lined with synovial cells of a variable structure is called tenosynovium, while one with a double layer sheath without synovial cells is known as tenovagium.2 The mechanical properties of tendon come from its highly oriented structure. Normal tendons display viscoelastic

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mechanical properties that confer time- and rate-dependent effects on the tissue. Specifically, tendons are more elastic at lower strain rates and stiffer at higher rates of tensile loading (see Chapter 2). Tendons deform less than ligaments under an applied load and are thus able to transmit the load from muscle to bone.7

CLINICAL PEARL At low rates of loading, tendons are more viscous or ductile and, consequently, can absorb more energy compared to high loading rates.13 ▶▶ At high rates of loading, tendons become more brittle and absorb less energy, but they are more effective at transferring loads.13 Therefore, tendon load can be increased in one of two ways when prescribing exercise: by the external load or by the speed of movement.13 ▶▶

Patients with tendinopathy display tendons that are thicker, but with reduced energy-storing capacity, meaning that for the same load, their tendons exhibit higher strains than those of healthy individuals.14 Material and structural properties of the tendon increase from birth through maturity and then decrease from maturity through old age.8 Although tendons withstand strong tensile forces well, they resist shear forces less well and provide little resistance to a compression force (see Chapter 2). In addition to the primary load-bearing part of the tendon, there is an extensive network of septae (endotendon), where the nerves and vessels are mainly located.14 A tendon can be divided into the following three main sections15:

The Musculoskeletal System

form a tendon.8 Tendon accommodates a high-tensile loading environment through a multiscale structural design: polypeptide hydrogen bonds create the strong triple-helical structure of a single collagen molecule; covalent bonds cross-linking between collagen molecules (fibrils) allow collagen fibers to withstand enormous forces; collagen fibers are bundled together within an ECM (fascicles) that limits the extent of neurovascular infiltration and maximizes mechanical integrity; and bundling of fascicles into primary, secondary, and tertiary fiber bundles reduces the impact of local fibril failure on the whole tissue.9,10 The position and length of tendons enable the muscle belly to be an optimal distance from the joint upon which it is acting. This creates space, but also allows the tendon to work like a lever arm (see Levers later), moving the point of action away from the center of rotation (COR), thereby reducing the forces required for movement.7 Also, due to their design, tendons provide a graduated change in material characteristics, which minimizes the development of areas of stress concentration where failure would likely occur. Tendons must be sufficiently stiff to enable efficient force transfer from the muscles to produce joint motion, but they must also incorporate a degree of elasticity to enable them to stretch and store elastic energy.7 Other tendons must modulate muscle contraction with extreme precision to allow it to perform intricate activities such as writing.7 The thickness of each tendon varies but is proportional to the size of the muscle from which it originates. Vascularity within the tendon is relatively sparse, but the extent of vascularity is not universally the same, and those tendons with less vascularity may be more vulnerable to both progressive degeneration and a reduced healing potential.11 Within the fascicles of tendons, which are held together by loose CT called endotenon, the collagen components are oriented in a unidirectional way. Endotenon contains blood vessels, lymphatics, and nerves, and permits longitudinal movements of individual fascicles when tensile forces are applied to the structure. The CT surrounding groups of fascicles, or the entire structure, is called the epitenon. The epitenon contains the vascular, lymphatic, and nerve supplies to the tendon. A peritendinous sheath (paratenon), which is composed of loose areolar CT in addition to sensory and autonomic nerve fibers, surrounds the entire tendon.12 This sheath consists of two layers: an inner (visceral) layer and an outer (parietal) layer with occasional connecting bridges (mesotenon). The paratenon is richly vascularized and is responsible for a significant portion of the blood supply to the tendon via a series of transverse vincula, which function as passageways for blood vessels to reach the tendon. In addition, the blood supply to the tendon comes from two other sources: the musculotendinous junction (MTJ) and the osseous insertion.

The bone–tendon junction. At most tendon–bone interfaces, the collagen fibers insert directly into the bone in a gradual transition of material composition. The physical junction of tendon and bone is referred to as an enthesis16 and is an interface that is vulnerable to acute and chronic injury.7,17 One role of the enthesis is to absorb and distribute the stress concentration that occurs at the junction over a broader area. ▶▶ The tendon midsubstance. Overuse tendon injuries can occur in the midsubstance of the tendon, but not as frequently as at the enthesis. ▶▶ MTJ. The MTJ is the site where the muscle and tendon meet. The MTJ comprises numerous interdigitations between muscle cells and tendon tissue, resembling interlocked fingers. ▶▶

Ligaments Skeletal ligaments are fibrous bands of dense CT that connect bones across joints. Ligaments can be named for the bones into which they insert (coracohumeral), their shape (deltoid of the ankle), or their relationships to each other (cruciate).18 The gross structure of a ligament varies according to location (intra-articular or extra-articular, capsular) and function.19 Ligaments, which appear as dense white bands or cords of

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ANATOMY

CT, are composed primarily of water (approximately 66%) and collagen (largely type I collagen [85%], but with small amounts of type III) making up most of the dry weight.2 The collagen in ligaments has a less unidirectional organization than it does in tendons, but its structural framework still provides stiffness (resistance to deformation—see Chapter 2). Small amounts of elastin (1% of the dry weight) are present in ligaments, with the exception of the ligamentum flavum and the nuchal ligament of the spine, which contain more. The cellular organization of ligaments makes them ideal for sustaining tensile loads and for tightening or loosening in different joint positions. At the microscopic level, closely spaced collagen fibers (fascicles) are aligned along the long axis of the ligament and are arranged into a series of bundles that are delineated by a cellular layer, the endoligament, and the entire ligament is encased in a neurovascular biocellular layer referred to as the epiligament.18 Ligaments contribute to the stability of joint function by preventing excessive motion, acting as guides or checkreins to direct motion, and providing proprioceptive information for joint function through sensory nerve endings (see Chapter 3) and as attachments to the joint capsule.2 Many ligaments share functions. For example, while the anterior cruciate ligament of the knee is considered to be the primary restraint to anterior translation of the tibia relative to the femur, the collateral ligaments and the posterior capsule of the knee also help in this function (see Chapter 20).18 The vascular and nerve distribution to ligaments is not homogenous. For example, the middle of the ligament is typically avascular, while the proximal and distal ends enjoy a rich blood supply. Similarly, the insertional ends of the ligaments are more highly innervated than the midsubstance.

and nerves.2 Most of the bones of the body form first as hyaline cartilage, and later become bone in a process called endochondral ossification. Articular cartilage functions to distribute the joint forces over a large contact area, thereby dissipating the forces associated with the load. This distribution of forces allows the articular cartilage to remain healthy and fully functional throughout decades of life. The normal thickness of articular cartilage is determined by the contact pressures across the joint—the higher the peak pressures, the thicker the cartilage.19 For example, the patellar has the thickest articular cartilage in the body. ▶▶

Articular cartilage may be grossly subdivided into four distinct zones with differing cellular morphology, biomechanical composition, collagen orientation, and structural properties, as follows: ■■ The superficial zone. The superficial zone, which lies adjacent to the joint cavity, comprises approximately 10–20% of the articular cartilage thickness and functions to protect deeper layers from shear stresses. The collagen fibers within this zone are packed tightly and aligned parallel to the articular surface. This zone is in contact with the synovial fluid and handles most of the tensile properties of cartilage. ■■

■■

Cartilage Cartilage tissue exists in three forms: hyaline, elastic, and fibrocartilage. ▶▶

Hyaline cartilage, also referred to as articular cartilage, covers the ends of long bones and permits almost frictionless motion to occur between the articular surfaces of a diarthrodial (synovial) joint. Articular cartilage is a highly organized viscoelastic material composed of cartilage cells called chondrocytes, water, and an ECM.

CLINICAL PEARL Chondrocytes are specialized cells that are responsible for the development of cartilage and the maintenance of the ECM. Chondrocytes produce aggrecan, link protein, and hyaluronan, all of which are extruded into the ECM, where they aggregate spontaneously.2 The aggrecan forms a strong, porous-permeable, fiber-reinforced composite material with collagen. The chondrocytes sense mechanical changes in their surrounding matrix through intracytoplasmic filaments and short cilia on the surface of the cells.19 ▶▶

6

Articular cartilage, the most abundant cartilage within the body, is devoid of any blood vessels, lymphatics,

Dutton_Ch01_p0001-p0027.indd 6

■■

The middle (transitional) zone. In the middle zone, which provides an anatomic and functional bridge between the superficial and deep zones, the collagen fibril orientation is obliquely organized. This zone comprises 40–60% of the total cartilage volume. Functionally, the middle zone is the first line of resistance to compressive forces. The deep or radial layer. The deep layer comprises 30% of the matrix volume. It is characterized by radially aligned collagen fibers that are perpendicular to the surface of the joint and have a high proteoglycan content. Functionally the deep zone is responsible for providing the greatest resistance to compressive forces. The tidemark. The tidemark distinguishes the deep zone from the calcified cartilage, the area that prevents the diffusion of nutrients from the bone tissue into the cartilage.

Elastic (yellow) cartilage is a very specialized CT, primarily found in locations such as the outer ear and portions of the larynx. ▶▶ Fibrocartilage, also referred to as white cartilage, functions as a shock absorber in both weight-bearing and non–weight-bearing joints. Its large fiber content, reinforced with numerous collagen fibers, makes it ideal for bearing large stresses in all directions. Fibrocartilage is an avascular, alymphatic, and aneural tissue and derives its nutrition by a double-diffusion system.2 Examples of fibrocartilage include the symphysis pubis, the intervertebral disk, and the menisci of the knee. ▶▶

Bone Bone is a highly vascular form of CT, composed of collagen, calcium phosphate, water, amorphous proteins, and cells. It is

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TABLE 1-2

General Structure of Bone

Comment

Conditions

Result

Epiphysis      

Mainly develops under pressure Apophysis forms under traction Forms bone ends Supports articular surface

Epiphyseal dysplasias Joint surface trauma Overuse injury Damaged blood supply

Distorted joints Degenerative changes Fragmented development Avascular necrosis

Physis      

Epiphyseal or growth plate Responsive to growth and sex hormones Vulnerable prior to growth spurt Mechanically weak

Physeal dysplasia Trauma Slipped epiphysis  

Short stature Deformed or angulated growth or growth arrest 

Metaphysis      

Remodeling expanded bone end Cancellous bone heals rapidly Vulnerable to osteomyelitis Affords ligament attachment

Osteomyelitis Tumors Metaphyseal dysplasia  

Sequestrum formation Altered bone shape Distorted growth  

Diaphysis      

Forms shaft of bone Large surface for muscle origin Significant compact cortical bone Strong in compression

Fractures Diaphyseal dysplasias Healing slower than at metaphysis  

Able to remodel angulation Cannot remodel rotation Involucrum with infection Dysplasia gives altered density and shape

 

Reproduced with permission from Reid DC. Sports Injury Assessment and Rehabilitation. New York, NY: Churchill Livingstone; 1991.

the most rigid of the CTs (Table 1-2). Despite its rigidity, bone is a dynamic tissue that undergoes constant metabolism and remodeling. The collagen of bone is produced in the same manner as that of ligament and tendon but by a different cell, the osteoblast. At the gross anatomical level, each bone has a distinct morphology comprising both cortical bone and cancellous bone. Cortical bone is found in the outer shell. Cancellous bone is found within the epiphyseal and metaphyseal regions of long bones, as well as throughout the interior of short bones. Skeletal development occurs in one of two ways: Intramembranous ossification. Mesenchymal stem cells within the mesenchyme or the medullary cavity of a bone initiate the process of intramembranous ossification. This type of ossification occurs in the cranium and facial bones and, in part, the ribs, clavicle, and mandible. ▶▶ Endochondral ossification. The first site of ossification occurs in the primary center of ossification, which is in the middle of the diaphysis (shaft). About the time of birth, a secondary ossification center appears in each epiphysis (end) of long bones. Between the bone formed by the primary and secondary ossification centers, cartilage persists as the epiphyseal (growth) plates between the diaphysis and the epiphysis of a long bone. This type of ossification occurs in the appendicular and axial bones. ▶▶

The periosteum is formed when the perichondrium, which surrounds the cartilage, becomes the periosteum. Chondrocytes in the primary center of ossification begin to grow (hypertrophy) and begin secreting alkaline phosphatase, an enzyme essential for mineral deposition. Calcification of the matrix follows, and apoptosis (a type of cell death involving a programmed sequence of events that eliminates certain cells) of the hypertrophic chondrocytes occurs. This creates cavities

Dutton_Ch01_p0001-p0027.indd 7

The Musculoskeletal System

Site

within the bone. The exact mechanism of chondrocyte hypertrophy and apoptosis is currently unknown. The hypertrophic chondrocytes (before apoptosis) also secrete a substance called vascular endothelial cell growth factor that induces the sprouting of blood vessels from the perichondrium. Blood vessels forming the periosteal bud invade the cavity left by the chondrocytes and branch in opposite directions along the length of the shaft. The blood vessels carry osteoprogenitor cells and hemopoietic cells inside the cavity, the latter of which later form the bone marrow. Osteoblasts, differentiated from the osteoprogenitor cells that enter the cavity via the periosteal bud, use the calcified matrix as a scaffold and begin to secrete osteoid, which forms the trabecular bone. Osteoclasts, formed from macrophages, break down the spongy bone to form the medullary cavity (bone marrow). The function of bone is to provide support, enhance leverage, protect vital structures, provide attachments for both tendons and ligaments, and store minerals, particularly calcium. Bones also may serve as useful landmarks during the palpation phase of the examination. The strength of bone is related directly to its density. Of importance to the clinician is the difference between maturing bone and mature bone. The epiphyseal plate or growth plate of a maturing bone can be divided into the following four distinct zones20: ▶▶

Reserve zone: It produces and stores matrix.

▶▶

Proliferative zone: It produces matrix and is the site for longitudinal bone cell growth.

▶▶

Hypertrophic zone: It is subdivided into the maturation zone, degenerative zone, and the zone of provisional calcification. It is within the hypertrophic zone that the matrix is prepared for calcification and is here that the matrix is ultimately calcified. The hypertrophic zone is the most susceptible of the zones to injury because of

7

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the low volume of bone matrix and the high amounts of developing immature cells in this region.2 ▶▶ Bone metaphysis: It is the part of the bone that grows during childhood.

eccentric-induced muscle damage, ischemia, and others (see Chapter 2).21 Because the nuclei of the myofibers are terminally postmitotic (i.e., they cannot divide anymore), muscle regeneration is ensured by a population of adult muscle stem cells, named satellite cells.21,23

ANATOMY

Skeletal Muscle Tissue

CLINICAL PEARL

Skeletal muscles constitute approximately 30–40% of total body mass and have many vital roles such as generation of movement, protection, breathing, thermal regulation, and metabolism.21 The microstructure and composition of skeletal muscle have been studied extensively. The class of tissue labeled skeletal muscle consists of individual muscle cells that work together to produce the movement of bony levers. A single muscle cell is long and cylindrical and is called a muscle fiber or myofiber. The myofiber is the most important part of skeletal muscle composition,22 and the integrity and function of a myofiber can be affected by different traumas such as strain, contusion, laceration, immobilization,

Satellite cells are essential to muscle regeneration post injury, and they also contribute to muscle hypertrophy.21 All muscles, depending on their size, are made up of thousands and, in some cases, hundreds of thousands of muscle fibers, which are wrapped in a CT sheath called epimysium (Fig. 1-1). As muscle cells differentiate within the mesoderm, individual myofibers are wrapped in a CT envelope called endomysium. Bundles of myofibers, which form a whole muscle (fasciculus), are encased in the perimysium (Fig. 1-1). The perimysium is continuous with the deep fascia. This

Epimysium Perimysium Fasciculus

Capillary

Nucleus Mitochondrion

Myofibril

8

Dutton_Ch01_p0001-p0027.indd 8

Endomysium Sarcolemma

FIGURE 1-1  Microscopic structure of the muscle.

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relationship allows the fascia to unite all of the fibers of a single motor unit and, therefore, adapt to variations in form and volume of each muscle according to muscular contraction and intramuscular modifications induced by joint movement.6 Under an electron microscope, it can be seen that each of the myofibers consists of thousands of myofibrils (Fig. 1-1), which extend throughout its length. Myofibrils are composed of sarcomeres arranged in series.2

CLINICAL PEARL

All skeletal muscles exhibit four characteristics: 1. Excitability, the ability to respond to stimulation from the nervous system. 2. Elasticity, the ability to change in length or stretch. The tension developed in skeletal muscle can occur passively (stretch) or actively (contraction). When an activated muscle develops tension, the amount of tension present is constant throughout the length of the muscle, in the tendons, and at the sites of the musculotendinous attachments to bone. The tensile force produced by the muscle pulls on the attached bones and creates torque at the joints crossed by the muscle. The magnitude of the tensile force is dependent on a number of factors. 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.

Myofibril

re

me

rco Sa

Myosin (thick filament) Actin (thin filament)

Tropomyosin Troponin complex

FIGURE 1-2  Troponin and tropomyosin action during a muscle contraction.

Dutton_Ch01_p0001-p0027.indd 9

CLINICAL PEARL The sarcoplasm is the specialized cytoplasm of a muscle cell that contains the usual subcellular elements along with the Golgi apparatus, abundant myofibrils, a modified endoplasmic reticulum known as the sarcoplasmic reticulum (SR), myoglobin, and mitochondria. Transversetubules (T-tubules) invaginate the sarcolemma, allowing impulses to penetrate the cell and activate the SR.

The Musculoskeletal System

The sarcomere (Fig. 1-2) is the contractile machinery of the muscle. The graded contractions of a whole muscle occur because the number of fibers participating in the contraction varies. Increasing the force of movement is achieved by recruiting more cells into cooperative action.

One of the most important roles of CT is to mechanically transmit the forces generated by the skeletal muscle cells to provide movement. Each of the myofibrils contains many fibers called myofilaments, which run parallel to the myofibril axis. The myofilaments are made up of two different proteins: actin (thin myofilaments) and myosin (thick myofilaments) that give skeletal muscle fibers their striated (striped) appearance (Fig. 1-2). The striations are produced by alternating dark (A) and light (I) bands that appear to span the width of the muscle fiber. The A bands are composed of myosin filaments, whereas the I bands are composed of actin filaments. The actin filaments of the I band overlap into the A band, giving the edges of the A band a darker appearance than the central region (H band), which contains only myosin. At the center of each I band is a thin, dark Z line. A sarcomere (Fig. 1-2) represents the distance between each Z line. Each muscle fiber is limited by a cell membrane called a sarcolemma (Fig. 1-1). The protein dystrophin plays an essential role in the mechanical strength and stability of the sarcolemma and is lacking in patients with Duchenne muscular dystrophy.21

Structures called cross-bridges serve to connect the actin and myosin filaments. Increased synthesis of actin and myosin stimulates new myofibrils that are added to the external layers of the preexisting myofibrils.24 The myosin filaments contain two flexible, hinge-like regions, which allow the cross-bridges to attach and detach from the actin filament. During contraction, the cross-bridges attach and undergo power strokes, which provide the contractile force. During relaxation, the cross-bridges detach. This attaching and detaching is asynchronous, so that some are attaching while others are detaching. Thus, at each moment, some of the cross-bridges are pulling, while others are releasing. The regulation of cross-bridge attachment and detachment is a function of two proteins found in the actin filaments: tropomyosin and troponin (Fig. 1-2). Tropomyosin attaches directly to the actin filament, whereas troponin is attached to the tropomyosin rather than directly to the actin filament.

CLINICAL PEARL Tropomyosin and troponin function as the switch for muscle contraction and relaxation. In a relaxed state, the tropomyosin physically blocks the cross-bridges from binding to the actin. For contraction to take place, the tropomyosin must be moved. 9

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At the level of voluntary control, the smallest functional unit that can be activated is the motor unit. A motor unit consists of a single α-motor neuron. The α-motor neurons of the spinal cord (anterior horn cells) are located in the anterior gray matter. When a contraction is initiated in the motor cortex of the brain, a depolarizing electrical current (action potential) is transmitted along the axon of the motor neuron and its branches, and at the neuromuscular junction (NMJ), a neurotransmitter (acetylcholine) is released resulting in the propagation of the action potential along the muscle fiber.25

ANATOMY

CLINICAL PEARL The area of contact between a nerve and muscle fiber is known as the motor end plate, or NMJ. The release of a chemical acetylcholine from the axon terminals at the NMJ causes electrical activation of the skeletal muscle fibers. Action potentials are the signals that relay information along the axons from one structure to another within the nervous system.2 An action potential arises from the temporary reversal of the membrane potential due to an increase in the permeability to sodium.2 When an action potential propagates into the transverse tubule system (narrow membranous tunnels formed from and continuous with the sarcolemma), the voltage sensors on the transverse tubule membrane signal the release of Ca2+ from the terminal cisternae portion of the SR (a series of interconnected sacs and tubes that surround each myofibril).2 The released Ca2+ then diffuses into the sarcomeres 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 of the muscle fibers that it innervates are stimulated and contract with all-or-none twitches. Although the muscle fibers produce all-or-none contractions, muscles are capable of a wide variety of responses, ranging from activities requiring a high level of precision to activities requiring high tension. At the end of the contraction (the neural activity and action potentials cease), the SR actively accumulates Ca2+ and muscle relaxation occurs. The return of Ca2+ to the SR involves active transport, requiring the degradation of adenosine triphosphate (ATP) to adenosine diphosphate (ADP).*,2 Because SR function is closely associated with both contraction and relaxation, changes in its ability to release or sequester Ca2+ markedly affect both the time course and magnitude of force output by the muscle fiber.2,26



TABLE 1-3

Comparison of Muscle Fiber Types

Characteristics

Type I

Type IIa

Type IIx

Size (diameter)

Small

Intermediate

Very large

Resistance to fatigue

High

Fairly high

Low

Capillary density

High

High

Low

Glycogen content

Low

Intermediate

High

Twitch rate

Slow

Fast

Fast

Energy system

Aerobic

Aerobic

Anaerobic

Maximum muscle Slow shortening velocity

Fast

Fast

Major storage fuel

Creatine phosphate glycogen

Creatine phosphate glycogen

Triglycerides

On the basis of their contractile properties, two major types of muscle fiber have been recognized within skeletal muscle based on their resistance to fatigue: type I (tonic, slow-twitch fibers) and type II (phasic fast-twitch fibers). Type II muscle fibers are further divided into two additional classifications (types IIa and IIx [formerly known as IIb and sometimes IId]) (Table 1-3). Type I fibers are richly endowed with mitochondria (and have a high capacity for oxygen uptake). Compared to type II fibers, type I fibers exhibit lower levels of isometric force production per unit area, demonstrate a longer time to contract and relax from a single electrical impulse, and have lower maximal speeds of shortening but are more resistant to fatigue. They are, therefore, suitable for activities of long duration or endurance (aerobic), including the maintenance of posture. In contrast, fast-twitch fibers, which generate a great amount of tension within a short period, are suited to quick, explosive actions (anaerobic), including such activities as sprinting. The type II (fast-twitch) fibers are separated based on mitochondria content into those that have a high complement of mitochondria (type IIa) and a high contractile speed and those that are mitochondria-poor (type IIx) but are the fastest to contract. This results in type IIx fibers having a tendency to fatigue more quickly than type IIa fibers (Table 1-3) but having a higher potential for generating ATP through anaerobic (glycotic) pathways.

CLINICAL PEARL The SR forms a network around the myofibrils, storing and providing the Ca2+ that is required for muscle contraction.

CLINICAL PEARL In fast-twitch fibers, the SR embraces every individual myofibril. In slow-twitch fibers, it may contain multiple myofibrils.

*

10

The most readily available energy for skeletal muscle cells is stored in the form of ATP and phosphocreatine (PCr). Through the activity of the enzyme ATPase, ATP promptly releases energy when required by the cell to perform any type of work, whether it is electrical, chemical, or mechanical.

Dutton_Ch01_p0001-p0027.indd 10

Each muscle comprises a mixture of fiber types. Theory dictates that a muscle with a large percentage of the total

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TABLE 1-4

Functional Division of Muscle Groups Stabilization Group

Primarily type IIa Prone to adaptive shortening Prone to develop hypertonicity Dominate in fatigue and new movement situations Generally cross two joints Examples Gastrocnemius/Soleus Tibialis posterior Short hip adductors Hamstrings Rectus femoris Tensor fascia lata Erector spinae Quadratus lumborum Pectoralis major Upper portion of trapezius Levator scapulae Sternocleidomastoid Scalenes Upper limb flexors

Primarily type I Prone to develop weakness Prone to muscle inhibition Fatigue easily Primarily cross one joint Examples Fibularis (peronei) Tibialis anterior Vastus medialis and lateralis Gluteus maximus, medius, and minimus Serratus anterior Rhomboids Lower portion of trapezius Short/deep cervical flexors Upper limb extensors Rectus abdominis        

 ata from Twomey LT, Taylor JR. Physical Therapy of the Low Back: Clinics in D Physical Therapy. New York, NY: Churchill Livingstone; 1987.

cross-sectional area occupied by slow-twitch type I fibers should be more fatigue resistant than one in which the fast-twitch type II fibers predominate. While there is little evidence of change in the relative proportions of the two fiber types, there is good evidence to show that there is in fact a decrease in the number of type IIx fibers accompanied by an increase in type IIa fibers with resistance training.25 Different activities place differing demands on a muscle (Table 1-4). For example, dynamic movement activities involve a predominance of fast-twitch fiber recruitment, whereas postural activities and those activities requiring stabilization entail more involvement of the slow-twitch fibers. In humans, most limb muscles contain a relatively equal distribution of each muscle fiber type, whereas the back and trunk demonstrate a predominance of slow-twitch fibers. Although it would seem possible that physical training may cause fibers to convert from slow twitch to fast twitch or the reverse, this has not been shown to be the case.25,27 However, fiber conversion from type IIB to type IIA, and vice versa, has been found to occur with training.25 In addition to structural changes during resistance and endurance training, a number of neural adaptations also occur25: ▶▶

Strength training produces (1) an enhanced drive from the higher centers of the brain after resistance training, resulting in the improvement in strength observed; (2) an increased synchronization of the motor units; (3) a decrease in the force threshold at which motor units are

Dutton_Ch01_p0001-p0027.indd 11

The effectiveness of muscle to produce movement depends on some factors. These include the location and orientation of the muscle attachment relative to the joint, the limitations or laxity present in the musculotendinous unit, the type of contraction, the point of application, and the actions of other muscles that cross the joint.

CLINICAL PEARL Following the stimulation of muscle, a brief period elapses before a muscle begins to develop tension. The length of this period, the electromechanical delay (EMD), varies considerably among muscles. Fast-twitch fibers have shorter periods of EMD when compared with slow-twitch fibers.28 EMD is affected by muscle fatigue, muscle length, muscle training, passive muscle stretching, and the type of muscle activation.28 Theoretically, a tissue injury may increase the EMD and, therefore, increase the susceptibility to future injury if full healing does not occur. One of the purposes of neuromuscular reeducation (see Chapter 14) is to return the EMD to a normal level.

The Musculoskeletal System

Movement Group

recruited; (4) an increase in motor unit firing rates; and (5) a decrease in the level of coactivation of antagonistic muscles after training. ▶▶ Endurance training produces (1) a decrease in the motor unit firing rate and (2) a lowering of the recruitment threshold, which improves fatigue resistance.

Muscles serve a variety of roles depending on the required movement: Prime mover (agonist).  This is a muscle that is directly responsible for producing a desired movement. ▶▶ Antagonist.  This is a muscle that has an effect directly opposite to that of the agonist. ▶▶ Synergist (supporter).  This is a muscle that performs a cooperative muscle function relative to the agonist. Synergists can function as stabilizers, neutralizers, or rotators. ■■ Stabilizers (fixators). Muscles that contract statically to steady or support some part of the body against the pull of the contracting muscles, against the pull of gravity, or against the effect of momentum and recoil in certain vigorous movements. ■■ Neutralizers. Muscles that act to prevent an undesired action from one of the movers. ■■ Rotators. A force couple is a pair of forces, equal in magnitude, oppositely directed, and displaced by perpendicular distance or moment. The best example of a force couple that controls rotation occurs at the scapula during arm elevation when the trapezius and serratus anterior contract. The basic function of muscle is to contract. The word contraction, used to describe the generation of tension within muscle fibers, conjures up an image of shortening of muscle fibers during a resistance exercise. However, a contraction ▶▶

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throughout the whole range of its related lever. Isokinetic contractions require the use of special equipment that produces an accommodating resistance. Both highspeed/low-resistance and low-speed/high-resistance regimens result in excellent strength gains.30 The major disadvantage of this type of exercise is its expense. Also, there is the potential for impact loading and incorrect joint axis alignment. Isokinetic exercises may also have questionable functional carryover.

can produce shortening or lengthening of the muscle, or no change in the muscle length. Thus, three types of contraction are commonly recognized: isometric, concentric, and eccentric (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. The strength of a muscle is defined as the force (or torque) generated about the joint during a maximum isometric contraction. ▶▶ Concentric contraction.  A concentric contraction produces a shortening of the muscle. This occurs when the tension generated by the agonist muscle is sufficient to overcome an external resistance and to move the body segment of one attachment toward the segment of its other attachment. Power is the rate at which a muscle does mechanical work and is determined by the product of the force of a contraction and velocity of shortening. ▶▶ Eccentric contraction.  An eccentric contraction occurs when a muscle slowly lengthens as it gives in to an external force that is greater than the contractile force it is exerting. In reality, the muscle does not lengthen, it merely returns from its shortened position to its normal resting length. Eccentric muscle contractions, which are capable of generating greater forces than either isometric or concentric contractions,29 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 filaments during an eccentric contraction, some of the myosin filaments probably are torn from the binding sites on the actin filament, while the remainder are completing the contraction cycle. The resulting force is substantially larger for a torn crossbridge than for one being created during a normal cycle of muscle contraction. Consequently, the combined increase in force per cross-bridge and the number of active crossbridges results in a maximum lengthening muscle tension that is greater than the tension that could be created during a shortening muscle action.29 ▶▶

ANATOMY

▶▶

Econcentric contraction.  This type of contraction, described by the Gray Institute (https://www.grayinstitute. com) and used in most functional movements, combines both a controlled concentric and a simultaneous eccentric contraction of the same muscle over two separate joints. Examples of an econcentric contraction include the standing hamstring curl, in which the hamstrings work concentrically to flex the knee while the hip tends to flex eccentrically, lengthening the hamstrings. When rising from a squat, the hamstrings work concentrically as the hip extends and work eccentrically as the knee extends. Conversely, the rectus femoris work eccentrically as the hip extends and work concentrically as the knee extends.

▶▶

Isolytic contraction.  An isolytic contraction is an osteopathic term used to describe a type of eccentric contraction that makes use of a greater force than the patient can overcome. The difference between an eccentric contraction and an isolytic contraction is that, in the former, the contraction is voluntary, whereas in the latter, it is involuntary. The isolytic contraction can be used in certain manual techniques to stretch fibrotic tissue (see Chapter 10).

As previously mentioned, depending on the type of muscular contraction, the length of a muscle can remain the same (isometric), shorten (concentric), or “lengthen” (eccentric). The rate of muscle length change substantially affects the force that a muscle can develop during contraction. ▶▶

Concentric contractions. The velocity at which muscle contracts significantly affects the tension that the muscle produces and subsequently affects a muscle’s strength and power. As the speed of a concentric contraction increases, the force it is capable of producing decreases. The slower speed of contraction is thought to produce greater forces than can be produced by increasing the number of cross-bridges formed. This relationship is a continuum, with the optimum velocity for the muscle somewhere between the slowest and fastest rates. At very slow speeds, the force that a muscle can resist or overcome rises rapidly up to 50% greater than the maximum isometric contraction.

▶▶

Eccentric contractions. During a maximum-effort eccentric contraction, as the velocity of active muscle “lengthening” increases, force production in the muscle initially increases, but then quickly levels off.31 The following changes in force production occur during an eccentric contraction:

CLINICAL PEARL Both concentric and eccentric muscle actions comprise the type of exercise called isotonic. An isotonic contraction is a contraction in which the tension within the muscle remains constant as the muscle shortens or lengthens. This state is very difficult 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 erroneous because in most exercise forms the muscle tension during exercise varies based upon the weight used, joint velocity, muscle length, and type of muscle contraction. The following three other contractions are worth mentioning: 12

▶▶

Isokinetic contraction.  An isokinetic contraction occurs when a muscle is maximally contracting at the same speed

Dutton_Ch01_p0001-p0027.indd 12

■■

Rapid eccentric contractions generate more force than do slow eccentric contractions.

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■■

During slow eccentric muscle actions, the work produced approximates that of an isometric contraction.

CLINICAL PEARL

▶▶

If the muscle is in a lengthened position compared with its optimum length, the actin filaments are pulled away from the myosin heads such that they cannot create as many cross-bridges. Passive insufficiency of the muscle occurs when the two-joint muscle cannot stretch to the extent required for full ROM in the opposite direction at all joints crossed. For example, when an individual attempts to make a closed fist with the wrist fully flexed, the active shortening of the finger and wrist flexors results in passive lengthening of the finger extensors. In this example, the length of the finger extensors is insufficient to allow full ROM at both the wrist and the fingers.32

The force and speed of a muscle contraction depend on the requirements of the activity, which in turn, are dependent on the ability of the central nervous system to control the recruitment of motor units. The motor units of slow-twitch fibers have lower thresholds and are easier to activate than those of the fast-twitch motor units. Consequently, the slowtwitch fibers are recruited first, even when the resulting limb movement is rapid.2 As the force requirement, speed requirement, or duration of activity increases, motor units with higher thresholds are recruited. Type IIa units are recruited before type IIb.2

CLINICAL PEARL The term temporal summation refers to the summation of individual contractile units. The summation can increase the muscular force by increasing the muscle activation frequency.33

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The Musculoskeletal System

The number of cross-bridges that can be formed is dependent on the extent of the overlap between the actin and myosin filaments. Thus, the force a muscle is capable of exerting depends on its length. For each muscle cell, there is an optimum length, or range of lengths, at which the contractile force is strongest. At the optimum length of the muscle, there is a near-optimal overlap of actin and myosin, allowing for the generation of maximum tension at this length. ▶▶ If the muscle is in a shortened position, the overlap of actin and myosin reduces the number of sites available for the cross-bridge formation. Active insufficiency of a muscle occurs when the muscle is incapable of shortening to the extent required to produce a full range of motion (ROM) at all joints crossed simultaneously. For example, the finger flexors cannot produce a closed fist when the wrist is fully flexed, as they can when it is in neutral position.

Although each muscle contains the contractile machinery to produce the forces for movement, it is the tendon that transmits these forces to the bones to achieve movement or stability of the body in space. The angle of insertion the tendon makes with a bone determines the line of pull, whereas the tension generated by a muscle is a function of its angle of insertion. A muscle generates the greatest amount of torque when its line of pull is oriented at a 90-degree angle to the bone, and it is attached anatomically as far from the joint center as possible.2 Just as there are optimal speeds of length change and optimal muscle lengths, there are optimal insertion angles for each of the muscles. The angle of insertion of a muscle, and therefore its line of pull, can change during dynamic movements. The angle of pennation is the angle created between the fiber direction and the line of pull. When the fibers of a muscle lie parallel to the long axis of the muscle, there is no angle of pennation. The number of fibers within a fixed volume of a muscle increases with the angle of pennation. Although pennation can enhance the maximum tension, the range of shortening of the muscle is reduced. Muscle fibers can contract to about 60% of their resting length. Since the muscle fibers in pennate muscles are shorter than the non-pennate equivalent, the amount of contraction is similarly reduced. Muscles that need to have large changes in length without the need for very high tension, such as the sartorius muscle, do not have pennate muscle fibers. In contrast, pennate muscle fibers are found in those muscles in which the emphasis is on a high capacity for tension generation rather than ROM (e.g., gluteus maximus).

CLINICAL PEARL Skeletal muscle blood flow increases 20-fold during muscle contractions.2 The muscle blood flow increases in proportion to the metabolic demands of the tissue, a relationship reflected by positive correlations between muscle blood flow and exercise. As body temperature elevates, the speeds of nerve and muscle functions increase, resulting in a higher value of maximum isometric tension and a higher maximum velocity of shortening possible with fewer motor units at any given load. Muscle function is most efficient at 38.5°C (101°F).2 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.34 The hydrolysis of ATP to ADP and inorganic phosphate (Pi) provides the power for muscular activity. Despite the large fluctuations in energy demand just mentioned, muscle ATP remains practically constant and demonstrates a remarkable precision of the system in adjusting the rate of the ATP-generating processes to the demand. There are three energy systems that contribute to the resynthesis of ATP via ADP rephosphorylation. These energy systems are as follows: ▶▶

Phosphagen system.  The phosphagen, or ATP-PCr, system is an anaerobic process—it can proceed

13

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ANATOMY

without oxygen (O2). The skeletal muscle cell stores the phosphocreatine (PCr) and ADP, of which PCr is the chemical fuel source. At the onset of muscular contraction, PCr represents the most immediate reserve for the rephosphorylation of ATP. The phosphagen system provides ATP primarily for short-term, high-intensity activities (i.e., sprinting), and it is the major source of energy during the first 30 seconds of intense exercise, but it is also active at the start of all exercises, regardless of intensity.35 Once a muscle returns to rest, the supply of ATP-PCr is replenished. While the maximum power of this system is great, one disadvantage of the phosphagen system is that because of its significant contribution to the energy yield at the onset of near maximal exercise, the concentration of PCr can be reduced to less than 40% of resting levels within 10 seconds of the start of intense exercise, which translates into a small maximum capacity of the system. ▶▶ Glycolytic system.  The glycolytic system is an anaerobic process that involves the breakdown of carbohydrates— either glycogen stored in the muscle or glucose delivered through the blood—into pyruvate to produce ATP in a process called glycolysis. Pyruvate is then transformed into lactic acid as a by-product of the anaerobic glycolysis. Because this system relies on a series of nine different chemical reactions, it is slower to become fully active. However, glycogenolysis has a greater capacity to provide energy than does PCr, and therefore it supplements PCr during maximal exercise and continues to rephosphorylate ADP during maximal exercise after PCr reserves have become essentially depleted.35 In essence, this system is the major source of energy from the 30th to 90th second of exercise. The process of glycolysis can be in one of two ways, termed fast glycolysis and slow glycolysis, depending on the energy demands within the cell. If energy must be supplied at a high rate, fast glycolysis is used primarily. If the energy demand is not so high, slow glycolysis is activated. The main disadvantage of the fast glycolysis system is that during very high-intensity exercise, hydrogen ions dissociate from the glycogenolytic end product of lactic acid. The accumulation of 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 interfere with muscle excitation–contraction and coupling, which can potentially impair contractile force during an exercise.35 This inhibition occurs once the muscle pH drops below a certain level, prompting the appearance of phosphofructokinase (PFK), resulting in local energy production ceasing until replenished by oxygen stores.

CLINICAL PEARL Lactic acid is the major energy source for providing the muscle with ATP during exercise bouts that last 1–3 minutes (e.g., running 400–800 m). 14

Dutton_Ch01_p0001-p0027.indd 14

▶▶

Oxidative system.  As its name suggests, the oxidative system requires O2 and is consequently termed the “aerobic” system. The fuel sources for this system are glycogen, fats, and proteins. This system is the primary source of ATP at rest and during low-intensity activities. The ATP is resynthesized in the mitochondria of the muscle cell such that the ability to metabolize oxygen and other substrates is related to the number and concentration of the mitochondria in cells. It is worth noting that at no time during either rest or exercise does any single energy system provide the complete supply of energy. While being unable to produce ATP at an equivalent rate to that produced by PCr breakdown and glycogenolysis, the oxidative system is capable of sustaining low-intensity exercise for several hours.35 However, because of increased complexity, the time between the onset of exercise and when this system is operating at its full potential is around 45 seconds.36

The relative contribution of these energy systems to ATP resynthesis has been shown to depend upon the intensity and duration of exercise, with the primary system used being based on the duration of the event37: 0–10 seconds: ATP–PCr. These bursts of activity develop muscle strength and stronger tendons and ligaments, with the ATP being supplied by the phosphagen system. ▶▶ 10–30 seconds: ATP–PCr plus anaerobic glycolysis. ▶▶ 30 seconds to 2 minutes: Anaerobic glycolysis. These longer bursts of activity, if repeated after 4 minutes of rest or mild exercise, enhance anaerobic power with the ATP being supplied by the phosphagen and anaerobic glycolytic system. ▶▶ 2–3 minutes: Anaerobic glycolysis plus oxidative system. ▶▶ More than 3 minutes and rest: oxidative system. These periods of activity using less than maximum intensity may develop aerobic power and endurance capabilities, and the phosphagen, anaerobic glycolytic, and anaerobic systems supply the ATP. ▶▶

Respiratory Muscles Although the respiratory muscles share some mechanical similarities with skeletal muscles, they are distinct from skeletal muscles in several aspects as follows2: Whereas skeletal muscles of the limbs overcome inertial loads, the respiratory muscles overcome primarily elastic and resistive loads. ▶▶ The respiratory muscles are under both voluntary and involuntary control. ▶▶ The respiratory muscles are similar to the heart muscles, in that they have to contract rhythmically and generate the required forces for ventilation throughout the entire lifespan of the individual. The respiratory muscles, however, unlike the cardiac muscles, do not contain pacemaker cells and are under the control of mechanical and chemical stimuli, requiring neural input from higher centers to initiate and coordinate contraction. ▶▶

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▶▶

CLINICAL PEARL The primary respiratory muscles of the body include the diaphragm; the internal, external, and transverse intercostals; the levator costae; and the serratus posterior inferior and superior.

JOINTS Arthrology is the study of the classification, structure, and function of articulations (joints or arthroses). A joint represents the junction between two or more bones. Joints are regions where bones are capped and surrounded by CTs that hold the bones together and determine the type and degree of movement between them.38 An understanding of the anatomy and biomechanics of the various joints is required to be able to assess and treat a patient thoroughly. When classified according to movement potential, joints may be classified into two broad categories: synarthrosis (nonsynovial) and diarthrosis (synovial).

Synarthrosis The type of tissue uniting the bone surfaces determines the major types of synarthroses38: ▶▶

Fibrous joints, which are joined by dense fibrous CT. The following three types exist: ■■ Suture (e.g., suture of the skull). ■■ Gomphosis (e.g., tooth and mandible or maxilla articulation). ■■ Syndesmosis (e.g., tibiofibular or radioulnar joints). These joints usually allow a small amount of motion.

▶▶

Cartilaginous joints, originally referred to as amphiarthrosis joints, are stable joints that allow for minimal or little movement. These joints exist in humans in one of 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.39 In a symphysis joint, the two bony components are covered with a thin lamina of hyaline cartilage and directly joined by fibrocartilage in the form of disks or pads.39

Diarthrosis This joint unites long bones and permits free bone movement and greater mobility. A fibroelastic joint capsule, which characterizes these joints, is filled with a lubricating substance called synovial fluid. Consequently, these joints are often referred to as synovial joints. Examples include, but are not limited to, the hip, knee, shoulder, and elbow joints. Synovial joints are further classified based on complexity: Simple (uniaxial): A single pair of articular surfaces one male, or convex, surface and one female, or concave, surface. Examples include hinge joint and trochoid (pivot) joints. ▶▶ Compound (biaxial): A single joint capsule that contains more than a single pair of mating articulating surfaces. The two types of biaxial joint in the body include the condyloid and saddle. ▶▶ Complex (triaxial or multiaxial): Contain an intraarticular inclusion within the joint class such as a meniscus or disk that increases the number of joint surfaces. The two types of joint in this category are plane joints and ball and socket joints. ▶▶

Synovial joints have five distinguishing characteristics: a joint cavity that is enclosed by the joint capsule, hyaline articular cartilage that covers the surfaces of the enclosed contiguous bones, synovial fluid that forms a film over the joint surfaces, synovial membrane that lines the inner surface of the capsule, and a joint capsule that is composed of two layers.39 All synovial joints of the body are provided with an array of corpuscular (mechanoreceptors) and noncorpuscular (nociceptors) receptor endings embedded in articular, muscular, and cutaneous structures with varying characteristic behaviors and distributions depending on the articular tissue (see Chapter 3). One intra-articular structure worth mentioning is the articular disk or meniscus. The term meniscus should be reserved for incomplete disks like those in the knee joint and occasionally the acromioclavicular joint. A meniscus, which consists of a dense ECM, is not covered by a synovial membrane and occurs between articular surfaces where congruity is low. The cells of the meniscus are referred to as fibrochondrocytes because they appear to be a mixture of fibroblasts and chondrocytes.40,41 A meniscal disk may extend across a synovial joint, dividing it structurally and functionally into two synovial cavities. Complete disks occur in the sternoclavicular and distal radioulnar joints, while that in the temporomandibular joint may be complete or incomplete.2 Peripherally disks are connected to fibrous capsules, usually by vascularized CT, so that they become invaded by vessels and afferent and motor nerves.2 Mechanoreceptors within the menisci function as transducers, converting the physical stimulus of tension and compression into a specific electrical nerve impulse (see Chapter 3).42 Synovial joints can be broadly classified according to structure or analogy (Fig. 1-3) into the following categories: ▶▶

The Musculoskeletal System

The resting length of the respiratory muscles is a relationship between the inward recoil forces of the lung and the outward recoil forces of the chest wall. Changes in the balance of recoil forces will result in changes in the resting length of the respiratory muscles. Thus, theoretically, simple and everyday life occurrences such as changes in posture may alter the operational length and the contractile strength of the respiratory muscles. If uncompensated, these length changes can potentially lead to decreases in the output of the muscles, and hence, a reduction in the ability to generate lung volume changes. The skeletal muscles of the limbs, on the other hand, are not constrained to operate at a particular resting length.

Spheroid. As the name suggests, a spheroid joint is a freely moving joint in which a sphere on the head of one bone fits into a rounded cavity in the other bone. Spheroid 15

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Head of humerus

Scapula

Radius

Ulna Pivot joint

Ball-and-socket

ANATOMY

Humerus

Ulna

Carpals Gliding joint Hinge joint Metacarpal

Carpal

Metacarpal Condyloid joint

Saddle joint

Phalanx FIGURE 1-3  Types of diarthrosis or synovial joints.

16

(ball and socket) joints allow motions in three planes (Fig. 1-3). Examples of a spheroid joint surface include the heads of the femur and humerus. ▶▶ Ellipsoid. Ellipsoid joints are similar to spheroid joints in that they allow the same type of movement albeit to a lesser magnitude. The ellipsoid joint allows movement in two planes (flexion, extension; abduction, adduction) and is biaxial. Examples of this joint can be found at the radiocarpal articulation at the wrist and the metacarpophalangeal articulation with the phalanges. ▶▶ Trochoid. The trochoid, or pivot, joint is characterized by a pivot-like process turning within a ring, or a ring on a pivot, the ring being formed partly of bone, partly of ligament (Fig. 1-3). Trochoid joints permit only rotation. Examples of a trochoid joint include the humeroradial joint and the atlantoaxial joint. ▶▶ Condyloid (ovoid). This joint is characterized by an ovoid articular surface, or condyle (Fig. 1-3). One bone may articulate with another by one surface or by two, but never

Dutton_Ch01_p0001-p0027.indd 16

more than two. If two distinct surfaces are present, the joint is called condylar or bicondylar. The elliptical cavity of the joint is designed in such a manner as to permit the motions of flexion, extension, adduction, abduction, and circumduction, but no axial rotation. The wrist joint is an example of this form of articulation. ▶▶ Ginglymoid. A ginglymoid joint is a hinge joint (Fig. 1-3). It is characterized by a spool-like surface and a concave surface. An example of a ginglymoid joint is the humeroulnar joint. ▶▶ Planar. As its name suggests, a planar joint is characterized by flat surfaces that slide over each other. Movement at this joint does not occur about an axis and is termed nonaxial. Examples of a planar joint include the intermetatarsal joints and some intercarpal joints. ▶▶ Saddle (sellar). Saddle joints are characterized by a convex surface in one cross-sectional plane and a concave surface in the plane perpendicular to it (Fig. 1-3). Examples of a saddle joint include the interphalangeal joints, the

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carpometacarpal joint of the thumb, the humeroulnar joint, and the calcaneocuboid joints. In reality, no joint surface is planar or resembles a true geometric form. Instead, joint surfaces are either convex in all directions or concave in all directions; that is, they resemble either the outer or inner surface of a piece of eggshell.

Synovial Fluid

KINESIOLOGY When describing movements, it is necessary to have a starting position as the reference position. This starting position is referred to as the anatomic reference position. The anatomic reference position for the human body is described as the erect standing position with the feet just slightly separated and the arms hanging by the side, the elbows straight, and the palms of the hand facing forward (Fig. 1-4).

Directional Terms Directional terms are used to describe the relationship of body parts or the location of an external object with respect to the body. The following are commonly used directional terms: Superior or cranial.  Closer to the head. ▶▶ Inferior or caudal.  Closer to the feet. ▶▶

Anterior or ventral.  Toward the front of the body. Posterior or dorsal.  Toward the back of the body. ▶▶ Medial.  Toward the midline of the body. ▶▶ Lateral.  Away from the midline of the body. ▶▶ Proximal.  Closer to the trunk. ▶▶ Distal.  Away from the trunk. ▶▶ Superficial.  Toward the surface of the body. ▶▶ Deep.  Away from the surface of the body in the direction of the inside of the body. ▶▶

CLINICAL PEARL Hyaluronan is a critical constituent component of normal synovial fluid and an important contributor to joint homeostasis. Hyaluronan imparts antiinflammatory and antinociceptive properties to normal synovial fluid and contributes to joint lubrication. It also is responsible for the viscoelastic properties of synovial fluid and contributes to the lubrication of articular cartilage surfaces.46

▶▶

The Musculoskeletal System

Articular cartilage is subject to a great variation of loading conditions, so joint lubrication through the synovial fluid is necessary to minimize frictional resistance between the weight-bearing surfaces. Fortunately, synovial joints are blessed with a very superior lubricating system, which permits a remarkably frictionless interaction at the joint surfaces. A cartilaginous lubricated interface has a coefficient of friction* of 0.002.43–45 By way of comparison, ice on ice has a higher coefficient of friction (0.03). The composition of synovial fluid is nearly the same as blood plasma, but with a decreased total protein content and a higher concentration of hyaluronan.43

A bursa can be a source of pain if it becomes inflamed or infected.

Indeed, synovial fluid is essentially a dialysate of plasma to which hyaluronan has been added.43 Hyaluronan is a GAG that is continually synthesized and released into the synovial fluid by specialized synoviocytes.47,48 The mechanical properties of synovial fluid permit it to act as both a cushion and a lubricant to the joint. Diseases, such as osteoarthritis, affect the thixotropic properties (thixotropy is the property of various gels becoming fluid when disturbed, as by shaking) of synovial fluid, resulting in reduced lubrication and subsequent wear of the articular cartilage and joint surfaces.43 It is well established that damaged articular cartilage in adults has a very limited potential for healing (see Chapter 2) because it possesses neither a blood supply nor lymphatic drainage.43

Bursae Closely associated with some synovial joints are flattened, saclike structures called bursae that are lined with a synovial membrane and filled with synovial fluid. The bursa produces small amounts of fluid, allowing for smooth and almost frictionless motion between contiguous muscles, tendons, bones, ligaments, and skin. A tendon sheath is a modified bursa. *

Coefficient of friction is a ratio of the force needed to make a body glide across a surface compared with the weight or force holding the two surfaces in contact.

Dutton_Ch01_p0001-p0027.indd 17

FIGURE 1-4  The anatomical position.

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MOVEMENTS OF THE BODY SEGMENTS In general, there are two types of motions: translation, which occurs in either a straight or curved line, and rotation, which involves a circular motion around a pivot point. Movements of the body segments occur in three dimensions along imaginary planes and around various axes of the body.

ANATOMY

Planes of the Body There are three traditional planes of the body corresponding to the three dimensions of space: sagittal, frontal, and transverse (Fig. 1-5). Sagittal.  The sagittal plane, also known as the anteriorposterior or median plane, divides the body vertically into left and right halves of equal size. ▶▶ Frontal.  The frontal plane, also known as the lateral or coronal plane, divides the body equally into front and back halves. ▶▶

ne

Frontal pla

▶▶

Transverse.  The transverse plane, also known as the horizontal plane, divides the body equally into top and bottom halves.

Because each of these planes bisects the body, it follows that each plane must pass through the center of gravity (COG) or center of mass (COM).* Every object or segment can be considered to have a single COG or COM—the point at which all the mass of the object or segment appears to be concentrated. In a symmetrical object, the COG is always located in the geometric center of the object. However, in an asymmetrical object such as the human body, the COG becomes the point at which the line of gravity balances the object. The line of gravity can best be visualized as a string with the weight on the end (a plumb-line), with a string attached to the COG of an object.49 If the human body is considered as a rigid object, the COG of the body lies approximately anterior to the second sacral vertebra (S2). Since the human body is not rigid, an individual’s COG continues to change with movement with the amount of change in the location depending on how disproportionately the segments are rearranged.49 The base of support (BOS) includes the part of the body in contact with the supporting surface and the intervening area. For example, during static standing, the BOS is between the individual’s feet. However, if an individual bends forward at the waist, the line of gravity moves outside of the BOS. The size of the BOS and its relation to the COG are important factors in the maintenance of balance and, thus, the stability of an object. The COG must be maintained over the BOS if an equilibrium is to be maintained. If the BOS of an object is large, the line of gravity is less likely to be displaced outside the BOS, which makes the object more stable.49

CLINICAL PEARL

Transvers e

If a movement described occurs in a plane that passes through the COG, that movement is deemed to have occurred in a cardinal plane. An arc of motion represents the total number of degrees traced between the two extreme positions of movement in a specific plane of motion.50 If a joint has more than one plane of motion, each type of motion is referred to as a unit of motion. For example, the wrist has two units of motion: flexion–extension and ulnar–radial deviation.50 Few movements involved with functional activities occur in the cardinal planes. Instead, most movements occur in an infinite number of vertical and horizontal planes parallel to the cardinal planes (see the discussion that follows).

plane

Axes of the Body Three reference axes are used to describe human motion: frontal, sagittal, and longitudinal (Fig. 1-6). The axis around which the movement takes place is always perpendicular to the plane in which it occurs. itta

ne l pla

Sag

18

FIGURE 1-5  Planes of the body.

Dutton_Ch01_p0001-p0027.indd 18

*

The center of gravity (COG), or center of mass (COM), may be defined as the point at which the three planes of the body intersect each other. The line of gravity is defined as the vertical line at which the two vertical planes intersect each other and is always vertically downward toward the center of the earth.

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Flexion, extension, hyperextension, dorsiflexion, and plantar flexion occur in the sagittal plane around an ML axis. Exceptions to this include carpometacarpal flexion and extension of the thumb. ▶▶ Abduction and adduction, side flexion of the trunk, elevation and depression of the shoulder girdle, radial and ulnar deviation of the wrist, and eversion and inversion of the foot occur in the frontal plane around an AP axis. ▶▶ Rotation of the head, neck, and trunk; internal rotation and external rotation of the arm or leg; horizontal adduction and abduction of the arm or thigh; and pronation and supination of the forearm usually occur in the transverse plane around the vertical axis. Rotary motions involve the curved movement of a segment around a fixed axis, or center of rotation. When a curved movement occurs around an axis that is not fixed, but instead shifts in space as the object moves, the axis around which the segment appears to move is referred to as the instantaneous axis of rotation or instantaneous center of rotation (ICR) (see Moment Arm). ▶▶ Arm circling and trunk circling are examples of circumduction. Circumduction involves an orderly sequence of circular movements that occur in the sagittal, frontal, and intermediate oblique planes, so that the segment as a whole incorporates a combination of flexion, extension, abduction, and adduction. Circumduction movements can occur at biaxial and triaxial joints. Examples of these joints include the tibiofemoral, radiohumeral, hip, glenohumeral, and the spinal joints. ▶▶

Vertical axis AP axis ML axis

The Musculoskeletal System

FIGURE 1-6  Axes of the body.

Both the configuration of a joint and the line of pull of the muscle acting at a joint determine the motion that occurs at a joint: A muscle whose line of pull is lateral to the joint is a potential abductor. ▶▶ A muscle whose line of pull is medial to the joint is a potential adductor. ▶▶ A muscle whose line of pull is anterior to a joint has the potential to extend or flex the joint. At the knee, an anterior line of pull may cause the knee to extend, whereas at the elbow joint, an anterior line of pull may cause flexion of the elbow. ▶▶ A muscle whose line of pull is posterior to the joint has the potential to extend or flex a joint (refer to preceding example). ▶▶

Mediolateral.  The mediolateral (ML), or frontal, axis passes horizontally from left to right and is formed by the intersection of the frontal and transverse planes. ▶▶ Vertical.  The vertical, or longitudinal, axis passes vertically from inferior to superior and is formed by the intersection of the sagittal and frontal planes. ▶▶ Anteroposterior.  The anteroposterior (AP), or sagittal, axis passes horizontally from anterior to posterior and is formed by the intersection of the sagittal and transverse planes. ▶▶

Most movements occur in planes and around axes that are somewhere in between the traditional planes and axes. Thus, nominal identification of every plane and axis of movement is impractical. The structure of the joint determines the possible axes of motion that are available. For example, at the humeroulnar joint, a hinge joint, flexion–extension occurs in sagittal plane about a frontal axis. At a ball-and-socket joint, abduction–adduction occurs in the frontal plane about a sagittal axis. The axis of rotation remains stationary only if the convex member of a joint is a perfect sphere and articulates with a perfect reciprocally shaped concave member. The planes and axes for the more common planar movements (Fig. 1-7) are as follows:

Dutton_Ch01_p0001-p0027.indd 19

Degrees of Freedom The number of degrees of freedom (DOF) is equal to the total number of independent displacements or aspects of motion of an object. At a joint, the DOF refers to the number of independent modes of motion available. A joint can have up to 3 degrees of angular freedom, corresponding to the number of available swings in the three dimensions of space. For example, if a joint can only swing in one direction or can only spin, it is said to have 1 DOF. The proximal interphalangeal joint and the humeroulnar joint are examples of a joint with 1 DOF. If a joint can spin and swing in one way only, or it can

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Cervical extension

Cervical flexion

Elbow flexion Shoulder abduction

Shoulder extension

Shoulder flexion

Elbow extension

ANATOMY

Hip flexion

Shoulder adduction Finger flexion

Shoulder circumduction

Knee flexion

Finger extension

Knee flexion Hip extension

Knee extension

A

Ankle dorsal flexion

Hip abduction

Ankle plantar flexion

Hip adduction Hip circumduction

B

Cervical lateral side bending Shoulder internal rotation Forearm pronation Forearm supination

Shoulder external rotation

Wrist extension

Wrist flexion

Wrist adduction

Wrist abduction

Foot and ankle inversion Foot and ankle eversion

C

Hip internal rotation

Hip external rotation

FIGURE 1-7  Movements of the body. A: Motions that occur in a sagittal plane about a frontal axis. B: Motions that occur in a frontal plane about a sagittal axis. C: Motions that occur in the transverse plane.

20

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swing in two completely distinct ways, but not spin, it is said to have 2 DOF. The tibiofemoral joint, temporomandibular joint, proximal and distal radioulnar joints, subtalar joint, and talocalcaneal joint are examples of joints with 2 DOF. If the bone can spin and also swing in two distinct directions, then it is said to have 3 DOF. Ball-and-socket joints, such as the shoulder and hip, have 3 DOF.

control in joints with 3 DOF. In joints with fewer than 3 DOF, the conjunct rotation occurs as part of the movement but is not under voluntary control. The implications for this become important when attempting to restore motion at these joints: the mobilizing techniques must take into consideration both the relative shapes of the articulating surfaces and the conjunct rotation that is associated with a particular motion (see Chapter 10).

CLINICAL PEARL

Because of the arrangement of the articulating surfaces— 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. This can best be illustrated using Codman’s paradox. 1. Stand with your arms by your side, palms facing inward, thumbs extended. Notice that the thumb is pointing forward. 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 position of 90 degrees of 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 from your thigh. Referring to the start position, and using the thumb as the reference, the arm has undergone an external rotation of 90 degrees. But where and when did the rotation take place? Undoubtedly, it occurred during the three separate, straightplane motions or swings that etched a triangle in space. What you have just witnessed is an example of a conjunct rotation— a rotation that occurs as a result of joint surface shapes—and the effect of inert tissues rather than contractile 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 of elbow flexion and extension. While fully flexing and extending your elbow a few times, watch the pisiform bone and forearm. If you watch carefully, you should notice that the pisiform and the forearm move in a direction of supination during flexion, and pronation during extension of the elbow. The pronation and supination motions are examples of conjunct rotations. Most habitual movements, or those movements that occur most frequently at a joint, involve a conjunct rotation. However, the conjunct rotations are not always under volitional control. In fact, the conjunct rotation is only under volitional

Dutton_Ch01_p0001-p0027.indd 21

JOINT KINEMATICS Kinematics is the study of motion and describes how something is moving without stating the cause. Kinetics is the term used to explain why an object moves the way it does due to the forces acting on that object (see Chapter 2). In studying joint kinematics, two major types of motion are involved: (1) osteokinematic and (2) arthrokinematic.

Osteokinematic Motion The normal ROM of a joint is sometimes called the physiologic or anatomic ROM. Physiologic movements of the bones termed osteokinematics are movements that can be performed voluntarily, for example, flexion of the shoulder. Osteokinematic motion occurs when any object forms the radius of an imaginary circle about a fixed point. The axis of rotation for osteokinematic motions is oriented perpendicular to the plane in which the rotation occurs. The 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 osteokinematic motions. Examples of osteokinematic motion include abduction or adduction of the arm, flexion of the hip or knee, and side bending of the trunk. A number of factors determine the amount of available physiologic joint motion, including

The Musculoskeletal System

Joint swing that occurs only in one plane is designated as having 1 DOF; in two planes, 2 DOF; and in three planes, 3 DOF. When including accessory motions (see Joint Kinematics), certain joints, such as the intervertebral joint, are free to move with 6 DOF—anterior/posterior glides, superior/inferior glides, and translational glides to the left/right, in addition to the available joint swings about the three axes of rotation.

the integrity of the joint surfaces and the amount of joint motion; ▶▶ the mobility and pliability of the soft tissues that surround a joint; ▶▶ the degree of soft-tissue approximation that occurs; ▶▶ the amount of scarring or adhesions that are present— interstitial scarring or fibrosis can occur in and around the joint capsules, within the muscles, and within the ligaments as a result of previous trauma; ▶▶ age—joint motion tends to decrease with increasing age due mainly to osteoarthritic changes; and ▶▶ gender—in general, females have more joint motion than males. ▶▶

ROM is considered to be pathological when motion at a joint either exceeds or fails to reach the normal physiologic limits of motion (see Chapter 2).39

Moment Arm To understand the concept of a moment arm, an understanding of the anatomy and movement (kinematics) of the joint

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ANATOMY

of interest is necessary. Although muscles produce linear forces, motions at joints are all rotary. For example, some joints can be considered to rotate about a fixed point. A good example of such a joint is the elbow. At the elbow joint, where the humerus and ulna articulate, the resulting rotation occurs primarily about a fixed point, referred to as the COR. In the case of the elbow joint, this COR is relatively constant throughout the joint ROM. However, in other joints (e.g., the knee) the COR moves through space as the knee joint flexes and extends because the articulating surfaces are not perfect circles. In the case of the knee, it is not appropriate to discuss a single COR—rather we must speak of a COR corresponding to a particular joint angle, or, using the terminology of joint kinematics, we must speak of the ICR, that is, the COR at any “instant” in time or space. Thus, the moment arm is defined as the perpendicular distance from the line of force application to the axis of rotation.

directly proportional to each other, with a small increment of arthrokinematic motion resulting in a larger increment of osteokinematic motion. Thus, a restriction of arthrokinematic motion results in a decrease in osteokinematic motion. A normal joint has an available range of active, or physiologic, motion, which is limited by a physiologic barrier as tension develops within the surrounding tissues, such as the joint capsule, ligaments, and CT. Beyond the available passive ROM, the anatomic barrier is found. This barrier cannot be exceeded without disruption to the integrity of the joint. At the physiologic barrier, there is an additional amount of passive ROM available. This small motion, which occurs at the joint surfaces, is referred to as joint-play motion. Three fundamental types of joint-play motions exist based on the different types of joint surfaces (Fig. 1-8): ▶▶

Arthrokinematic Motion At each synovial articulation, the articulating surface of each bone moves in relation to the shape of the other articulating surface. The term arthrokinematics is used to describe the motions of the bone surfaces within the joint. The type and amount of motion occurring at the joint surfaces is influenced by the shape of their respective joint surfaces. Arthrokinematic movements cannot be performed 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 or accessory (arthrokinematic) motions occur simultaneously during movement and are

A

Roll.  A roll occurs when the points of contact on each incongruent joint surface are constantly changing so that new point on one surface meets a new point on the opposite surface (see Fig. 1-8). This type of movement is analogous to a tire on a car as the car rolls forward. In a normal functioning joint, pure rolling does not occur alone but instead occurs in combination with joint sliding and spinning. The term rock is often used to describe small rolling motions. Rolling is always in the same direction as the swinging bone motion irrespective of whether the surface is convex or concave (Fig. 1-8). If the rolling occurs alone, it causes compression of the surfaces on the side to which the bone is swinging and separation on the other side.

B Extension Spin Femur stationary

Roll

Slide

Roll and slide Tibia stationary

22

Dutton_Ch01_p0001-p0027.indd 22

Spin

Extension

FIGURE 1-8  Arthrokinematics of motion.

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A ion mot ne Bo

i Joint gl

Stationary

de

n Re

s tr ic ti o

surface Join t

Stationary

FIGURE 1-9  Gliding motions according to joint surfaces.

Slide.  A slide is a pure translation if the two surfaces are congruently flat or curved. It occurs if only one point on the moving surface makes contact with new points on the opposing surface (see Fig. 1-8). This type of movement is analogous to a car tire skidding when the brakes are applied suddenly on a wet road. This type of motion also is referred to as translatory motion. Although the roll of a joint always occurs in the same direction as the swing of a bone, the direction of the slide is determined by the shape of the articulating surface (Fig. 1-9). This rule is often referred to as the concave–convex rule: if the joint surface is convex relative to the other surface, the slide occurs in the opposite direction to the osteokinematic motion (see Fig. 1-9). If, on the other hand, the joint surface is concave, the slide occurs in the same direction as the osteokinematic motion (see Fig. 1-9). The clinical significance of the concave–convex rule is described in Chapter 10. ▶▶ Spin.  A spin is defined as any movement in which the bone moves, but the mechanical axis remains stationary. A spin involves a rotation of one surface on an opposing surface around a vertical axis (see Fig. 1-8). This type of motion is analogous to the pirouette performed by a ballet dancer. Spinning rarely occurs alone in joints but instead occurs in combination with rolling and sliding. Spin motions in the body include internal and external rotation of the glenohumeral joint when the humerus is abducted to 90 degrees; and at the radial head during forearm pronation and supination. ▶▶

Most anatomic joints demonstrate composite motions involving a roll, slide, and spin. As osteokinematic and arthrokinematic motions are proportional to each other, such that one cannot occur completely without the other, it follows that if an active motion

Dutton_Ch01_p0001-p0027.indd 23

CLINICAL PEARL Two other accessory motions are used by clinicians in various 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 fluid and maintain cartilage health. ▶▶ Distraction. This involves an increase in the joint space between bony partners. The terms traction and distraction are not synonymous, as the former involves a force applied to the long axis of a bone, which does not always result in the joint space increasing between the bony partners. For example, if traction is applied to the shaft of the femur, it results in a glide occurring at the hip joint surface, whereas if a distraction force is applied at right angles to the acetabulum, distraction at the hip joint occurs.

In the extremities, osteokinematic motion is controlled by the amount of flexibility of the surrounding soft tissues of the joint, where flexibility is measured as the amount of internal resistance to motion. In contrast, the arthrokinematic motion is controlled by the integrity of the joint surfaces and the supporting tissues of the joint. This characteristic can be noted clinically in a chronic rupture of the anterior cruciate ligament of the knee. Upon examination of that knee, the arthrokinematic motion (joint slide or glide) is found to be increased, illustrated by a positive Lachman test, but the ROM of the knee, its osteokinematic motion, is not affected (see Chapter 20). In contrast, in the spine, the osteokinematic motion is controlled by both the flexibility of the surrounding soft tissues and by the integrity of the joint surfaces and the supporting tissues of the joint. This 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 suboccipital muscle (see Chapter 23). The examination of these motions and their clinical implications are described in Chapters 4 and 10.

The Musculoskeletal System

B

is decreased compared to the same joint on the other side of the body, one or both of these motions may be at fault. 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 specific as possible. This is particularly important when trying to regain motion using traditional stretching methods (which employ osteokinematic motions) in the presence of a restricted arthrokinematic motion, as these methods magnify the force at the joint and cause compression of the joint surfaces in the direction of the rolling bone. In contrast, using an arthrokinematic technique to increase the joint play allows the force to be applied close to the joint surface and in the direction that replicates the sliding component of the joint mechanics.

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Levers A lever is a rigid object that is used to either multiply the mechanical force (effort) or resistance force (load) applied to it around an axis. The effort force attempts to cause movement of the load. For simplicity sake, levers are usually described using a straight bar, which is the lever, and the fulcrum, which is the point on which the bar is resting and around which the lever rotates. That part of the lever between the fulcrum and the load is referred to as the load arm. Three types of levers are commonly cited:

ANATOMY

First-class: It occurs when two forces are applied on either side of the axis, and the fulcrum lies between the effort and the load (Fig. 1-10), like a seesaw. Examples in the human body include the contraction of the triceps at the elbow joint, or tipping of the head forward and backward. ▶▶ Second-class: It occurs when the load (resistance) is applied between the fulcrum and the point where the effort is exerted (Fig. 1-10). The magnifying effects of the effort require less force to move the resistance. Examples of second-class levers in everyday life include the nutcracker, and the wheelbarrow—with the wheel acting as the fulcrum. Examples of second-class levers in the human body include weight-bearing plantarflexion (rising up on the toes) (Fig. 1-10). Another would be an isolated contraction of the brachioradialis to flex the elbow, which could only occur if the other elbow flexors are paralyzed. ▶▶ Third class: It occurs when the load is located at the end of the lever (Fig. 1-10), and the effort lies between the fulcrum and the load, like a drawbridge or a crane. The effort is exerted between the load and the fulcrum. The effort expended is greater than the load, but the load is moved a greater distance. Most movable joints in the human body function as third-class levers—flexion at the elbow. ▶▶

When a machine puts out more force than is put in, the machine is said to have a mechanical advantage (MA). The MA of the musculoskeletal lever is defined as the ratio of the internal moment arm to the external moment arm. Depending on the location of the axis of rotation, the first-class lever can have an MA equal to, less than, or greater than 1.51 Second-class levers always have an MA greater than 1. Thirdclass levers always have an MA less than 1. The majority of muscles throughout the musculoskeletal system function with an MA of much less than 1. Therefore, the muscles and underlying joints must “pay the price” by generating and dispersing relative large forces, respectively, even for seemingly low-load activities.51

KINEMATIC CHAINS When a body moves, it does so by its kinematics, which in the human body takes place through arthrokinematic and osteokinematic movements. The expression kinematic chain is used in rehabilitation to describe the function or activity of an extremity or trunk in terms of a series of linked chains (see Chapter 12). A kinematic chain refers to a series of articulated, segmented links, such as the connected pelvis, thigh, leg, and foot of the lower extremity.52 According to kinematic chain theory, each of the joint segments of the body involved in a particular movement constitutes a link in the kinematic chain. Because each motion of a joint is often a function of other joint motions, the efficiency of an activity can be dependent on how well these chain-links work together.

CLINICAL PEARL The number of links within a particular kinematic chain varies, depending on the activity. In general, longer kinematic chains are involved with more strenuous activities.

Effort

Effort

Fulcrum

Load

Load

Effort

Fulcrum Fulcrum

A First-class lever 24

Dutton_Ch01_p0001-p0027.indd 24

B Second-class lever

Load

C Third-class lever

FIGURE 1-10  The three classes of levers.

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TABLE 1-5

Differential Features of OKC and CKC Exercises Characteristics

Advantages

Disadvantages

Open kinematic chain      

1.  Single muscle group 2.  Single axis and plane 3.  Emphasizes concentric contraction 4. Non–weight-bearing

1.  Isolated recruitment 2.  Simple movement pattern 3.  Isolated recruitment 4.  Minimal joint compression

1.  Limited function 2.  Limited function 3.  Limited eccentrics 4.  Less proprioception and joint stability with increased joint shear forces

Closed kinematic    

1.  Multiple muscle groups 2.  Multiple axes and planes 3.  Balance of concentric and eccentric contractions 4.  Weight-bearing exercise

1.  Functional recruitment 2.  Functional movement patterns 3.  Functional contractions 4.  Increased proprioception and joint stability

1.  Difficult to isolate 2.  More complex 3.  Loss of control of target joint 4. Compressive forces on articular surfaces

 

 eproduced with permission from Greenfield BH, Tovin BJ. The application of open and closed kinematic chain exercises in rehabilitation of the lower extremity. R J Back Musculoskelet Rehabil. 1992 Jan 1;2(4):38–51.

Two types of kinematic chain systems are recognized: closed kinematic chain (CKC) system and the open kinematic chain (OKC) system (Table 1-5).

Closed Kinematic Chain A CKC activity can be defined as any movement if both ends of the kinetic chain are connected to an immovable framework, or if the distal segment is fixed (supporting the body weight), in a situation where there are greater joint compressive forces, greater joint congruity, and enhanced dynamic stabilization. Examples of closed kinematic chain exercises (CKCEs) involving the lower extremities include the squat and the leg press. The activities of walking, running, jumping, climbing, and rising from the floor all incorporate closed kinetic chain components. An example of a CKCE for the upper extremities is the push-up, or when using the arms to push down on the armrests to rise out of a chair.

CLINICAL PEARL In most activities of daily living, the activation sequence of the links involves a closed chain whereby the activity is initiated from a firm BOS and transferred to a more mobile distal segment.

These definitions are not always clear-cut. For example, many activities, such as swimming and cycling, traditionally viewed as OKC activities, include a load on the end segment; yet the end segment is not “fixed” and restricted from movement. This ambiguity of definitions for CKC and OKC activities has allowed some activities to be classified in opposing categories. Thus, there has been a growing need for clarification of OKC and CKC terminology, especially when related to functional activities.

The Musculoskeletal System

Exercise Mode

CLOSE-PACKED AND OPEN-PACKED POSITIONS OF THE JOINT Joint movements usually are accompanied by a relative compression (approximation) or distraction (separation) of the opposing joint surfaces. These relative compressions or distractions affect the level of congruity of the opposing surfaces. The position of maximum congruity of the opposing joint surfaces is termed the close-packed position of the joint. The position of least congruity is termed the open-packed position. Thus, movements toward the close-packed position of a joint involve an element of compression, whereas movements out of this position involve an element of distraction.

Close-Packed Position Open Kinematic Chain It is accepted that the difference between OKC and CKC activities is determined by the movement of the end segment. The traditional definition for an open-chain activity included all activities that involved the end segment of an extremity moving freely through space, resulting in isolated movement of a joint.53 Examples of an open-chain activity include lifting a drinking glass and kicking a soccer ball. Open kinematic chain exercises (OKCEs) involving the lower extremity include the seated knee extension and prone knee flexion. Upper extremity examples of OKCE include the biceps curl and the military press.

Dutton_Ch01_p0001-p0027.indd 25

The close-packed position of a joint is the joint position that results in the maximal tautness of the major ligaments; maximal surface congruity; ▶▶ minimal joint volume; and ▶▶ maximal stability of the joint. ▶▶ ▶▶

Once the close-packed position is achieved, no further motion in that direction is possible. This is the often-cited reason most fractures and dislocations occur when an external force is applied to a joint that is in its close-packed position. Also, many of the traumatic injuries of the upper extremities result from falling on a shoulder, elbow, or wrist,

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TABLE 1-6

Close-Packed Position of the Joints

Joint

Position

Zygapophyseal (spine)

Extension

Temporomandibular

Teeth clenched

Glenohumeral

Abduction and external rotation

Acromioclavicular

Arm abducted to 90 degrees

Sternoclavicular



TABLE 1-7

 pen-Packed (Resting) Position of the O Joints

ANATOMY

Joint

Position

Zygapophyseal (spine)

Midway between flexion and extension

Temporomandibular

Mouth slightly open (freeway space)

Glenohumeral

55 degrees of abduction, 30 degrees of horizontal adduction

Maximum shoulder elevation

Acromioclavicular

Arm resting by side

Ulnohumeral

Extension

Sternoclavicular

Arm resting by side

Radiohumeral

Elbow flexed 90 degrees, forearm supinated 5 degrees

Ulnohumeral

70 degrees of flexion, 10 degrees of supination

Proximal radioulnar

5 degrees of supination

Radiohumeral

Full extension, full supination

Distal radioulnar

5 degrees of supination

Proximal radioulnar

Radiocarpal (wrist)

Extension with radial deviation

70 degrees of flexion, 35 degrees of supination

Metacarpophalangeal

Full flexion

Distal radioulnar

10 degrees of supination

Carpometacarpal

Full opposition

Radiocarpal (wrist)

Neutral with slight ulnar deviation

Interphalangeal

Full extension

Carpometacarpal

Midway between abduction–adduction and flexion–extension

Hip

Full extension, internal rotation, and abduction

Metacarpophalangeal

Slight flexion

Tibiofemoral

Full extension and external rotation of tibia

Interphalangeal

Slight flexion

Hip

10–30 degrees of flexion, 10–30 degrees of abduction, and 0–5 degrees of external rotation

Tibiofemoral

25 degrees of flexion

Talocrural (ankle)

10 degrees of plantar flexion, midway between maximum inversion and eversion

Subtalar

Midway between extremes of range of movement

Midtarsal

Midway between extremes of range of movement

Tarsometatarsal

Midway between extremes of range of movement

Metatarsophalangeal

Neutral

Interphalangeal

Slight flexion

Talocrural (ankle)

Maximum dorsiflexion

Subtalar

Supination

Midtarsal

Supination

Tarsometatarsal

Supination

Metatarsophalangeal

Full extension

Interphalangeal

Full extension

which are in their close-packed position. This type of injury, a fall on an outstretched hand is often referred to as a FOOSH injury. The close-packed positions for the various joints are depicted in Table 1-6.

Open-Packed Position In essence, any position of the joint, other than the closepacked position, could be considered as an open-packed position. The open-packed position, also referred to as the loose-packed position of a joint, is the joint position that results in slackening of the major ligaments of the joint; ▶▶ minimal surface congruity; ▶▶ minimal joint surface contact; ▶▶ maximal joint volume; and ▶▶ minimal stability of the joint. ▶▶

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Dutton_Ch01_p0001-p0027.indd 26

The open-packed position permits maximal distraction of the joint surfaces. Because the open-packed position causes the brunt of any external force to be borne by the joint capsule or surrounding ligaments, most capsular or ligamentous sprains occur when a joint is in its open-packed position. The openpacked positions for the various joints are depicted in Table 1-7.

CLINICAL PEARL The open-packed position is commonly used during joint mobilization techniques (see Chapter 10).

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REFERENCES

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The Musculoskeletal System

1. Buckingham M, Bajard L, Chang T, et al. The formation of skeletal muscle: from somite to limb. J Anat. 2003;202:59–68. 2. Standring S, Gray H. Gray’s Anatomy: The Anatomical Basis of Clinical Practice. 41st ed. London, England: Elsevier; 2015. 3. Sharma P, Maffulli N. Tendon injury and tendinopathy: healing and repair. J Bone Joint Surg Am. 2005;87:187–202. 4. Starcher BC. Lung elastin and matrix. Chest. 2000;117(5 Suppl 1): 229S–234S. 5. Barnes JF. Myofascial Release, Healing Ancient Wounds. 2nd ed. Paoli, PA: MFR Treatment Centers & Seminars; 2017. 6. Day JA. Fascial anatomy in manual therapy: introducing a new biomechanical model. Orthop Phys Ther Pract. 2011;23:68–74. 7. Screen H. Tendon and tendon pathology. In: Jull G, Moore A, Falla D, Lewis J, McCarthy C, Sterling M, eds. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. London, England: Elsevier; 2015:106–112. 8. McCarthy MM, Hannafin JA. The mature athlete: aging tendon and ligament. Sports Health. 2014;6:41–48. 9. Ryan M, Bisset L, Newsham-West R. Should we care about tendon structure? The disconnect between structure and symptoms in tendinopathy. J Orthop Sports Phys Ther. 2015;45:823–825. 10. Lodish H, Berk A, Kaiser CA, et al. Protein structure and function. In: Lodish H, Berk A, Kaiser CA, Krieger M, Bretscher A, Ploegh H, et al., eds. Molecular Cell Biology. 8th ed. New York, NY: Macmillan Higher Education/W.H. Freeman; 2016:67–128. 11. Michener LA, Kulig K. Not all tendons are created equal: implications for differing treatment approaches. J Orthop Sports Phys Ther. 2015;45:829–832. 12. Lian Ø, Dahl J, Ackermann PW, Frihagen F, Engebretsen L, Bahr R. Pronociceptive and antinociceptive neuromediators in patellar tendinopathy. Am J Sports Med. 2006;34:1801–1808. 13. Silbernagel KG, Crossley KM. A proposed return-to-sport program for patients with midportion achilles tendinopathy: rationale and implementation. J Orthop Sports Phys Ther. 2015;45:876–886. 14. Scott A, Backman LJ, Speed C. Tendinopathy: update on pathophysiology. J Orthop Sports Phys Ther. 2015;45:833–841. 15. Curwin SL. Tendon pathology and injuries: pathophysiology, healing, and treatment considerations. In: Magee D, Zachazewski JE, Quillen WS, eds. Scientific Foundations and Principles of Practice in Musculoskeletal Rehabilitation. St. Louis, MO: WB Saunders; 2007:47–78. 16. Benjamin M, Toumi H, Ralphs JR, Bydder G, Best TM, Milz S. Where tendons and ligaments meet bone: attachment sites (‘entheses’) in relation to exercise and/or mechanical load. J Anat. 2006;208(4):471–490. 17. Maganaris CN, Narici MV, Almekinders LC, Maffulli N. Biomechanics and pathophysiology of overuse tendon injuries: ideas on insertional tendinopathy. Sports Med. 2004;34(14):1005–1017. 18. Hildebrand KA, Hart DA, Rattner JB, et al. Ligament injuries: pathophysiology, healing, and treatment considerations. In: Magee D, Zachazewski JE, Quillen WS, eds. Scientific Foundations and Principles of Practice in Musculoskeletal Rehabilitation. St. Louis, MO: WB Saunders; 2007:23–46. 19. Vereeke West R, Fu F. Soft tissue physiology and repair. Orthopaedic Knowledge Update 8: Home Study Syllabus. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2005:15–27. 20. Tippett SR. Considerations for the pediatric patient. In: Voight ML, Hoogenboom BJ, Prentice WE, eds. Musculoskeletal Interventions: Techniques for Therapeutic Exercise. New York, NY: McGraw-Hill; 2007:803–820. 21. Duchesne E, Dufresne SS, Dumont NA. Impact of inflammation and anti-inflammatory modalities on skeletal muscle healing: from fundamental research to the clinic. Phys Ther. 2017;97:807–817. 22. Frontera WR, Ochala J. Skeletal muscle: a brief review of structure and function. Calcif Tissue Int. 2015;96(3):183–195. 23. Dumont NA, Bentzinger CF, Sincennes MC, Rudnicki MA. Satellite cells and skeletal muscle regeneration. Compr Physiol. 2015;5:1027–1059. 24. Folland JP, Williams AG. The adaptations to strength training: morphological and neurological contributions to increased strength. Sports Med. 2007;37:145–168. 25. Pollock R, Harridge S. Neuromuscular adaptations to exercise. In: Jull G, Moore A, Falla D, Lewis J, McCarthy C, Sterling M, eds. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. London, England: Elsevier; 2015:68–77. 26. Williams JH, Klug GA. Calcium exchange hypothesis of skeletal muscle fatigue: a brief review. Muscle Nerve. 1995;18(4):421–434. 27. Fitts RH, Widrick JJ. Muscle mechanics: adaptations with exercise training. Exerc Sport Sci Rev. 1996;24:427–473.

28. Chen HY, Chien CC, Wu SK, Liau JJ, Jan MH. Electromechanical delay of the vastus medialis obliquus and vastus lateralis in individuals with patellofemoral pain syndrome. J Orthop Sports Phys Ther. 2012;42:791–796. 29. Hanci E, Sekir U, Gur H, Akova B. Eccentric training improves ankle evertor and dorsiflexor strength and proprioception in functionally unstable ankles. Am J Phys Med Rehabil. 2016;95:448–458. 30. Dekerle J, Barstow TJ, Regan L, Carter H. The critical power concept in all-out isokinetic exercise. J Sci Med Sport. 2014;17:640–644. 31. Beyer R, Kongsgaard M, Hougs Kjær B, Øhlenschlæger T, Kjær M, Magnusson SP. Heavy slow resistance versus eccentric training as treatment for achilles tendinopathy: a randomized controlled trial. Am J Sports Med. 2015;43:1704–1711. 32. Chleboun G. Muscle structure and function. In: Levangie PK, Norkin CC, eds. Joint Structure and Function. 5th ed. Philadelphia, PA: FA Davis Company; 2011:108–137. 33. Magee DJ, Zachazewski JE. Principles of stabilization training. In: Magee D, Zachazewski JE, Quillen WS, eds. Scientific Foundations and Principles of Practice in Musculoskeletal Rehabilitation. St. Louis, MO: WB Saunders; 2007:388–413. 34. Tonkonogi M, Sahlin K. Physical exercise and mitochondrial function in human skeletal muscle. Exerc Sport Sci Rev. 2002;30:129–137. 35. McMahon S, Jenkins D. Factors affecting the rate of phosphocreatine resynthesis following intense exercise. Sports Med. 2002;32:761–784. 36. Bangsbo J. Muscle oxygen uptake in humans at onset and during intense exercise. Acta Physiol Scand. 2000;168:457–464. 37. American College of Sports Medicine. ACSM’s Guidelines for Exercise Testing and Prescription. 8th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010. 38. Junqueira LC, Carneciro J. Bone. In: Junqueira LC, Carneciro J, eds. Basic Histology. 10th ed. New York, NY: McGraw-Hill; 2003:141–159. 39. Curwin S. Joint structure and function. In: Levangie PK, Norkin CC, eds. Joint Structure and Function. 5th ed. Philadelphia, PA: FA Davis Company; 2011:64–107. 40. Huang L, Li M, Li H, Yang C, Cai X. Study of differential properties of fibrochondrocytes and hyaline chondrocytes in growing rabbits. Br J Oral Maxillofac Surg. 2015;53:187–193. 41. Liang Y, Idrees E, Andrews SHJ, et al. Plasticity of human meniscus fibrochondrocytes: a study on effects of mitotic divisions and oxygen tension. Sci Rep. 2017;7(1):12148. 42. Fox AJ, Bedi A, Rodeo SA. The basic science of human knee menisci: structure, composition, and function. Sports Health. 2012;4(4):340–351. 43. Barreto G, Soliymani R, Baumann M, et al. Functional analysis of synovial fluid from osteoarthritic knee and carpometacarpal joints unravels different molecular profiles. Rheumatology (Oxford). 2018. 44. Hartjen N, Brauer L, Reiss B, et al. Evaluation of surfactant proteins A, B, C, and D in articular cartilage, synovial membrane and synovial fluid of healthy as well as patients with osteoarthritis and rheumatoid arthritis. PloS One. 2018;13:e0203502. 45. Necas D, Vrbka M, Krupka I, Hartl M. The effect of kinematic conditions and synovial fluid composition on the frictional behaviour of materials for artificial joints. Materials (Basel). 2018;11(5):767. 46. Huang LLH, Chen YA, Zhuo ZY, et al. Medical applications of collagen and hyaluronan in regenerative medicine. Adv Exp Med Biol. 2018;1077:285–306. 47. Marshall KW. Intra-articular hyaluronan therapy. Curr Opin Rheumatol. 2000;12:468–474. 48. Namba RS, Shuster S, Tucker P, Stern R. Localization of hyaluronan in pseudocapsule from total hip arthroplasty. Clin Orthop Relat Res. 1999;363:158–162. 49. Ward SR. Biomechanical applications to joint structure and function. In: Levangie PK, Norkin CC, eds. Joint Structure and Function. 5th ed. Philadelphia, PA: FA Davis Company; 2011:3–63. 50. American Medical Association. In: Cocchiarella L, Andersson GBJ, eds. Guides to the Evaluation of Permanent Impairment. 5th ed. Chicago, IL: American Medical Association; 2001. 51. Sara LK, Neumann DA. Basic structure and function of human joints. In: Neumann DA, ed. Kinesiology of the Musculoskeletal System: Foundations for Physical Rehabilitation. 3rd ed. St. Louis, MO: Mosby; 2016:28–46. 52. Neumann DA. Getting started. In: Neumann DA, ed. Kinesiology of the Musculoskeletal System: Foundations for Physical Rehabilitation. 3rd ed. St. Louis, MO: Mosby; 2016:3–27. 53. Blanpied PR, Neumann DA. Biomechanical principles. In: Neumann DA, ed. Kinesiology of the Musculoskeletal System: Foundations for Physical Rehabilitation. 3rd ed. St. Louis, MO: Mosby; 2016:77–114.

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Tissue Behavior, Injury, Healing, and Treatment

CHAPTER OBJECTIVES At the completion of this chapter, the reader will be able to: 1. Describe the various types of stress that are applied to the body. 2. Describe the various physiological processes by which the body adapts to stress. 3. Define the various common mechanisms of injury. 4. Describe the etiology and pathophysiology of musculoskeletal injuries associated with various types of body tissue. 5. Outline the pathophysiology of the healing process and the various stages of healing of the various connective tissues. 6. Describe the factors that can impede the healing process. 7. Outline the more common surgical procedures available for musculoskeletal injuries. 8. Outline the principles behind postsurgical rehabilitation. 9. Describe the detrimental effects of immobilization.

OVERVIEW Tissues in the body are designed to function while undergoing the stresses of everyday living. Body weight, friction, and air or water resistance are all types of stresses that commonly act on the body. The ability of the tissues to respond to stress is due to their differing viscoelastic properties, with each tissue responding to stress in an individual manner based on design. Maintaining the health of the various tissues is a delicate balance because insufficient, excessive, or repetitive stresses can prove deleterious. Fortunately, most tissues have an inherent ability to self-heal—a process that is an intricate phenomenon.

CHAPTER 2

THE RESPONSE OF TISSUE TO STRESS Kinetics is the term applied to define the forces acting on the body. Posture and movement are both governed by the body’s ability to control these forces. The same forces that move and stabilize the body also have the potential to deform and injure the body.1 A wide range of external and internal forces are either generated or resisted by the human body during daily activities. Examples of these external forces include ground reaction force, gravity, and applied force through contact. Examples of internal forces include structural tension, joint compression, and joint shear forces (Fig. 2-1). Tissue failure will result if stress is applied too quickly, exceeds the tolerance limits of the tissues, or if it is applied repetitively without sufficient time for recovery.2 This type of failure, which may be a result of an acceleration or deceleration injury, has been termed dynamic overload2: Acceleration. This type, which is typically related to a contact injury, occurs when the body or body parts are stationary or moving slower than the applied force, and the injury-producing force accelerates the body or body part beyond the tissue’s ability to withstand or resist that force. For example, when a soccer player is being tackled and the force of contact by the opposing player’s foot against the lateral aspect of the leg exceeds the medial collateral ligament’s ability to resist the force. ▶▶ Deceleration. In this type of injury, which is not typically related to contact, the body or body parts are rapidly decelerated. Examples include landing from a jump or attempting to stop and quickly change direction (cutting). ▶▶

While the prevention of contact injuries may be difficult, deceleration injuries may be reduced or potentially removed by developing sufficient strength to counteract the loads applied, combined with appropriate neuromuscular control strategies to apply the strength in an appropriate manner.2 Biological tissues are anisotropic, which means they can demonstrate differing mechanical behavior as a function of test direction. The properties of extensibility and elasticity are common to many biologic tissues. Extensibility is the ability to be stretched, and elasticity is the ability to return to normal length after lengthening or shortening.3 It is the concentration

28

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▶▶

= Original shape

Strain is defined as the change in length of a material due to an imposed load, divided by the original length.4 The two basic types of strain are a linear strain, which causes a change in the length of a structure, and shear strain, which causes a change in the angular relationships within a structure.

CLINICAL PEARL

Shear

Strain is the amount of elongation divided by the length of the structure. ▶▶ Stress is the force in a structure divided by the crosssectional area. ▶▶

=

Compression

Tension

FIGURE 2-1  Internal forces acting on the body.

of proteoglycans in solution (see Chapter 1) that is responsible for influencing the mechanical properties of the tissue, including the regulation of hydration, compressive stiffness, sheer stiffness, and osmotic pressure. Under the right circumstances, the body can respond and adapt to stress. The terms stress and strain have specific mechanical meanings. ▶▶

Stress, or load, is defined in units of force per area and is used to describe the type of force applied. Stress is independent of the amount of material, but it is directly related to the magnitude of force and inversely related to the unit area.4

The inherent ability of a tissue to tolerate load can be observed experimentally in graphic form using a load– deformation curve. The load–deformation curve, or stress– strain curve, of a structure (Fig. 2-2) depicts the relationship between the amount of force applied to a structure and the structure’s response in terms of deformation or acceleration. The shape of the resulting load–deformation curve depends on the kind of material involved. The horizontal axis (deformation or strain) represents the ratio of the tissue’s deformed length compared to its original length. The vertical axis of the graph (load or stress) denotes the internal resistance generated as the tissue resists its deformation, divided by its crosssectional area. The load–deformation curve can be divided into four regions, each region representing a biomechanical property of the tissue (Fig. 2-2): ▶▶

Toe region. In this region, the collagen fibers have a wavy, or folded, appearance at rest or on slack. When a force that lengthens the collagen fibers is initially applied to connective tissue (CT), this slack range is affected first,

Tissue Behavior, Injury, Healing, and Treatment

=

Regions Load (Stress)

(B)

Elastic

Plastic

Failure

(A)

Toe I Slack range

II Linear physiological range

III Primary failure loss of mechanical properties

IV Deformation Complete (Strain) failure

FIGURE 2-2  The stress–strain curve.

29

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ANATOMY

and the fibers unfold as the slack is taken up (see Crimp later). The toe region is an artifact caused by this take-up of slack, alignment, and/or seating of the test specimen. The size of the toe region depends on the type of material and the waviness of the collagen pattern. ▶▶ Elastic region. Within the elastic deformation region, the structure imitates a spring—the geometric deformation in the structure increases linearly with increasing load, and after the load is released the structure returns to its original shape. The slope of the elastic region of the load–deformation curve from one point in the curve to another, which corresponds to the physiological range of a structure, is called the modulus of elasticity or Young’s modulus (stress divided by the strain), and represents the extrinsic stiffness or rigidity of the structure—the stiffer the tissue, the steeper the slope. All normal tissues within the musculoskeletal system exhibit some degree of stiffness. The greater the Young’s modulus for a material, the better it can withstand greater forces. Larger structures will have greater rigidity than smaller structures of similar composition. Stiffness is not necessarily a negative characteristic—tendons transmit force more effectively and efficiently when they are stiffer.5 Plastic region. The end of the elastic deformation range, and the beginning of the plastic deformation range, represents the point where an increasing level of stress on the tissue results in progressive failure, microscopic tearing of the collagen fibers, and permanent deformation. The permanent change results from the breaking of bonds and their subsequent inability to contribute to the recovery of the tissue. Unlike the elastic region, removal of the load in this region will not result in a return of the tissue to its original length. ▶▶ Failure region. Deformations exceeding the ultimate failure point (Fig. 2-2) produce mechanical failure of the structure, which in the human body may be represented by the fracturing of bone or the rupturing of a soft tissue. ▶▶

CLINICAL PEARL Stiffness = force/deformation. The gradient in the linear portion of the load–deformation graph immediately after the toe region of the load–displacement curve represents the stiffness value. The load–deformation curve does not indicate the variable of time. ▶▶ Elastic modulus = stress/strain. The larger the Young’s modulus for a material, the greater stress needed for a given strain. ▶▶

CLINICAL PEARL

30

Unloading a tendon significantly influences the mechanical properties. For example, one study that looked at the effects of 4 weeks of unilateral lower limb suspension followed by 6 weeks of rehabilitation found that there was a 17% decrease in the elastic modulus (lower stiffness) after suspension, and the restoration of normal stiffness after rehabilitation.6

Dutton_Ch02_p0028-p0060.indd 30

Some protective mechanisms exist in CT to help respond to stress and strain, including crimp, viscoelasticity, creep and stress relaxation, plastic deformation, and stress response.

Crimp The crimp of collagen is one of the major factors behind the viscoelastic properties of CT. Crimp, a collagen tissue’s first line of response to stress, is different for each type of CT, and provides each with different viscoelastic properties. Collagen fibers are oriented obliquely when relaxed. However, when a load is applied, the fibers line up in the direction of the applied force as they uncrimp. Crimping is seen primarily in ligaments, tendons, and joint capsules, and occurs in the toe phase of the stress–strain curve (Fig. 2-2).

CLINICAL PEARL If a load is applied to the CT and then removed immediately, the material recoils to its original size. If, however, the load is allowed to remain, the material continues to stretch. After a period of a sustained stretch, the stretching tends to reach a steady-state value. Realignment of the collagen fibers in the direction of the stress occurs, and water and proteoglycans are displaced from between the fibers.

Viscoelasticity Viscoelasticity is the time-dependent mechanical property of a material to stretch or compress over time, and to return to its original shape when a force is removed. The mechanical qualities of a tissue can be separated into categories based on whether the tissue acts primarily as a solid, fluid, or a mixture of the two. Solids are described according to their elasticity, strength, hardness, and stiffness. Bone, ligaments, tendons, and skeletal muscle are all examples of elastic solids. Biological tissues that demonstrate attributes of both solids and fluids are viscoelastic. The viscoelastic properties of a structure determine its response to loading. For example, a ligament demonstrates more viscous behavior at lower loads, whereas, at higher loads, elastic behaviors dominate.7

Creep and Stress Relaxation Creep and stress relaxation are two characteristics of viscoelastic materials that are used to document their behavior quantitatively.3 Creep is the gradual rearrangement of collagen fibers, proteoglycans, and water that occurs because of a constantly applied force after the initial lengthening caused by crimp has ceased. Creep is a time-dependent and transient biomechanical phenomenon. Short duration stresses (90%) are caused either by excessive strain of the muscle or by contusion. Muscle strains may be graded by severity (Table 2-2). A number of factors contribute to muscle strain injury including17 inadequate flexibility; inadequate strength or endurance; ▶▶ dyssynergistic muscle contraction; ▶▶ insufficient warm-up; and ▶▶ inadequate rehabilitation from the previous injury. ▶▶ ▶▶

A distraction strain occurs in muscle to which an excessive pulling force is applied, resulting in overstretching.21 A contusion may occur if a muscle is injured by a heavy compressive force, such as a direct blow. At the site of the direct blow, a hematoma may develop. Two types of hematoma can be identified as22,23: 1. Intramuscular. This type of hematoma is associated with a muscle strain or bruise. The size of the hematoma is limited by the muscle fascia. Clinical findings may include pain and loss of function. 2. Intermuscular. This type of hematoma develops if the muscle fascia is ruptured, and the extravasated blood spreads into the interfascial and interstitial spaces. The pain is usually less severe with this type.

Healing

36

Skeletal muscle has considerable regenerative capabilities, and the process of skeletal muscle regeneration after injury is a well-studied cascade of events. The essential process of muscle regeneration is similar, irrespective of the cause of injury, but the outcome and time course of regeneration vary according to the type, severity, and extent of the injury. Broadly speaking, there are three phases in the healing process of an

Dutton_Ch02_p0028-p0060.indd 36



TABLE 2-2

Classification of Muscle Injury

Type

Related Factors

Exercise-induced muscle injury (delayed muscle soreness)  

Increased activity Unaccustomed activity Excessive eccentric work Viral infections Secondary to muscle cell damage

Strains First degree (mild): minimal structural damage; minimal hemorrhage; early resolution

  Onset at 24–48 hours after exercise Sudden overstretch Sudden contraction Decelerating limb Insufficient warm-up Lack of flexibility

Second degree (moderate): partial tear; large spectrum of injury; significant early functional loss Third degree (severe): complete tear; may require aspiration; may require surgery       Contusions Mild, moderate, severe Intramuscular vs. intermuscular

Increasing severity of strain associated with greater muscle fiber death, more hemorrhage, and more eventual scarring Steroid use or abuse Previous muscle injury Collagen disease Direct blow, associated with increasing muscle trauma and tearing of fiber proportionate to severity

Reproduced with permission from Reid DC. Sports Injury Assessment and Rehabilitation. New York, NY: Churchill Livingstone; 1991.

injured muscle: the destruction phase, the repair phase, and the remodeling phase.

Destruction Phase The pathology of skeletal muscle damage varies, depending on the initiating cause. One of the potential consequences of muscle injury is atrophy. The amount of muscle atrophy that occurs depends on the usage prior to bed rest and the function of the muscle.24 Antigravity muscles (such as the quadriceps) tend to have greater potential for atrophy than antagonist muscles (such as the hamstrings). Research has shown that a single bout of exercise protects against muscle damage.25 A reconditioning program with gradual progression from lower intensity activities with minimal eccentric actions is recommended to protect against muscle damage.24,26 Following an injury, satellite cells activate and become myoblasts that proliferate extensively for the first few days. Unlike the multinucleated myofibers, satellite cells are mononuclear that maintain mitotic potential and respond to cellular signals by entering the cell cycle to provide the substrate for muscle regeneration and growth.27 The destructive phase is characterized by the necrosis of muscle tissue, degeneration, and an

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infiltration by PMN leukocytes as a hematoma and edema begin to form at the site of injury.

Repair Phase The repair phase usually involves the following steps: ▶▶

Hematoma formation.  The gap between the ruptured ends of the fibers is at first filled by a hematoma. During the first day, the hematoma is invaded by inflammatory cells, including phagocytes, which begin disposal of the blood clot.

One of the major roles of the early mediators of inflammation released by resident cells is to increase vasodilation, vascular permeability, and the expression of adhesion molecules to allow the infiltration of inflammatory cells into peripheral tissues from the blood circulation.11,28

Treatment The intervention depends on the stage of healing (see Chapter 8). The following principles should guide the clinician when rehabilitating a muscle injury17: ▶▶

The onset, development, and resolution of the inflammatory process have a critical role on the guidance of satellite cell function and, thus, on muscle regeneration.11,29 The blood coagulation cascade, among other roles, leads to the formation of small molecules called anaphylatoxins that activate sentinel cells residing in muscle tissue (residence cells), such as mast cells, which in turn trigger the inflammatory response.11,30 The factors released by the mast cells directly stimulate the proliferation of satellite cells.31 Satellite cells (see Chapter 1), myoblastic precursor cells, proliferate to reconstitute the injured area.32 In addition to the release of anaphylatoxins, tissue damage also liberates intracellular proteins and molecules normally sequestered in the ECM, which activate resident cells once they are released at the site of the injury.11,33

CLINICAL PEARL The mechanical stress induced by a traumatic muscle injury releases a wide variety of factors that activate different resident cell types to initiate the healing process.11,34–36 During the first week of healing, the injury site is the weakest point of the muscle–tendon unit. During the first few weeks, the newly formed myofibers grow to form new mature myofibers.11 The regeneration of the myofibers begins with the activation of satellite cells, located between the basal lamina and the plasma membrane of each myofiber.27 The final stage in the regenerative process involves the integration of the neural elements and the formation of a functional neuromuscular junction. Provided that the continuity of the muscle fiber is not disrupted, and the innervation, vascular supply, and ECM are left intact, muscle will regenerate without loss of normal tissue architecture and function.11

Remodeling Phase In this phase, the regenerated muscle matures and contracts with the reorganization of the scar tissue. There is often

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Prevention is easier than treatment. Patient education is important to inform the patient about the expected duration and extent of symptoms, and any precautions or contraindications to prevent reinjury or disruption of the healing process.

Controlled mobility and activity are better than absolute rest. ▶▶ Medications and modalities are important adjuncts to care. ▶▶ It is important to develop strong, flexible tissue using pain as the guiding factor. ▶▶

The typical exercise progression involves PROM, then AAROM, then AROM, and then submaximal isometrics, initially in a protective range before progressing throughout the range (see Chapter 12). Once the patient can tolerate submaximal isometrics, a progression to maximal isometrics is made at multiangles and then throughout the range, before progressing to progressive resistive exercises (see Chapter 12).

Tissue Behavior, Injury, Healing, and Treatment

CLINICAL PEARL

complete restoration of the functional capacity of the injured muscle. The tensile strength of the healing muscle tissue increases over time. However, whereas normal intramuscular collagenous tissue has a greater proportion of type I collagen than type III collagen, initially after injury, type III collagen demonstrates a significant increase over type I collagen in the area of repair. Over time, the proportion of type I to type III collagen returns to normal. Controlled mobility and stress are key considerations in the post-acute period to allow scar formation, muscle regeneration, correct orientation of new muscle fibers, and the normalization of the tensile properties of muscle.

Muscle and Aging With age, there is a reduction in the ability to produce and sustain the muscular power. This age-related phenomenon, termed senescence sarcopenia, can result in a 20–25% loss of skeletal muscle mass (see Chapter 30).

CLINICAL PEARL Sarcopenia (sarco = muscle, penia = lack of ) is not a disease, but rather refers specifically to the universal, involuntary decline in lean body mass that occurs with age, primarily as a result of the loss of skeletal muscle volume. Sarcopenia has important consequences. The loss of lean body mass reduces function, and a loss of approximately 40% of lean body mass is fatal.37,38 Sarcopenia is distinct from wasting—involuntary weight loss resulting from inadequate intake, which is seen in starvation, advanced cancer, or acquired immunodeficiency syndrome.

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ANATOMY

While a variety of studies have investigated the underlying mechanisms and treatments of age-related muscle loss, very few epidemiologic studies have looked at the prevalence, incidence, pathogenesis, and consequences of sarcopenia in elderly populations. It is likely that the determinants of sarcopenia are multifactorial and include genetic factors, environmental factors, and age-related changes in muscle tissue. The effects of aging on muscle morphology have been studied. Aging causes a decrease in muscle volume, with type II fiber apparently being more affected by gradual atrophy. These losses of muscular strength and muscle mass can have important health consequences because they can predispose the elderly to disability, an increased risk of falls and hip fractures, and a decrease in bone mineral density.

rapidly creating the linear region of the load–deformation curve (Fig. 2-2). The stress–strain behavior of the tendon is then reasonably linear until close to failure at which point material microrupture leads to a steady drop in stiffness as the fibers pull apart and the tendon fails.43 Most tendons likely function in the toe and early linear regions under physiological loading conditions.44 Positional tendons, which experience very small loads during use, likely only operate in the linear region, whereas energy storing tendons are often loaded to values close to the absolute failure stress of the tissue.43,45

CLINICAL PEARL As the amount of crimp in a tendon decreases with age, the toe region becomes smaller.

CLINICAL PEARL When older people maintain muscular activity, the losses in strength with age are reduced substantially. Age-related muscle fiber atrophy and weakness may be completely reversed in some individuals with resistance training (see Chapter 30).

TENDON BEHAVIOR, INJURY, HEALING, AND TREATMENT As outlined in Chapter 1, a tendon is a type of regular, dense CT that transfers muscle forces to the skeleton and plays an important role in the development of power and the efficiency of muscular contractions through the storage and release of elastic energy.39,40

Behavior

38

The organization of the tendon determines its mechanical behavior. As tendons have more parallel collagen fibers than ligaments, and less realignment occurs during initial loading, the toe region of the load–deformation curve is smaller in tendons than in ligaments.41 The compliance of tendons varies. Tendons of the digital flexors and extensors are very stiff, and their length changes very little when muscle forces are applied through them. This allows for very precise movements, and these types of tendons are often referred to as positional tendons. In contrast, the tendons of some muscles, particularly those involved in locomotion and ballistic performance, are more elastic, giving them the capability of storing energy. For example, the Achilles tendon is stretched during the late stance phase in gait as the triceps surae is stretched as the ankle dorsiflexes. Near the beginning of the plantar flexion contraction, the muscle activation ceases and energy stored in the stretched tendon helps to initiate plantar flexion. These types of tendons are often referred to as energy storing tendons. Total tendon strains (percentage deformity) of 1–2% result in the straightening of the crimp pattern of unloaded tendon collagen.42 As the load increases beyond the toe region, the collagen fibrils stretch, and the stiffness of the tendon increases

Dutton_Ch02_p0028-p0060.indd 38

There is little question that tendinopathy affects tendon structure. Tendon tissue homeostasis is based on the ability of the tendon cells to sense and respond to mechanical load through mechanotransduction.46 As with all CT, tendons have a positive adaptive response to repeated physiologic mechanical loading, which results in biologic and mechanical changes.44 The exact level of mechanical and biological stimulation required to maintain normal tendon homeostasis is not currently known, but it is widely believed that an abnormal level of stimulation (underload or overload) may play a role in the pathogenesis of tendinopathy.46 A tendon can resist tensile stress in the directional of its fibers orientation because of the collagen structure, and it can resist some compressive stress because of its proteoglycan content. The total amount of load the tendon can resist and the amount it stretches during loading depend on its cross-sectional area, composition, and length. Strain injuries are common at the musculotendinous junction (MTJ), the weakest point in the muscle tendon unit.47

CLINICAL PEARL The MTJ is the location of most common muscle strains caused by tensile forces in a normal muscle–tendon unit. In particular, a predilection for a tear near the MTJ has been reported in the biceps and triceps brachii, rotator cuff muscles, flexor pollicis longus, fibularis (peroneus) longus, medial head of the gastrocnemius, rectus femoris, adductor longus, iliopsoas, pectoralis major, semimembranosus, and the entire hamstring group.47

Injury Despite the wealth of knowledge about tendon structure and function, there remains a surprising dearth of knowledge concerning tendon pathophysiology. This is because although tendinopathies are common conditions, they present differently, depending on the site and nature of the injury process, but share common features of pain during tendon loading, diffuse or localized swelling, and limitations in activity potential or performance.48 Recently, it has been recommended that the term tendinopathy replace the traditional term tendinitis

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CLINICAL PEARL Tendinopathy can be persistent and recalcitrant to treatment and symptoms may continue for a number of years. Although the etiology of tendinopathy is still unclear, histological evidence consistently demonstrates an absence of prostaglandin-mediated inflammation. However, there is indeed an inflammatory reaction within chronically painful tendinopathy, but to a lesser extent than that of immunedriven rheumatological disorders.57 This would appear to be contradictory, but the problem is with semantics, particularly the definition of inflammation, and the presence of what substances, cells, or processes indicate inflammation. What is clear is that there are peripheral and, likely, central nervous system (CNS) changes involving inflammatory and noninflammatory pathways, resulting in hyperalgesia and allodynia in selected populations with tendon injury.40 Perhaps the presence of an excess overload can imbalance any repair attempts and lead to an inappropriate cell metabolic response and more significant matrix breakdown.58

CLINICAL PEARL It is important to note that tendon pain is not consistent with a triphasic inflammatory process, so clinicians should consider avoiding therapy such as absolute rest, ice, and antiinflammatory medications as definitive treatments for tendinopathy.59 Structural changes that occur with tendinopathy include tendon thickening, focal hypoechogenicity (ultrasound),

Dutton_Ch02_p0028-p0060.indd 39

hypervascularity (color Doppler ultrasound), and increased signal intensity (magnetic resonance imaging [MRI]).40 Specimens taken from torn tendons show disorientation of collagen fibers, thinning of the fibers, myxoid degeneration, chondroid metaplasia, calcification, and vascular infiltration.60 It is hypothesized that there is a resident population of fibroblastlike cells within a tendon that, after injury, can differentiate into several lineages (osteoblast, chondrocyte, adipocyte, tenocyte), leading to metaplasia (e.g., bony, cartilaginous, or adipocyte transformation).57,61 Despite knowledge of the structural changes, the source of pain in tendons cannot currently be seen on tendon imaging, as there is an inconsistent relationship between pain and pathological changes identified on imaging.59 This might be explained by the fact that pain is an output from the CNS which may or may not be associated with a physiological nociceptive input caused by tissue disruption.59 Thus, changes to brain and spinal cord excitability and cortical reorganization may be occurring with tendon pain.62 In the International Classification of Functioning, Disability and Health (ICF) language (see Chapter 4), the health condition of tendinopathy includes impairments in body structure and function (e.g., pain, muscle power and endurance), activity limitations (twisting, lifting, jumping), and participation restrictions (e.g., work and sport).48 Although sport activity is the most common source of tendinopathy, it can be work-related, drug-related (e.g., cortisone, cyclosporine, statins, and quinolone antibiotics), or due to a metabolic disorder such as disturbed glucose metabolism and atherosclerosis.52 Most tendon trauma tends to occur from loading (sudden overload or repetitive) or rapid unloading. Tendons and their insertions are rarely loaded purely in tension as there is often compression of the tendon as well, either internally (e.g., one fascicle or bundle of fibers against another) or against external structures (paratendon, retinacula, bone).57 This combination of tension and compression results in shearing and friction.57 The mechanical loading is anabolic and marked by an increased synthesis of collagen proteins, which peaks around 24 hours after exercise and remains elevated for up to 70–80 hours.52 Simultaneously, there is a degradation of collagen proteins, although the timing of this catabolic peak occurs earlier than the anabolic peak, resulting in a net loss of collagen around the first 24–36 hours after training, followed by a net gain in collagen.54 This would tend to indicate that a certain restitution time interval in between exercise bouts is critical for the tissue to adapt and to avoid a net catabolic situation.

Tissue Behavior, Injury, Healing, and Treatment

for describing tendon pathology as this does not denote an underlying pathology, but rather signals that all is not well in the tendon.49 However, confusing the issue is the fact that the non-inflammatory etiology of tendinopathy has lately been questioned, as inflammation may play a role in the initial phase of the disease.50 Tendinitis, which is seen to a much lesser extent (3 days or major surgery within 4 weeks of application of clinical decision rule

1

Localized tenderness along distribution of the deep venous system (assessed by firm palpation in the center of the posterior calf, the popliteal space, and along the area of the femoral vein in the anterior thigh and groin)

1

Entire lower extremity swelling

1

Calf swelling by >3 cm compared with asymptomatic lower extremity (measured 10 cm below tibial tuberosity)

1

Pitting edema (greater in the symptomatic lower extremity)

1

Collateral superficial veins (nonvaricose)

1

Alternative diagnosis as likely or greater than that of DVT (most common alternative diagnoses on cellulitis, calf strain, and postoperative swelling)

−2

a

Score interpretation: ≤0 = probability of proximal lower extremity deep vein thrombosis (PDVT) of 3% (95% confidence interval = 1.7–5.9%), 1 or 2 = probability of PDVT of 17% (95% confidence interval = 12–23%), ≥3 = probability of PDVT of 75% (95% confidence interval = 63–84%). Reproduced with permission from Wells PS, Anderson DR, Bormanis J, et al. Value of assessment of pretest probability of deep-vein thrombosis in clinical management. Lancet. 1997 Dec 20–27;350(9094):1795–1798.

Prevention is the key with DVT. Methods of prevention may be classified as pharmacological and nonpharmacological. Pharmacological prevention includes anticoagulant drugs such as low-dose Coumadin (warfarin), low-molecular-weight heparin, adjusted-dose heparin, and heparin antithrombin III combination. These drugs work by altering the body’s normal blood-clotting process. Second tier drugs include dextran, aspirin, and low-dose subcutaneous heparin. Nonpharmacological prevention attempts to counteract the effects of immobility, including calf and foot/ankle exercises, and compression stockings. Finally, inferior vena cava (IVC) filters and Greenfield filters may be employed with a patient who has a contraindication to anticoagulation, previous complications with anticoagulants, or if anticoagulants have proved ineffective in the past. Pulmonary embolus.155  This is a part of the spectrum of diseases associated with VTE. Under normal conditions, micro-thrombi (tiny aggregates of red cells, platelets, and fibrin) are formed and lysed continually within the venous circulatory system. This dynamic equilibrium ensures local hemostasis in response to injury without

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Although a D-dimer blood test can be used to detect the presence of an inappropriate thrombus, a pulmonary angiography remains the criterion standard for the diagnosis of PE but is rapidly being replaced by multidetector computed tomographic angiography (MDCTA), since the latter modality is significantly less invasive, is easier to perform, and offers equal sensitivity and specificity. Poor wound healing.  Wound-healing abnormalities cause great physical and psychological stress to the affected patients and are extremely expensive to treat. The rate of healing in acute surgical wounds is affected by both extrinsic factors (surgical technique, tension of wound suturing, maintenance of adequate oxygenation, cigarette smoking, prevention or eradication of infection, and types of wound dressing) and intrinsic factors (presence of shock or sepsis, control of diabetes mellitus, and the age, nutritional, and immune status of the patient).156 Although many studies have documented relationships between malnutrition and poor wound healing, the optimal nutrient intake to promote wound healing is unknown. It is known, however, that vitamins A, C, and E, protein, arginine, zinc, and water play a role in the healing process.157 ▶▶ Scars and adhesions.  A surgery is a form of controlled macrotrauma to the musculoskeletal system. The tissues respond to this trauma in much the same way that they do to any other form of trauma or injury. As part of the postsurgical rehabilitation process, the involved structure is usually immobilized to protect the surgical site from injury. However, prolonged immobilization of a CT can produce significant changes in its histochemical and biomechanical structure. These changes include a

Tissue Behavior, Injury, Healing, and Treatment

Clinical Finding

▶▶

permitting uncontrolled propagation of a clot. Under pathological conditions, micro-thrombi may escape the normal fibrinolytic system to grow and propagate. PE occurs when these propagating clots break loose and embolize to block pulmonary blood vessels. PE most commonly results from DVT occurring in the deep veins of the lower extremities, proximal to and including the popliteal veins and in the axillary or subclavian veins (deep veins of the arm or shoulder). PE is an extremely common and highly lethal postsurgical condition that is a leading cause of death in all age groups. A good clinician actively seeks the diagnosis as soon as any suspicion of PE whatsoever is warranted, because prompt diagnosis and treatment can dramatically reduce the mortality rate and morbidity of the disease. Unfortunately, the diagnosis is missed more often than it is made because PE often causes only vague and nonspecific symptoms. Symptoms that should provoke a suspicion of PE must include chest pain, chest wall tenderness, back pain, shoulder pain, upper abdominal pain, syncope, tachycardia, hemoptysis, shortness of breath, painful respiration, new onset of wheezing, any new cardiac arrhythmia, or any other unexplained symptom referable to the thorax. It is important to remember that many patients with PE are initially completely asymptomatic and most of those who do have symptoms have an atypical presentation.

 linical Decision Rule for Outpatients C Suspected of Having a Proximal Deep Vein Thrombosis

▶▶

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ANATOMY

fibro-fatty infiltration that can progress into fibrosis, creating adhesions around the healing site, and an increase in the microscopic cross-linking of collagen fibers resulting in an overall loss of extensibility of the CTs. Unlike CT, which is mature and stable with limited pliability, scar tissue is more vulnerable to break down. Fortunately, controlled and skilled therapeutic interventions can reverse the detrimental effects of shortterm immobilization. These include mobilization of the CT with passive mobility techniques or active range of motion that help to restore the extensibility of the tissue. To assist with the overall healing of the incision, scar mobilization techniques may be performed to the patient’s tolerance with lotion.

Cartilage degeneration.  Immobilization of a joint causes atrophic changes in articular cartilage through a reduction of matrix proteoglycans and cartilage softening. Softened articular cartilage is vulnerable to damage during weight bearing. The reduction of the matrix proteoglycan concentration has been demonstrated to be highest in the superficial zone but also occurs throughout the uncalcified cartilage, diminishing with distance from the surface of the articular cartilage. ▶▶ Decreased mechanical and structural properties of ligaments.  ▶▶

CLINICAL PEARL Following a period of immobilization, CTs are more vulnerable to deformation and breakdown than normal tissues subjected to similar amounts of stress.

DETRIMENTAL EFFECTS OF IMMOBILIZATION Continuous immobilization of connective and skeletal muscle tissues can cause some undesirable consequences. These include the following:



TABLE 2-8

Decreased bone density.  Mechanical forces acting on bone stimulate osteogenesis, and the absence of such forces inhibits osteogenesis.

Structural Changes in the Various Types of Muscle Following Immobilization in a Shortened Position

 

56

▶▶

Muscle Fiber Type and Changes 

Structural Characteristics

Slow Oxidative

Fast Oxidative Glycolytic

Fast Glycolytic

Number of fibers

Moderate decrease

Minimal increase

Minimal increase

Diameter of fibers

Significant decrease

Moderate decrease

Moderate decrease

Fiber fragmentation

Minimal increase

Minimal increase

Significant increase

Myofibrils

Minimal decrease and disoriented

—

Wavy

Nuclei

Degenerated and rounded

Degenerated and rounded

Degenerated and rounded

Mitochondria

Moderate decrease, degenerated

Moderate decrease, degenerated

Minimal decrease, degenerated, swollen

Sarcoplasmic reticulum

Minimal decrease, orderly arrangement

Minimal decrease

Minimal decrease

Myofilaments

Minimal decrease, disorganized

Moderate decrease

Minimal decrease, wavy

Z band

Moderate decrease

—

Faint or absent

Vesicles

Abnormal configuration

—

—

Basement membrane

Minimal increase

—

—

Register of sarcomeres

Irregular projections, shifted with time

—

—

Fatty infiltration

Minimal increase

—

—

Collagen

Minimal increase between fibers

—

—

Macrophages

Minimal increased invasion

Minimal increased invasion

Minimal increased invasion

Satellite cells

Minimal increase

—

—

Target cells

Minimal increase

—

—

Data from Gossman MR, Sahrmann SA, Rose SJ. Review of length-associated changes in muscle. Experimental evidence and clinical implications. Phys Ther. 1982 Dec;62(12):1799–1808.

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▶▶

Weakness or atrophy of muscles.  Muscle atrophy is an imbalance between protein synthesis and degradation. General and selective muscle atrophy can occur with immobilization. General muscle atrophy typically occurs in one-joint muscles as two-joint muscles are “less” immobilized by typical immobilization methods.158 Selective muscle atrophy occurs more often in type I fibers as they are more susceptible to the effects of inactivity and, as their numbers decline, the proportion of type IIa fibers increases.

Change in muscle resting length ▶▶ Decrease in total muscle weight ▶▶ Increase in muscle contraction time ▶▶ Decrease in muscle tension produced ▶▶ Decrease in protein synthesis ▶▶ Increase in lactate concentration with exercise ▶▶

The extent of the negative impact of immobilization depends on the general health of the patient, duration of the immobilization, and the position of the limb during immobilization. The clinician must remember that the restoration of full strength and range of motion may prove difficult if muscles are allowed to heal without early active motion, or in a shortened position, and that the patient may be prone to repeated strains.100 The cause of muscle damage during exercised recovery from atrophy involves an altered ability of the muscle fibers to bear the mechanical stress of external loads (e.g., weight bearing) and movement associated with exercise. Strenuous exercise of atrophied muscle can result in primary or secondary sarcolemmal disruption, swelling or disruption of the sarcotubular system, distortion of the contractile components of myofibrils, cytoskeletal damage, and extracellular myofiber matrix abnormalities.24 These pathologic changes are similar to those seen in healthy young adults after sprint running or resistance training.24 Thus, range-of-motion exercises should be started once the swelling and tenderness have subsided to the point that the exercises are not unduly painful.100

REFERENCES 1. Neumann DA. Getting started. In: Neumann DA, ed. Kinesiology of the Musculoskeletal System: Foundations for Physical Rehabilitation. 3rd ed. St. Louis, MO: Mosby; 2016:3–27. 2. Herrington L. Acute knee injuries. In: Jull G, Moore A, Falla D, Lewis J, McCarthy C, Sterling M, eds. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. London, England: Elsevier; 2015:522–527. 3. Goel VK, Khandha A, Vadapalli S. Musculoskeletal biomechanics. Orthopaedic Knowledge Update 8: Home Study Syllabus. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2005:39–56. 4. Topoleski LD. Mechanical properties of materials. In: Oatis CA, ed. Kinesiology: The Mechanics and Pathomechanics of Human Movement. Philadelphia, PA: Lippincott Williams and Wilkins; 2004:21–35. 5. Houck J. Biomechanics of the Foot and Ankle for the Physical Therapist. In: Hughes C, ed. La Crosse, WI: Orthopedic Section, APTA; 2014. 6. Shin D, Finni T, Ahn S, et al. Effect of chronic unloading and rehabilitation on human Achilles tendon properties: a velocity-encoded phasecontrast MRI study. J Appl Physiol. 2008;105:1179–1186. 7. Hildebrand KA, Hart DA, Rattner JB, et al. Ligament injuries: pathophysiology, healing, and treatment considerations. In: Magee D,

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Tissue Behavior, Injury, Healing, and Treatment

In addition to those effects listed in Table 2-8, immobilization can have the following negative effects on muscle:

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35. Dufresne SS, Frenette J, Dumont NA. Inflammation and muscle regeneration, a double-edged sword. Med Sci (Paris). 2016;32:591–597. 36. Yang W, Hu P. Skeletal muscle regeneration is modulated by inflammation. J Orthop Translat. 2018;13:25–32. 37. Kotler D, Tierney A, Pierson R. Magnitude of body cell mass depletion and the timing of death from wasting in AIDS. Am J Clin Nutr. 1989;50:444–447. 38. Roubenoff R, Castaneda C. Sarcopenia-understanding the dynamics of aging muscle. JAMA. 2001;286:1230–1231. 39. Lichtwark GA, Barclay CJ. The influence of tendon compliance on muscle power output and efficiency during cyclic contractions. J Exp Biol. 2010;213:707–714. 40. Ryan M, Bisset L, Newsham-West R. Should we care about tendon structure? The disconnect between structure and symptoms in tendinopathy. J Orthop Sports Phys Ther. 2015;45:823–825. 41. Vereeke West R, Fu F. Soft tissue physiology and repair. In: Vaccaro AR, ed. Orthopaedic Knowledge Update 8: Home Study Syllabus. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2005:15–27. 42. Screen HR, Lee DA, Bader DL, Shelton JC. An investigation into the effects of the hierarchical structure of tendon fascicles on micromechanical properties. Proc Inst Mech Eng H. 2004;218:109–119. 43. Screen H. Tendon and tendon pathology. In: Jull G, Moore A, Falla D, Lewis J, McCarthy C, Sterling M, eds. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. London, England: Elsevier; 2015:106–112. 44. Curwin SL. Tendon pathology and injuries: pathophysiology, healing, and treatment considerations. In: Magee D, Zachazewski JE, Quillen WS, eds. Scientific Foundations and Principles of Practice in Musculoskeletal Rehabilitation. St. Louis, MO: WB Saunders; 2007:47–78. 45. Birch HL, Thorpe CT, Rumian AP. Specialisation of extracellular matrix for function in tendons and ligaments. Muscles Ligaments Tendons J. 2013;3:12–22. 46. McCarthy MM, Hannafin JA. The mature athlete: aging tendon and ligament. Sports Health. 2014;6:41–48. 47. Rehorn MR, Blemker SS. The effects of aponeurosis geometry on strain injury susceptibility explored with a 3D muscle model. J Biomech. 2010;43:2574–2581. 48. Macdermid JC, Silbernagel KG. Outcome evaluation in tendinopathy: foundations of assessment and a summary of selected measures. J Orthop Sports Phys Ther. 2015;45:950–964. 49. Vicenzino B. Tendinopathy: evidence-informed physical therapy clinical reasoning. J Orthop Sports Phys Ther. 2015;45:816–818. 50. Battery L, Maffulli N. Inflammation in overuse tendon injuries. Sports Med Arthrosc Rev. 2011;19:213–217. 51. Maffulli N, Wong J, Almekinders LC. Types and epidemiology of tendinopathy. Clin Sports Med. 2003;22:675–692. 52. Ackermann PW, Renstrom P. Tendinopathy in sport. Sports Health. 2012;4:193–201. 53. Ackermann PW, Salo PT, Hart DA. Neuronal pathways in tendon healing. Front Biosci. 2009;14:5165–5187. 54. Magnusson SP, Langberg H, Kjaer M. The pathogenesis of tendinopathy: balancing the response to loading. Nat Rev Rheumatol. 2010;6: 262–268. 55. Kaux JF, Forthomme B, Goff CL, Crielaard JM, Croisier JL. Current opinions on tendinopathy. J Sports Sci Med. 2011;10:238–253. 56. Jayaseelan DJ, Moats N, Ricardo CR. Rehabilitation of proximal hamstring tendinopathy utilizing eccentric training, lumbopelvic stabilization, and trigger point dry needling: 2 case reports. J Orthop Sports Phys Ther. 2014;44:198–205. 57. Scott A, Backman LJ, Speed C. Tendinopathy: update on pathophysiology. J Orthop Sports Phys Ther. 2015;45:833–841. 58. Scott A. The fundamental role of inflammation in tendon injury. Curr Med Res Opin. 2013;29(Suppl 2):3–6. 59. Cook J, Rio E, Lewis J. Managing tendinopathy. In: Jull G, Moore A, Falla D, Lewis J, McCarthy C, Sterling M, eds. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. London, England: Elsevier; 2015:112–115. 60. Hashimoto T, Nobuhara K, Hamada T. Pathologic evidence of degeneration as a primary cause of rotator cuff tear. Clin Orthop Relat Res. 2003;415:111–120. 61. Salingcarnboriboon R, Yoshitake H, Tsuji K, et al. Establishment of tendon-derived cell lines exhibiting pluripotent mesenchymal stem cell-like property. Exp Cell Res. 2003;287:289–300. 62. Ngomo S, Mercier C, Roy JS. Cortical mapping of the infraspinatus muscle in healthy individuals. BMC Neurosci. 2013;14:52. 63. Kaeding C, Best TM. Tendinosis: pathophysiology and nonoperative treatment. Sports Health. 2009;1:284–292.

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110. Schmidt H, Pedersen TL, Junge T, Engelbert R, Juul-Kristensen B. Hypermobility in adolescent athletes: pain, functional ability, quality of life, and musculoskeletal injuries. J Orthop Sports Phys Ther. 2017;47:792–800. 111. McGill SM, Cholewicki J. Biomechanical basis for stability: an explanation to enhance clinical utility. J Orthop Sports Phys Ther. 2001;31:96–100. 112. Sophia Fox AJ, Bedi A, Rodeo SA. The basic science of articular cartilage: structure, composition, and function. Sports Health. 2009;1:461–468. 113. Pearle AD, Warren RF, Rodeo SA. Basic science of articular cartilage and osteoarthritis. Clin Sports Med. 2005;24:1–12. 114. Tetteh ES, Bajaj S, Ghodadra NS. Basic science and surgical treatment options for articular cartilage injuries of the knee. J Orthop Sports Phys Ther. 2012;42:243–253. 115. Lundon K, Walker JM. Cartilage of human joints and related structures. In: Magee D, Zachazewski JE, Quillen WS, eds. Scientific Foundations and Principles of Practice in Musculoskeletal Rehabilitation. St. Louis, MO: WB Saunders; 2007:144–174. 116. Barry F, Murphy M. Mesenchymal stem cells in joint disease and repair. Nat Rev Rheumatol. 2013;9:584–594. 117. Bijlsma JW, Berenbaum F, Lafeber FP. Osteoarthritis: an update with relevance for clinical practice. Lancet. 2011;377:2115–2126. 118. Hunter DJ. Osteoarthritis. Best Pract Res Clin Rheumatol. 2011;25: 801–814. 119. Richmond SA, Fukuchi RK, Ezzat A, Schneider K, Schneider G, Emery CA. Are joint injury, sport activity, physical activity, obesity, or occupational activities predictors for osteoarthritis? A systematic review. J Orthop Sports Phys Ther. 2013;43:515–B19. 120. Fox AJ, Wanivenhaus F, Burge AJ, Warren RF, Rodeo SA. The human meniscus: a review of anatomy, function, injury, and advances in treatment. Clin Anat. 2014;28:269–287. 121. Redondo ML, Naveen NB, Liu JN, Tauro TM, Southworth TM, Cole BJ. Preservation of knee articular cartilage. Sports Med Arthrosc Rev. 2018;26:e23–e30. 122. Armiento AR, Stoddart MJ, Alini M, Eglin D. Biomaterials for articular cartilage tissue engineering: learning from biology. Acta Biomater. 2018;65:1–20. 123. Wolfstadt JI, Cole BJ, Ogilvie-Harris DJ, Viswanathan S, Chahal J. Current concepts: the role of mesenchymal stem cells in the management of knee osteoarthritis. Sports Health. 2015;7:38–44. 124. Chandra R, Mahajan S. Role of viscosupplementation in osteo-arthritis of knee joint. J Indian Med Assoc. 2013;111:337–340, 342. 125. Lo GH, LaValley M, McAlindon T, Felson DT. Intra-articular hyaluronic acid in treatment of knee osteoarthritis: a meta-analysis. JAMA. 2003;290:3115–3121. 126. Behrens SB, Deren ME, Matson A, Fadale PD, Monchik KO. Stress fractures of the pelvis and legs in athletes: a review. Sports Health. 2013;5:165–174. 127. Loitz-Ramage B, Zernicke RF. Bone biology and mechanics. In: Magee D, Zachazewski JE, Quillen WS, eds. Scientific Foundations and Principles of Practice in Musculoskeletal Rehabilitation. St. Louis, MO: WB Saunders; 2007:122–143. 128. Warden SJ, Creaby MW, Bryant AL, Crossley KM. Stress fracture risk factors in female football players and their clinical implications. Br J Sports Med. 2007;41(Suppl 1):i38–i43. 129. Lehman TP, Belanger MJ, Pascale MS. Bilateral proximal third fibular stress fractures in an adolescent female track athlete. Orthopedics. 2002;25:329–332. 130. Shah MK, Stewart GW. Sacral stress fractures: an unusual cause of low back pain in an athlete. Spine. 2002;27:E104–E108. 131. Jones GL. Upper extremity stress fractures. Clin Sports Med. 2006; 25:159–174, xi. 132. Tuan K, Wu S, Sennett B. Stress fractures in athletes: risk factors, diagnosis, and management. Orthopedics. 2004;27:583–591; quiz 592–593. 133. Schneiders AG, Sullivan SJ, Hendrick PA, et al. The ability of clinical tests to diagnose stress fractures: a systematic review and meta-analysis. J Orthop Sports Phys Ther. 2012;42:760–771. 134. Schlundt C, El Khassawna T, Serra A, et al. Macrophages in bone fracture healing: their essential role in endochondral ossification. Bone. 2018;106:78–89. 135. Cassuto J, Folestad A, Gothlin J, Malchau H, Karrholm J. The key role of proinflammatory cytokines, matrix proteins, RANKL/OPG and Wnt/β-catenin in bone healing of hip arthroplasty patients. Bone. 2018;107:66–77.

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88. Michener LA, Kulig K. Not all tendons are created equal: implications for differing treatment approaches. J Orthop Sports Phys Ther. 2015;45:829–832. 89. Heales LJ, Lim EC, Hodges PW, Vicenzino B. Sensory and motor deficits exist on the non-injured side of patients with unilateral tendon pain and disability—implications for central nervous system involvement: a systematic review with meta-analysis. Br J Sports Med. 2014;48:1400–1406. 90. Plinsinga ML, Brink MS, Vicenzino B, van Wilgen CP. Evidence of nervous system sensitization in commonly presenting and persistent painful tendinopathies: a systematic review. J Orthop Sports Phys Ther. 2015;45:864–875. 91. Ruedl G, Ploner P, Linortner I, et al. Are oral contraceptive use and menstrual cycle phase related to anterior cruciate ligament injury risk in female recreational skiers? Knee Surg Sports Traumatol Arthrosc. 2009;17:1065–1069. 92. Dragoo JL, Padrez K, Workman R, Lindsey DP. The effect of relaxin on the female anterior cruciate ligament: analysis of mechanical properties in an animal model. Knee. 2009;16:69–72. 93. Negahi Shirazi A, Chrzanowski W, Khademhosseini A, Dehghani F. Anterior cruciate ligament: structure, injuries and regenerative treatments. Adv Exp Med Biol. 2015;881:161–186. 94. Fu FH, Nagai K. Editorial commentary: the anterior cruciate ligament is a dynamic structure. Arthroscopy. 2018;34:2476–2477. 95. Chen X, Jones IA, Park C, Vangsness CT Jr. The efficacy of platelet-rich plasma on tendon and ligament healing: a systematic review and metaanalysis with bias assessment. Am J Sports Med. 2018;46:2020–2032. 96. Frahs SM, Oxford JT, Neumann EE, et al. Extracellular matrix expression and production in fibroblast-collagen gels: towards an in vitro model for ligament wound healing. Ann Biomed Eng. 2018;46(11):1882–1895. 97. Xu C, Zhang Y, Sutrisno L, Yang L, Chen R, Sung KLP. Bay11-7082 facilitates wound healing by antagonizing mechanical injury- and TNFalpha-induced expression of MMPs in posterior cruciate ligament. Connect Tissue Res. 2018:1–12. 98. Murphy PG, Loitz BJ, Frank CB, Hart DA. Influence of exogenous growth factors on the expression of plasminogen activators by explants of normal and healing rabbit ligaments. Biochem Cell Biol. 1993;71:522–529. 99. Pierce GF, Mustoe TA, Lingelbach J, et al. Plateletderived growth factor and transforming growth factor-[beta] enhance tissue repair activities by unique mechanisms. J Cell Biol. 1989;109:429–440. 100. Booher JM, Thibodeau GA. The body’s response to trauma and environmental stress. In: Booher JM, Thibodeau GA, eds. Athletic Injury Assessment. 4th ed. New York, NY: McGraw-Hill; 2000:55–76. 101. Hildebrand KA, Frank CB. Scar formation and ligament healing. Can J Surg. 1998;41:425–429. 102. van Grinsven S, van Cingel RE, Holla CJ, van Loon CJ. Evidence-based rehabilitation following anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2010;18:1128–1144. 103. Bleakley C, McDonough S, MacAuley D. The use of ice in the treatment of acute soft-tissue injury: a systematic review of randomized controlled trials. Am J Sports Med. 2004;32:251–261. 104. Richter M, Bosch U, Wippermann B, Hofmann A, Krettek C. Comparison of surgical repair or reconstruction of the cruciate ligaments versus nonsurgical treatment in patients with traumatic knee dislocations. Am J Sports Med. 2002;30:718–727. 105. Hildebrand KA, Frank CB, Hart DA. Gene intervention in ligament and tendon: current status, challenges, future directions. Gene Ther. 2004;11:368–378. 106. Magee DJ, Zachazewski JE. Principles of stabilization training. In: Magee D, Zachazewski JE, Quillen WS, eds. Scientific Foundations and Principles of Practice in Musculoskeletal Rehabilitation. St. Louis, MO: WB Saunders; 2007:388–413. 107. Maffey LL. Arthrokinematics and mobilization of musculoskeletal tissue: the principles. In: Magee D, Zachazewski JE, Quillen WS, eds. Scientific Foundations and Principles of Practice in Musculoskeletal Rehabilitation. St. Louis, MO: WB Saunders; 2007:487–526. 108. Pacey V, Nicholson LL, Adams RD, Munn J, Munns CF. Generalized joint hypermobility and risk of lower limb joint injury during sport: a systematic review with meta-analysis. Am J Sports Med. 2010;38:1487–1497. 109. Sohrbeck-Nohr O, Kristensen JH, Boyle E, Remvig L, Juul-Kristensen B. Generalized joint hypermobility in childhood is a possible risk for the development of joint pain in adolescence: a cohort study. BMC Pediatr. 2014;14:302.

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The Nervous System

CHAPTER 3

CHAPTER OBJECTIVES At the completion of this chapter, the reader will be able to: 1. Describe the various components of the central nervous system (CNS) and peripheral nervous system (PNS). 2. Describe the anatomic and functional organization of the nervous system. 3. Describe the various components and distributions of the cervical, brachial, and lumbosacral plexuses. 4. Describe the difference between balance and proprioception. 5. Describe the role proprioception plays in function. 6. Describe and differentiate among the various joint mechanoreceptors. 7. Recognize the characteristics of a lesion to the CNS. 8. Outline the neurophysiology of pain and the methods by which pain is controlled. 9. Define concussion and describe its associated signs and symptoms. 10. List the findings and the impairments associated with the more common peripheral nerve lesions. 11. Perform a comprehensive examination of the neurologic system. 12. Describe some of the common pathologies of the nervous system.

OVERVIEW In order to perform a comprehensive neuromusculoskeletal examination, the clinician must have a clear understanding of the anatomy, physiology, and function of the various components of the nervous system, and be able to recognize those signs and symptoms that indicate a compromise of the nervous system.

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The nervous system is composed of only two principal types of cells—neurons and supporting cells. The neuron, which is classified according to structure or function, serves to store and process information, and is the functional unit of the nervous system. The supporting cell called the neuroglial cell, or simply glial, functions to provide structural and metabolic support for the neurons.1 Unlike many cells, neurons cannot divide by mitosis, but they do have some capability to regenerate. In contrast, glial cells retain limited mitotic abilities.

Anatomy The human nervous system can be subdivided into two anatomic divisions: the CNS, comprising the brain and the spinal cord, and the PNS, formed by the nerves and ganglia (cluster of nerve cell bodies located outside of the CNS). The PNS is further subdivided into somatic and autonomic divisions. The somatic division, which includes the cranial (with the exception of cranial II) and the spinal nerves, innervates the skin, the muscles, and the joints, while the autonomic division innervates the glands and the smooth muscle of the viscera and the blood vessels.1 Neurons can broadly be divided into four types based on anatomical and functional criteria2: Aα fibers: Thick myelinated fibers transmitting signals to and from muscles. ▶▶ Aβ fibers: Thick myelinated fibers conducting sensations such as touch and proprioception. ▶▶ Aδ fibers: Thin myelinated fibers transmitting nociceptive signals evoked by stimuli such as cold and pinprick. ▶▶ C fibers: Small-diameter unmyelinated nerve fibers subserving nociception evoked by heat or mechanical stimuli as well as innocuous temperature changes (e.g., warm detection) and itch. C fibers can be further subdivided into four main groups: ■■ C-polymodal fibers, which are activated by mechanical thermal and chemical stimuli. ■■ Mechanoreceptors, which are activated by specific modalities. ■■ Low threshold C fibers, which mediate pleasant touch. ▶▶

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Dendrites

Axon from another neuron

Cell body

Nissl bodies

ANATOMY

Synapse Initial segment of axon Oligodendrocyte

Perikaryon Axon hillock Myelin sheath Axon

Collateral axonal branch

Node of ranvier Central nervous system Peripheral nervous system

Schwann cell Collateral branch

Axon terminal

Motor end plates FIGURE 3-1  Schematic drawing of a neuron. (Reproduced with permission from Junqueira LC, Carneiro J. Junqueira’s Basic Histology: Text and Atlas. 13th ed. New York, NY: McGraw-Hill Education; 2013.)

Silent (sleeping) nociceptors, which are not normally activated by thermal or mechanical stimuli, but become sensitized after exposure to inflammatory stimuli. Although neurons come in various sizes and shapes, there are four functional parts for each nerve fiber (Fig. 3-1): ■■

Dendrite. Dendrites serve a receptive function and receive information from other nerve cells, or the environment. ▶▶ Axon. The axon cylinder, in which there is a bidirectional flow of axoplasm, conducts information and nutrition to ▶▶

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the nerve cells and the tissues that the nerve innervates. Many axons are covered by myelin, a lipid-rich insulating membrane. In myelinated fibers, there is a direct proportional relationship between fiber diameter and conduction velocity.3 This membrane is divided into segments, approximately 1-mm long, by small gaps, called nodes of Ranvier, in which the myelin is absent.1 Myelin, which has a high electrical resistance and low capacitance, serves to increase the nerve conduction velocity of neural transmissions through a process called salutatory conduction. The Schwann cell can be myelinating (responsible for laying down myelin around axons), or non-myelinating. ▶▶ Cell body. The cell body contains the nucleus of the cell and has important integrative functions. ▶▶ Axon terminal. The axon terminal is the transmission site for action potentials, the messengers of the nerve cell. Peripheral nerves are enclosed in three layers of tissue of differing character. From the inside outward, these are the endoneurium, perineurium, and epineurium.1 The endoneurium, which surrounds single axons and is in close contact with Schwann cells, has an important mechanical and physiological protective function for the nerve fascicles.2 The nerve fibers embedded in endoneurium form a funiculus surrounded by perineurium, a thin but strong sheath of connective tissue. A fluid exists in the endoneurial spaces, which following nerve injury can produce intraneural edema, which in turn can play a major role in acute and chronic nerve lesions.3 The nerve bundles are embedded in a loose areolar connective tissue framework, called the epineurium. The epineurium that extends between the fascicles is termed the inner or the interfascicular epineurium, whereas that surrounding the entire nerve trunk is called the epifascicular epineurium.1 The connective tissue outside the epineurium is referred to as the adventitia of the nerve or the epineural tissue. Although the epineurium is continuous with the surrounding connective tissue, its attachment is loose, so that nerve trunks are relatively mobile, except where tethered by entering vessels or exiting nerve branches (see Chapter 11). Peripheral nerves also contain a small amount of adipose tissue, which may protect the nerves from excessive pressure.2 There are no connective tissue components in the spinal nerves comparable to the epineurium and the perineurium of the peripheral nerve; at least they are not developed to the same degree.1 As a result, the spinal nerve roots are more sensitive to both tension and compression. The spinal nerve roots also are devoid of lymphatics and, thus, are predisposed to prolonged inflammation.1 The communication of information from one nerve cell to another occurs at junctions called synapses, where a chemical is released in the form of a neurotransmitter. A difference in concentration exists across the cell membrane of potassium, sodium, and chloride ions. These ions can selectively permeate ion channels in the membrane so that an unequal distribution of net charge occurs. The resting membrane potential results from an internal negativity resulting from the active transport of sodium from inside to outside the cell, and potassium from outside to inside the cell.3

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Central Nervous System The CNS consists of the brain and an elongated spinal cord. The spinal cord participates directly in the control of body movements, the processing and transmission of sensory information from the trunk and the limbs, and the regulation of visceral functions.1 The spinal cord also provides a conduit for the two-way transmission of messages between the brain and the body. These messages travel along the pathways, or tracts, that are fiber bundles of similar groups of neurons. These tracts may descend or ascend.

Aggregates of spinal tracts are referred to as columns or lemnisci. The spinal cord is normally 42–45-cm long in adults and is continuous with the medulla and brain stem at its upper end (Fig. 3-2A).1 The conus medullaris serves as the distal end of the cord, and, in adults, the conus ends at the L1 or L2 level of the vertebral column. A series of specializations, the filum terminales and the coccygeal ligament, anchor the spinal cord and the dural sac inferiorly and ensure that the tensile forces applied to the spinal cord are distributed throughout its entire length.1 The spinal cord has an external segmental organization. Each of the 31 pairs of spinal nerves that arise from the spinal cord has an anterior (ventral) root and a posterior (dorsal) root, with each root consisting of one to eight rootlets and bundles of nerve fibers. A spinal (sensory) ganglion (posterior [dorsal] root ganglion), a swelling that contains nerve cell bodies, is located in the posterior (dorsal) root (Fig. 3-2B) of a typical spinal nerve. The cauda equina (Fig. 3-2C) is a bundle of spinal nerves and spinal nerve rootlets, consisting of the second through fifth lumbar nerve pairs, the first through fifth sacral nerve pairs, and the coccygeal nerve, all of which arise from the lumbar enlargement and the conus medullaris of the spinal cord. Three membranes, or meninges, envelop the structures of the CNS: dura mater, arachnoid, and pia mater (Fig. 3-3). The meninges and related spaces are important to both the nutrition and the protection of the spinal cord. The cerebrospinal fluid that flows through the meningeal spaces, and within the ventricles of the brain, provides a cushion for the spinal cord. The meninges also form barriers that resist the entrance of various noxious organisms.

Dura Mater The dura mater (Latin, tough mother) (Fig. 3-3) is the outermost and the strongest of the membranes and is composed of an inner meningeal layer and an outermost periosteal layer. The dura runs uninterrupted from the interior of the cranium through the foramen magnum and surrounds the spinal cord throughout its distribution from the cranium to the coccyx at the second sacral level (S2). The dura also is attached to the posterior surfaces of C2 and C3.1 The dura forms a vertical sac (dural sac) around the spinal cord, and its short lateral projections blend with the

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Arachnoid The arachnoid is a thin and delicate avascular layer, coextensive with the dura mater and the pia mater (Fig. 3-3). Even though the arachnoid and the pia mater are interconnected by trabeculae, there is a space between them, called the subarachnoid space (Fig. 3-3), which contains the cerebrospinal fluid. The supposedly rhythmic flow of this cerebrospinal fluid is the rationale used by craniosacral therapists to explain their techniques, although there is no evidence of this finding in the literature.

Pia Mater The pia mater (Fig. 3-3) is the deepest of the layers. It is intimately related and firmly attached, via connective tissue investments, to the outer surface of the spinal cord and the nerve roots. The pia mater conveys the blood vessels that supply the spinal cord and has a series of lateral specializations, the denticulate (dentate) ligaments, which anchor the spinal cord to the dura mater. These ligaments, which derive their name from their tooth-like appearance, extend the whole length of the spinal cord.

The Nervous System

CLINICAL PEARL

epineurium of the spinal nerves. The dura is separated from the bones and the ligaments that form the walls of the vertebral canal by an epidural space, which can become partly calcified or even ossified with age.

Peripheral Nervous System: Somatic Nerves The somatic portion of the PNS consists of the cranial nerves (CNs) and the spinal nerves. The main functional component of peripheral neurons consists of the axon and dendrite as well as their cell body (e.g., in the dorsal root ganglion for sensory neurons).2

Cranial Nerves The CNs, typically, are described as comprising 12 pairs, which are referred to by the Roman numerals I through XII (Fig. 3-4). The CN roots enter and exit the brain stem to provide sensory and motor innervation to the head and the muscles of the face. CN I (olfactory) and CN II (optic) are not true nerves but rather fiber tracts of the brain. The examination of the CN system is described later in this chapter (see section “Orthopaedic Neurologic Testing”). CN I (olfactory). The olfactory tract (Fig. 3-4) arises from the olfactory bulb on the inferior aspect of the frontal lobe, just above the cribriform plate. From here it continues posteriorly as the olfactory tract and terminates just lateral to the optic chiasm. The olfactory nerve handles the sense of smell. ▶▶ CN II (optic). The fibers of the optic nerve arise from the inner layer of the retina and proceed posteriorly to enter the cranial cavity via the optic foramen, to form the optic chiasm (Fig. 3-4). The fibers from the nasal half of the retina decussate within the optic chiasm, whereas ▶▶

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Vertebral levels

Spinal cord levels

1

C1

2

C2 C3

5

C4

6

ANATOMY

7

T1

Dorsal root

8 1 2 3 4

Ventral root

C1

4

3

C7

Spinal nerve levels

C5 C6 C7 C8 T1

Spinal n. Vertebra

Ventral ramus

Spinal cord

Dorsal ramus

Dorsal horn of gray matter

Motor nerve to muscle

T2 T3

5

T4

6

T5

7

T6

8

T7

B

Sensory nerve from skin

9

T8 10 11 12

T9 T10

1

T12

2 3 4 5 1 2 3 4 5 1

L1

T11 T12

Cauda equina L4 vertebra L4 spinal n.

L5 spinal n.

L1 L2

S1 spinal n.

L3 L4

L5

S3 spinal n.

L5 S1

S5 spinal n. S1 S2 S3 S4 S5

S5

Spinal n.

C

Coccyx

A FIGURE 3-2  Schematic illustration of the spinal cord. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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Scalp

Skull Dura mater Arachnoid mater

The Nervous System

Cerebral a. Subarachnoid space Bridging v. Pia mater Arachnoid villus

Cerebral a. FIGURE 3-3  Schematic illustration of the relationship of the dura mater, arachnoid, and pia mater. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

and middle cranial fossa. The nerve innervates the lateral rectus muscle.

those from the lateral half do not. The optic nerve handles vision. ▶▶

CN III (oculomotor). The oculomotor nerve arises in the oculomotor nucleus and leaves the brain on the medial aspect of the cerebral peduncle (Fig. 3-4). It then extends from the interpeduncular fossa and runs between the posterior cerebral artery and the superior cerebellar artery, before leaving the cranial cavity and entering the cavernous sinus by way of the superior orbital fissure. The somatic portion of the oculomotor nerve supplies the levator palpebrae superioris muscle; the superior, medial, and inferior rectus muscles; and the inferior oblique muscles (Fig. 3-4). These muscles handle some eye movements. The visceral efferent portion of this nerve innervates two smooth intraocular muscles: the ciliary and the constrictor pupillae. These muscles handle papillary constriction.

▶▶

CN IV (trochlear). The trochlear nerve arises from the trochlear nucleus, just inferior to the oculomotor nucleus at the anterior border of the periaqueductal gray (PAG) matter (Fig. 3-4). The fibers cross within the midbrain and then emerge contralaterally on the posterior surface of the brain stem, before entering the orbit via the superior orbital fissure, to supply the superior oblique muscle.

Note: Because nerves III, IV, and VI are examined together, CN V is described after CN VI. ▶▶

CN VI (abducens). The abducens nerve originates from the abducens nucleus within the inferior aspect of the pons. Its long intracranial course to the superior orbital fissure makes it vulnerable to pathology in the posterior

Dutton_Ch03_p0061-p0160.indd 65

CN V (trigeminal). The trigeminal nerve (labelled CN VI in Fig. 3-4) is so named because of its tripartite division into the maxillary, ophthalmic, and mandibular branches (V-1, V-2, and V-3 respectively in Fig. 3-4). All three of these branches contain sensory cells, but the ophthalmic and the maxillary are exclusively sensory, the latter supplying the soft and hard palate, maxillary sinuses, upper teeth and upper lip, and mucous membrane of the pharynx. The mandibular branch not only carries sensory information but also represents the motor component of the nerve, supplying the muscles of mastication, both pterygoids, the anterior belly of digastric, tensor tympani, tensor veli palatini, and mylohyoid.   The spinal nucleus and the tract of the trigeminal nerve cannot be distinguished either histologically or on the basis of afferent reception from the cervical nerves. Consequently, the entire column can be viewed as a single nucleus and, legitimately, may be called the trigeminocervical nucleus. ▶▶ CN VII (facial). The facial nerve is made up of a sensory (intermediate) root, which conveys taste, and a motor root, the facial nerve proper, which supplies the muscles of facial expression, the platysma muscle, and the stapedius muscle of the inner ear (Fig. 3-4). The intermediate root, together with the motor nerve and CN VIII, travels through the internal acoustic meatus to enter the facial canal of the temporal bone. From here, the intermediate nerve swells to form the geniculate ganglion and gives off the greater superficial petrosal nerve, which ▶▶

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V-1

V-2

V-3

CN VI CN IV

ANATOMY

CN II CN I

V-1

V-2 V-3

CN III

V-3

CN V

CN VII

CN VIII CN IX

CN X

CN XII

CN XI

KEY

Somatic motor Branchial motor Visceral motor

General sensory Special sensory Visceral sensory

FIGURE 3-4  The CNs. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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The vestibular system includes the vestibular apparatus of the inner ear, the vestibular nuclei and their neural projections, and the exteroreceptors throughout the body, especially in the upper cervical spine and the eyes.1 The apparatus of the inner ear consists of the static labyrinth, which comprises three semicircular canals (SCC) (Fig. 3-5A), each orientated at right angles to the other. The labyrinth includes specialized sensory areas that are located in the utricle and the saccule (Fig. 3-5A), within which otoliths (hair cells) are located (Fig. 3-5B). A series of filaments line the basement membrane of the SCC and project into endolymph, which deforms these filaments when head motion occurs. This deformation is registered by receptor cells, and when sudden perturbations occur, the frequency of nerve impulses along the afferent nerve supply of the cell body is altered. Unlike the filaments of the SCC, the filaments of the utricle and saccule do not project into endolymph but instead insert into a gelatinous mass, within which the otolith is embedded. Deformation of these filaments is produced by the weight of the otolith against the cilia, as the gelatinous mass is displaced during head movement. The otoliths are responsible for providing information about gravitational forces, as well as vertical and horizontal motion. The filaments of the saccule also provide information about vertical motion. At rest, the endolymphatic fluid, or the gelatinous membrane, is stationary. When motion of the head occurs, the endolymphatic fluid, or the gelatinous membrane, initially remains stationary because of its inertia, while the canals move. This relative motion produces a dragging effect on the filaments and either increases or decreases the discharge rate, depending on the direction of shear. At the end of the head movement, the fluid and the membrane continue to move, and the cilia are now dragged in the opposite direction before coming to rest. In essence, the SCC receptors transmit a positive signal when movement begins, no signal when the motion has finished, and a normal level after the sensory cell has returned to its original position. As this occurs, other sensory cells orientated in the opposite direction react in the reverse fashion. ▶▶

CN IX (glossopharyngeal). The glossopharyngeal nerve (Fig. 3-4) contains a somatic motor, visceral efferent, visceral sensory, and somatic sensory fiber. The motor fibers originate in the nucleus ambiguous, leaving the lateral medulla to join the sensory nerve, which arises from cells in the superior and petrous ganglia. The

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glossopharyngeal nerve exits the skull through the jugular foramen and serves some functions, including supplying taste fibers for the posterior third of the tongue. ▶▶ CN X (vagus). The functions of the vagus nerve (Fig. 3-4) are numerous and include the motor parasympathetic fibers to all the organs except the suprarenal (adrenal) glands, from its origin down to the second segment of the transverse colon. The vagus also controls some skeletal muscles, including the ■■ cricothyroid muscle; ■■ levator veli palatini muscle; ■■ salpingopharyngeus muscle; ■■ palatoglossus muscle; ■■ palatopharyngeus muscle; ■■ superior, middle, and inferior pharyngeal constrictors; and ■■ muscles of the larynx. The vagus nerve is thus responsible for such varied tasks as heart rate, gastrointestinal peristalsis, sweating, speech, and breathing. It also has some afferent fibers that innervate the inner (canal) portion of the outer ear.

The Nervous System

eventually innervates the lacrimal and salivary glands via the pterygopalatine ganglion and the chorda tympani nerve, respectively. The facial nerve proper exits the skull through the stylomastoid foramen. ▶▶ CN VIII (vestibulocochlear). The vestibulocochlear nerve subserves two different senses: balance and hearing. The cochlear portion of the nerve arises from spiral ganglia, and the vestibular portion arises from the vestibular ganglia in the labyrinth of the inner ear (Fig. 3-4). The cochlear portion is concerned with the sense of hearing, whereas the vestibular portion is a part of the system of equilibrium, the vestibular system.

CN XI (accessory). The accessory nerve consists of a cranial component and a spinal component. The cranial root originates in the nucleus ambiguous and is often viewed as an aberrant portion of the vagus nerve. The spinal portion of the nerve arises from the lateral parts of the anterior horns of the first five or six cervical cord segments and ascends through the foramen magnum. The spinal portion of the accessory nerve supplies the sternocleidomastoid (SCM) and the trapezius muscles (Fig. 3-4). ▶▶ CN XII (hypoglossal). The hypoglossal nerve is the motor nerve of the tongue, innervating the ipsilateral side of the tongue (Fig. 3-4) as well as forming the descendens hypoglossi, which anastomoses with other cervical branches to form the ansa hypoglossi. The latter, in turn, innervates the infrahyoid muscles. ▶▶

Spinal Nerves There are a total of 31 symmetrically arranged pairs of spinal nerves, each derived from the spinal cord.4 The spinal nerves are divided topographically into eight cervical pairs (C1–8), 12 thoracic pairs (T1–12), five lumbar pairs (L1–5), five sacral pairs (S1–5), and a coccygeal pair (Fig. 3-2A). The posterior (dorsal) and anterior (ventral) roots of the spinal nerves are located within the vertebral canal (Fig. 3-2B). The portion of the spinal nerve that is not within the vertebral canal, and that usually occupies the intervertebral foramen, is referred to as a peripheral nerve. As the nerve roots begin to exit the vertebral canal, they must penetrate the dura mater before passing through dural sleeves within the intervertebral foramen. The dural sleeves are continuous with the epineurium of the nerves.

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A

Stapes in the vestibular window Vestibule Utricle Semicircular Semicircular canals duct Saccule

Petrous part of temporal bone CN VII CN VIII

ANATOMY

Internal acoustic meatus Cochlear n. Vestibular n. Helicotrema

Tympanic membrane

B

Cochlear window

Scala vestibuli Cochlea

Vestibular membrane Scala vestibuli (containing perilymph)

Cochlear duct Scala tympani

Cochlear duct (containing endolymph)

Auditory tube

Tectorial membrane

Spiral ganglion (CN VIII)

C

Hair cells

Auricle Scala tympani (containing perilymph)

Basilar membrane

External acoustic meatus Tympanic membrane

Footplate of stapes in vestibular window

Malleus Incus Stapes

Arrows indicate direction of propagated wave Vestibular membrane

Scala vestibuli (containing perilymph) Hairs Hair cells

Sound waves

Helicotrema Basilar membrane Cochlear window External ear

Middle ear

Scala tympani (containing perilymph)

Auditory tube Inner ear

FIGURE 3-5  The apparatus of the inner ear. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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Essentially, there are four branches, or rami, of spinal nerves:

There are three functional types of nerve fibers in the major nerve trunks, which vary in quantity depending on the particular nerve: afferent (sensory), autonomic (visceral efferent) (see Peripheral Nervous System: Autonomic Nervous System), and motor (somatic efferent) (Table 3-1). The faster nerve fibers such as the Aδ fibers are more concerned with speed and quality of human movement whereas the C fibers conduct far more slowly and are more involved with nociception and, by the compounds they release, the health of surrounding tissue.3 Afferent (Sensory) Nerves. The sensory nerves carry afferents (a nerve conveying impulses from the periphery to the CNS) from a portion of the skin. They also carry efferents (a nerve conveying impulses from the CNS to the periphery) to the skin structures. When a sensory nerve is compressed, symptoms occur in the area of the nerve distribution. This area of distribution, called a dermatome, is a well-defined

TABLE 3-1

Classification of Afferent, Cutaneous, and Efferents

Type

Conduction Velocity (m/s)

Aα

70–120

Aα (type Ia) Aα (type Ib) Aβ (type II)

70–120 70–120 30–120

Aδ (type III)

12–30

Aγ B

15–30 R)

Esophagus (T5–6)

Pharynx, lower neck, arms, midline chest from upper to lower sternum

Gastric (T6–10)

Lower thoracic to upper abdomen

ANATOMY

Gallbladder (T7–9) Upper abdomen, lower scapular, and thoracolumbar Pancreas

Upper lumbar or upper abdomen

Kidneys (T10–L1)

Upper lumbar, occasionally anterior abdomen approximately 4–5 cm lateral to umbilicus

Urinary bladder (T11–12)

Lower abdomen or low lumbar

Uterus

Lower abdomen or low lumbar

Reproduced with permission from Head H. Studies in Neurology. London: Oxford Medical Publications; 1920.

116

the side effects of medications, or fear of reinjury. Some individuals are motivated to avoid activities in which they have experienced acute episodes of pain in order to reduce the likelihood of re-experiencing pain or causing further physical damage.147 While this is a normal adaptive behavioral strategy for dealing with situations involving acute pain, it can become maladaptive when dealing with chronic pain.147 The basic premise of fear-avoidance behavior is that if an individual interprets the experience of pain (which is associated with or without an actual injury) as significantly threatening, and begins to catastrophize about it, then pain-related fear evolves.147 For patients who interpret the pain as nonthreatening, and who do not catastrophize, pain-related FA does not develop, and normalization of daily activities and rapid recovery are likely to occur.147 Somatosensory amplification refers to the tendency to experience somatic sensation as intense, noxious, and disturbing. Somatosensory amplification is observed in patients whose extreme anxiety leads to an increase in their perception of pain. In 1980, Professor Gordon Waddell first described a group of eight clinical physical signs that have come to be known as Waddell signs. These signs were initially developed as a method to identify patients with LBP who were likely to experience a poor surgical outcome from lower back surgery.148 More recently, the Waddell signs have been employed to detect abnormal, sometimes inappropriately labeled nonorganic, manifestations of LBP in patients who have depression, emotional disturbance, or anxiety states.149 This usage has since expanded to identify malingering in patients, such as discrediting the legitimacy of motor vehicle accident claims as well as identifying psychogenic components in other non-lumbar pain syndromes.148 However, in 1998, Main and

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TABLE 3-8

 ommon Signs and Symptoms of C Pathologies Associated with Abdominal and Back Pain

Pathology/ Condition

Signs/Symptoms

AAA        

Pain located in central lumbar region Palpable pulsating abdominal mass Pain described as pulsating or throbbing Patient unable to find comfortable position History of AAA or vascular claudication

Cancer (i.e., pancreatic, ovarian, and prostate metastasis to spine)

Night pain that disrupts sleep Pain that is unrelieved by rest Unexplained weight loss Fever and sweats Extreme fatigue Altered gastrointestinal or genitourinary function

Intestinal obstruction (i.e., volvulus, adhesions, tumor, and functional)

Colicky abdominal pain Abdominal distention Nausea/vomiting/sweating Constipation

Gastrointestinal infection/ inflammation (i.e., peritonitis, appendicitis, and pancreatitis)

Abdominal pain and muscle guarding Rebound tenderness Any movement aggravates pain Fever, chills, sweating, and vomiting Pain relieved by sitting and leaning forward (pancreatitis)

Renal disorders (i.e., Severe pain along upper urinary tract pain pattern nephrolithiasis, urinary tract Altered urinary tract function (frequency, infection, and urgency, and dysuria) pyelonephritis) Hematuria Gynecological (i.e., endometriosis, pelvic inflammatory disease, and ovarian cysts)

Lumbopelvic and lower abdominal pain Cyclical pain, nausea, and vomiting Dysmenorrhea Abnormal uterine bleeding

AAA, abdominal aortic aneurysm. Reproduced with permission from Stowell T, Cioffredi W, Greiner A, et al. Abdominal differential diagnosis in a patient referred to a physical therapy clinic for low back pain. J Orthop Sports Phys Ther. 2005 Nov; 35(11):755–764.

Waddell stated that these physical signs have been misinterpreted, are not tests of credibility, and have been misused both clinically and medicolegally as they felt the behavioral signs may be a response affected by fear from injury and development of chronic incapacity.150 The Somatosensory Amplification Rating Scale (SARS; Table 3-9) is a version of the Waddell’s nonorganic physical signs, which has been modified to allow for a more accurate appraisal of the patient with exaggerated illness behavior.

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TABLE 3-9

Somatosensory Amplification Rating Scale Percent

Scorea

Sensory examination 1.  No deficit or deficit well localized to dermatome Deficit related to dermatome(s) but some inconsistency Nondermatomal or very inconsistent deficit Blatantly impossible (i.e., split down midline or entire body with positive tuning fork test) 2.  Amount of body involved: Evaluate similar to burn (% of surface areas for an entire leg is 18%) 

            60%

   0  1  2  3    0  1  2  3

Motor examination 1.  No deficit or deficit well localized to myotomes Deficit related to myotome(s) but some inconsistency Non-myotomal or very inconsistent weakness, exhibits cogwheeling or giving way, weakness is coachable Blatantly impossible, significant weakness that disappears when distracted 2.  Amount of body involved      

       

   0  1  2

  60%

 3  0  1  2  3

Tenderness 1. No tenderness or tenderness clearly localized to discrete, anatomically sensible structures Tenderness not well localized, some inconsistency Diffuse or very inconsistent tenderness, multiple anatomic structures involved (skin, muscle, bone, etc.) Blatantly impossible, significant tenderness of multiple anatomic structures (skin, muscle, bone, etc.), which disappears when distracted 2.  Amount of body involved      

       

   0  1  2

 

 3

60%

 0  1  2  3

Additional tests: distraction tests Distraction SLR rating determined by the difference in measurements between supine and seated     SLR supine at less than 45 degrees Standing flexion versus long sit test Rating determined by two factors Difference between hip ROM, standing versus supine       Distance measurement from middle finger to toes, standing versus supine (long sit)       Total score possible

  45 degrees       50 degrees 18 cm  

 1  2  3    1  0  1  2  3  0  1  2  3 27

The Nervous System

Examination

ROM, range of motion; SARS, Somatosensory Amplification Rating Scale; SLR, straight-leg raise. a

SARS scores of 5 or greater are indicative of inappropriate illness behavior. The higher the score, the greater the exaggerated behavior.

Data from Barsky AJ, Goodson JD, Lane RS, et al. The amplification of somatic symptoms. Psychosom Med. 1988 Sep-Oct;50(5):510–519.

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CLINICAL PEARL It is important to remember that the Waddell and SARS assessment tools are not designed to detect whether patients are malingering, but only to indicate whether they have behavioral signs that may be in response to a fear from injury and the potential for long-term incapacity.

Pain-Control Mechanisms ANATOMY 118

One of the earliest pain-control mechanisms proposed a concept called the gate control theory. This theory proposed that Aβ mechanoreceptor inputs to spinal pain transmission neurons are gated, or modulated via a feedforward inhibition. A 2018 study postulated that capsaicin-activated nociceptor inputs reduce Iα and sensitize the spinal pain transmission neurons, allowing Aβ inputs to cause firing before inhibitory inputs arrive, which addresses the timing problem underlying the gating by feedforward inhibition, and that their modulation offers a way to bypass the gate control.151 The key brain sites involved in pain perception include the anterior cingulate cortex, anterior insular cortex, primary somatosensory cortex, secondary somatosensory cortex, a number of regions in the thalamus and cerebellum, and, interestingly, areas such as the premotor cortex that are normally linked to motor function.85,152 Indeed, it is clear that both the basal ganglia (associated with planned action), the PAG of the midbrain region, and the raphe nucleus in the pons and the medulla receive nociceptive input as well as coordinating important aspects of movement and motor control.43,85,153,154 The PAG area of the upper pons sends signals to the raphe magnus nucleus in the lower pons and the upper medulla.1 This nucleus relays the signal down the cord to a pain-inhibitory complex located in the posterior (dorsal) horn of the cord.43 The nerve fibers derived from the PAG area secrete enkephalin and serotonin, whereas the raphe magnus releases enkephalin only.43 The PAG is also believed to be involved in complex behavioral responses to stressful or life-threatening situations or to promote recuperative behavior after a defense reaction. Enkephalin is believed to produce presynaptic inhibition of the incoming pain signals to lamina I–V, thereby blocking pain signals at their entry point into the cord.155,156 It is further believed that the chemical releases in the upper end of the pathway can inhibit pain signal transmission in the reticular formation and the thalamus. The inhibition from this system is effective on both fast and slow pains. In the cortex, a negative-feedback loop, called the corticofugal system, originates at the termination point of the various sensory pathways.43 Excessive stimulation of this feedback loop results in a signal being transmitted down from the sensory cortex to the posterior horn of the level from which the input arose. This response produces lateral or recurrent inhibition of the cells adjacent to the stimulated cell, thereby preventing the spread of the signal. This is an automatic gain control system to prevent overloading of the sensory system. Finally, two other neuroactive peptides, beta endorphin and dynorphin, are theorized to be used as analgesics in the

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body to numb or dull pain in addition to promoting feelings of well-being and increasing relaxation.

The Assessment of Pain A number of biological, psychological, and social factors can influence how pain is experienced, expressed, and interpreted. The expression of pain may be verbal, self-reported, or an observation of behavior, and this may be self-initiated by the person in pain or elicited by an observer’s question.114,157 The timely assessment of pain is critical for the effective management of neuromusculoskeletal pain conditions. Also critical is the use of an accurate and reliable method for the assessment of pain as this determines a better understanding of a person’s pain experience, allows the identification of appropriate treatment options, helps monitor any change in a person’s pain condition, and minimizes the potential for any adverse physiological and psychological consequences of unrelieved or inadequately managed pain.114,158

CLINICAL PEARL Fundamental differences exist between the expressions of the pain experience in infants, children, adolescents, and adults, which highlights the need to assess and interpret pain in a way that is specific to each age group.114 Whenever possible, evidence-based measures of pain intensity must be used as any inconsistency in the assessment, measurement, and documentation of pain means that, in many instances, pain may be underestimated and undertreated.114 One of the simplest methods to quantify the intensity of pain in adults and adolescents (12–18 years) is to use a 10-point visual analog scale (VAS) (see Chapter 4). The VAS is a numerically continuous scale that requires the pain level be identified by making a mark on a 100-mm line, or by circling the appropriate number in a 1–10 series. The patient is asked to rate his or her present pain compared with the worst pain ever experienced, with 0 representing no pain, 1 representing pain that is minimally perceived, and 10 representing pain that requires immediate attention. The Brief Pain Inventory (BPI), previously known as the Brief Pain Questionnaire, rapidly assesses the severity of pain and its impact on functioning. It is available in a short (9 items) and long (17 items) form. The BPI measures both the intensity of pain (sensory dimension) and interference of pain in the patient’s life (reactive dimension). It also questions the patient about pain relief, pain quality, and patient perception of the cause of pain. Pressure pain threshold (PPT), commonly used in the evaluation of tenderness, is defined as the minimum force applied which induces pain.159 The PPT is measured using a pressure algometer. The assessment of pain in children is somewhat more challenging and the choice of approach will depend on the age and abilities of the child. The three main approaches to measuring pain intensity in children are as follows114:

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Although it is not within the scope of this text to describe all of the available pediatric pain assessment tools, the following can serve as a reference114:

contributors and acknowledging the important role of pain-inhibitory processes related to reducing the fear of pain. One of the goals of the CFT approach is to determine the presence of any painful postures (e.g., sitting, lying, standing) and painful movements (e.g., sitto-stand, squatting, bending forward) and then modifying the offending posture or movement while introducing helpful techniques, such as relaxed breathing, during the movement. The aim of decreasing the symptoms is for the patient to be able to repeat the movement multiple times and then introduce that movement into meaningful functional tasks, and, in so doing, “disrupt” the previous memory and association of that task with symptoms.161–163 ▶▶ Graded Motor Imagery (GMI). GMI is a precise sequence of intervention strategies, which evolved from the growing understanding of the fundamental neuroplasticity of complex pain states, that is aimed at the treatment of complex pain syndromes.164 This relatively new approach is backed up with neuroscience theory including neuromatrix paradigm, neuroplasticity, and mirror neurones. The sequences of interventions are as follows165–169:

Infant (3 Years or Younger).  The suggested scale for this age group is the The Face, Legs, Activity, Cry and Consolability (FLACC) Scale. ▶▶ Preschool Child (3–5 Years).  The suggested scale for this age group is the Pieces of Hurt Tool, supplemented by parent/guardian report and observation. ▶▶ Child (6–11 Years).  The suggested scale for this age group is the Faces Pain Scale Revised (FPS-R). ▶▶

Nonpharmacological Control of Pain



The pharmacological control of pain is discussed in Chapter 9. Clinicians can use several nonpharmacological therapeutic interventions to manage pain. These include, in addition to thermotherapy and cryotherapy (see Chapter 8), the following:



Exercise. Physical therapists use a combination of different forms of exercise (stretching, strengthening, motor control, coordination, endurance, and aerobic) to individualize a program to the person with pain.160 Numerous studies have shown the effectiveness of exercise for preventing and controlling pain, and for reducing the chronicity of pain. However, with the exception of strengthening anaerobic exercises, there are insufficient data to make recommendations regarding the frequency, duration, and intensity of an effective exercise program for controlling or reducing pain. The methods by which exercise helps with pain have focused on the production of endogenous opioids, and serotonin that are released with exercise. ▶▶ Cognitive Functional Therapy (CFT). CFT is an approach that aims to address the multidimensional nature of pain while simultaneously addressing any biomechanical ▶▶

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Pain neuroscience education. There are two homunculi, one that represents the skin and the other that represents movement. In the sensory homunculus, the areas which require enhanced sensation have a larger representation. Imaging studies have shown that chronic pain results in changes in the virtual representation (referred to as smudging) of the area affected, so that there is no longer a clear defined outline of the body part and an overlapping of neighboring body parts.170,171 Theoretically, in addition to the nervous system, the immune and endocrine systems play a large role in complex pain syndromes. Other factors include past experiences, stress, environment, and cognitions. Laterality. This involves the restoration of the patient’s accuracy and speed of identifying whether a picture or actual body part is a right or left part of the body, or identifying if the body part is turned to the right or the left (e.g., the direction of neck rotation). Motor imagery/visualization. Involves the observation and imaging of movements and postures which are progressively more complex and contextually variable. The patient imagines performing movements or adopting postures without pain before attempting to perform them without pain. It is thought that there are representations within the spinal cord, thalamic and cortical structures that have a role in the guidance of imagined and actual movements. By performing educated movements, the smudging can normalize the virtual representations in the brain. Sensory retraining. According to GMI, the sensitivity threshold for pain transmission can increase or decrease based on a number of factors. The goals of the interventions are to decrease the sensitivity of the pain system and to increase the patient’s tolerance for activities. Mirror therapy. Involves using a mirror to present a reverse image of a limb to try and trick the patient’s brain.

The Nervous System

Physiological. Physiological indicators (e.g., increased heart rate, blood pressure, sweating) are associated with a generalized (nonspecific) stress reaction and more strongly associated with distress and anxiety than selfreport pain measures. For this reason, physiological indicators should not be used in isolation to estimate the presence, quality, or intensity of pain. ▶▶ Observations of behavior. Observational measures involve observing an individual’s nonverbal behavior (e.g., crying, facial expression, torso and limb movements) and interactions (e.g., social, appetite). Observational measures are particularly useful for assessing pain in children aged less than 4 years, who do not have the language skills necessary to communicate pain. ▶▶ Self-report. The ability of a child to understand and report the presence and intensity of pain requires cognitive skills, including receptive language and understanding, knowledge and memory of pain, executive function (e.g., cognitive flexibility, working memory), and the ability to understand and estimate magnitudes and symbolic processing. ▶▶

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Transcutaneous electrical nerve stimulation (TENS). TENS is frequently used to treat a number of pain conditions including back pain, osteoarthritis, and fibromyalgia to name a few (see Chapter 8). TENS is generally applied at low frequencies (50 Hz), at varying sensory threshold intensities.160 It is thought that TENS produces its analgesic effect by activating opioid receptors—lowfrequency activates m-opioid receptors whereas highfrequency activates d-opioid receptors.172 ▶▶ Interferential current (see Chapter 8). Clinically, interferential current therapy is beneficial for treating painful conditions such as osteoarthritic pain. The potential mechanisms behind this pain control include an increase in blood flow, and the same mechanisms as TENS—segmental inhibition and activation of descending inhibitory pathways. ▶▶ Manual therapy (see Chapter 10). Clinical evidence supports the use of massage, joint mobilizations, and joint manipulations for a variety of pain conditions.160 These techniques likely have local peripheral effects, as well as more systemic and CNS effects that either directly or indirectly reduce pain.

prolonged concussion, or may herald the development of postconcussion syndrome (PCS).178

Patient education. Patients can be educated on pain management techniques (relaxation, cognitive behavioral approaches, and biofeedback), positions and activities to avoid, and positions and activities to adopt.

Sex differences among concussed athletes are well documented and demonstrate dissimilarities between male and female athletes that range from anthropometrics, neuromuscular, and strength differences, to postconcussion symptoms and cognitive dysfunctions that can influence an individual’s recovery time.179 There are number of potential explanations for this disparity179:

▶▶

ANATOMY

▶▶

More recently, a number of joint-specific approaches have been introduced. For example, the Shoulder Symptom Modification Procedure (SSMP) involves a comprehensive management method that includes advice, education, exercises for the rotator cuff, and, frequently, whole-body rehabilitation.173 The symptomatic movement is identified, and then the clinician makes various changes in three areas (thoracic spine, scapula, G-H region) to determine whether shoulder-related symptoms change.173

Concussion

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A concussion is classified as a form of mild TBI that results from trauma to the head. It is a complex pathology and may cause numerous symptoms, including vestibular, balance, and visual ocular abnormalities.174,175 The Centers for Disease Control and Prevention describe concussion as: “a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces secondary to direct or indirect forces to the head.” A loss of consciousness is not necessary to diagnosis concussion. There are usually no findings on routine imaging such as computed tomography (CT) with a concussion, which complicates the diagnosis.176 While concussions can occur in nearly every walk of life, the greatest frequency occurs in collision and contact sports, including football, lacrosse, hockey, rugby, soccer, and basketball. While the majority of patients with a sports-related concussion may recover within a 7–10 day period, children and adolescents require more time to recover than do collegiate or professional athletes.177 Persistence of symptoms beyond the generally accepted time frame for recovery may represent a

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CLINICAL PEARL Based on a fact sheet available from the Centers for Disease Control and Prevention (http://cdc.gov/concussion/ HeadsUp/high_school.html), an individual who is suspected of suffering from a concussion should not be left alone, and should be brought to the emergency department if any of the following is present: ▶▶ a headache that worsens ▶▶ drowsiness or inability to be woken up ▶▶ inability to recognize people or places ▶▶ repeated vomiting ▶▶ worsening confusion/irritability ▶▶ seizures ▶▶ hemiparesis/hemisensory loss ▶▶ unsteadiness or ▶▶ slurred speech

Females have longer cervical spine segments and may not be as efficient at transmitting impact forces from their head into their torso via their cervical musculature during a concussive event. ▶▶ Females may also be more likely to seek medical treatment for concussion symptoms and to honestly report symptoms when they suffer a concussion. ▶▶

With increased awareness of the rate of concussion injury in sports and the potential detrimental long-term effects, a number of efforts have been made to identify the health consequences of repeated blows to the head while concurrently seeking to implement strategies to better protect the athlete from these injuries.180 It is important to note that concussion can result in a constellation of physical, cognitive, emotional, and sleep-related symptoms.181 Acute signs and symptoms of a concussion can include confusion, loss of consciousness, posttraumatic amnesia, retrograde amnesia, balance deficits, dizziness, visual problems, personality changes, fatigue, sensitivity to light/noise, numbness, and vomiting.182 Chronic signs and symptoms of a concussion have a degree of overlap and include cognitive deficits in attention or memory, and at least two or more of the following symptoms: fatigue, sleep disturbance, headache, dizziness, irritability, affective disturbance, apathy, or personality change.183 Since most cognitive deficits resolve within 1–3 months after a mild TBI in the majority of patients, there is considerable controversy regarding PCS because of the nonspecificity of its symptoms.184

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The following two findings can help determine whether the prolonged symptoms reflect a version of the concussion pathophysiology or a manifestation of a secondary process, such as premorbid clinical depression185:

CLINICAL PEARL The rate of lower extremity musculoskeletal injuries is reportedly higher in collegiate and professional athletes following concussions.186–188 The increased risk for lower extremity injury following concussion was 1.47–2.48 times greater within 90-day follow-up.186 Increased risk of injury within 1 year varied considerably between studies, from 1.64 to 4.07 times greater risk.186–188   It is hypothesized that this increased risk for lower extremity injury is due to the persistence of postconcussive symptoms or neuromotor deficits.

Given that no single clinical test can determine whether concussion has occurred, published guidelines189–191 for the diagnosis and treatment of concussion recommend a comprehensive, multidisciplinary assessment of concussion history, symptoms, and balance, in addition to neurocognitive testing.192 The nature, burden, and duration of symptoms appear to be the primary determinant of injury severity in concussion.174,193 A history of multiple concussions appears to increase the risk for PCS.178 The diagnosis and subsequent management of concussion continues to evolve and several tests now exist to identify the deficits found in this population. What is clear is that concussion symptoms may be immediate after injury, or appear in a delayed fashion post injury, so it is important to stay vigilant.176 The sideline assessment of concussion is best accomplished with standardized instruments that are widely available, including the Sport Concussion Assessment Tool-2 (SCAT-2),174 which has been adopted by nearly every professional sports team and many college teams. The Modified Maddocks Score can be used to assess orientation by asking the athlete about game events that day and the week before.176 Other tests include, the Immediate Postconcussion Assessment and Cognitive Testing (ImPact), the postconcussion symptom scale, the Balance Error Scoring System (BESS) (see Neuromuscular Control and Balance Testing), and dual-task gait testing. The physical examination should include an assessment of concentration (e.g., drills such as stating the months of the year in reverse), memory (recall of three words at 5 minutes), the cervical spine, gait, balance, cerebellar testing (e.g., finger to nose test), and an examination of the CNs. The CN examination is particularly important as recent research has highlighted eye movement

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The Nervous System

1. If symptoms that were experienced early after the injury are exacerbated by exertion, but improved with rest, then the original concussion pathophysiology is likely persisting. 2. If ongoing symptoms are exacerbated even minimal activity and no longer respond to rest, this may represent psychological symptoms related to prolonged inactivity and frustration with inability to return to usual activities.

abnormalities, especially smooth pursuit saccadic eye movements, as an indication for impaired function in concussed patients.174,178,194–196 As described in the balance section, The integration of the vestibular, vision, and somatosensory systems is essential for the maintenance of balance. The vestibular system is intricately related to the balance system through the vestibulospinal reflex (VSR) and to the visual system through the vestibulo-ocular reflex (VOR).175 The VSR promotes appropriate motor responses in the extremities for the maintenance of balance while the VOR provides connections to the ocular muscles in order to keep clear vision with head movement.175 Besides the VOR, additional visual functions such as near point convergence (NPC), smooth pursuit, and saccades are used to maintain clear vision and focus when the head is not moving.175 A number of clinical assessment tools have been designed to examine the vestibular, balance, and visual ocular systems after a concussion. One such tool is the King-Devick (K-D) test,197,198 a rapid number-naming task that broadly captures visual function and saccadic eye movements as well as attention and language function by requiring a participant to correctly identify single digits that are variably spaced on three handheld cards.199 An increase in the time taken to complete the K-D compared with baseline is indicative of a concussion with sensitivity of 86% and specificity of 90%.197,200 A recent pilot study found that poor K-D testing performance of adolescents with concussion may indicate a range of vestibular/ocular motor deficits that need to be further identified and addressed to maximize recovery.199 Another assessment tool, the vestibular/ocular motor screening (VOMS),201 provides a comprehensive examination of various saccadic eye movements with the intention of provoking symptoms after each assessment. Specifically, the VOMS accurately differentiates between controls and athletes with concussion in the evaluation of smooth-pursuit eye movements, saccadic eye movements, NPC, VOR, and visual motion sensitivity.202 Interestingly, the VOMS does not provoke symptoms in healthy controls.175 A recent study reported that the VOMS items measured unique aspects of vestibular function other than those measured by the BESS or K-D with good reliability, and concluded that clinicians should consider implementing the VOMS as part of a comprehensive concussion assessment if vestibular impairment is suspected.175

CLINICAL PEARL Gait performance during a dual-task test condition is a viable measure for use in the clinical setting, as individuals with concussion exhibit decreased gait velocity, increased medial-lateral displacement, and more cognitive errors with dual-task testing.192 The type of cognitive task to be performed in a dual-task gait assessment has yet to be determined, but question-and-answer tasks appear to be the most discriminating.192 Current recommendations are that the athlete undergo baseline testing in these areas prior to the season and, if a concussion is suspected, undergo the same battery of tests so that scores may be compared.

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TABLE 3-10

Cantu Grading Scale

Grade

Description

1

Includes posttraumatic amnesia less than 30 minutes and no loss of consciousness

2

Defined as loss of consciousness less than 5 minutes, or amnesia 30 minutes to 24 hours

3

Includes loss of consciousness greater than 5 minutes or amnesia greater than 24 hours

ANATOMY

Reproduced with permission from Cantu RC. Guidelines for return to contact sports after a cerebral concussion. Phys Sportsmed. 1986 Oct; 14(10):75–83.

CLINICAL PEARL A standardized process projecting the length of recovery time after concussion has remained an elusive piece of the puzzle. The recovery time associated with such an injury once diagnosed can last anywhere from 1 week to several months. Parents are typically advised to keep the patient at rest and, for at least 24 hours, to have the patient avoid strenuous activity, recreational drugs, alcohol, sleeping medication, and aspirin or nonsteroidal antiinflammatory drugs. Obviously, moves toward prevention would seem prudent. The most common attempted prevention strategy of concussion has occurred with American Football that has seen modifications to helmets that include innovations in design, padding, mouth guards, and product materials. However, despite aggressive enforcement of helmet and protective padding use, epidemiological and laboratory studies have not shown significant reductions in concussion instances or the extent of concussive injury to the brain.203 One hypothesis is that such devices and equipment do little to nothing to prevent or mitigate the rapid acceleration and deceleration of the brain and related fluids inside the rigid cranium.180 Based on the science of fluid dynamics, slosh refers to the movement of liquid inside containers that are also typically undergoing motion. When the head is exposed to rapid acceleration/ deceleration, the brain may be at risk for slosh-induced injury as tissues of differing density (i.e., blood, spine, brain, and skull) decelerate at different rates, thereby creating shear and cavitation (vapor bubble creation and implosion).180 Current management guidelines recommend a period of cognitive and physical rest in the early post injury. However, there is no scientific evidence that prolonged rest for more than several weeks in concussed patients is beneficial.178 Neurocognitive rehabilitation, which uses cognitive tasks to improve cognitive processes and attention processes, can be used once the concussion symptoms have subsided.178 Once the patient is asymptomatic at rest, a progression from light aerobic activity such as walking, to sport- or work-specific activities can be introduced.174 The Cantu204 grading scale has been helpful in assessing severity of concussion and for making return to play decisions (Table 3-10).

Orthopaedic Neurologic Testing

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(UMN/CNS) lesion, a lower motor neuron (LMN/PNS) lesion, or both. In essence, neurological tissue is tested during active, passive, and resisted isometric movement, as well as those tests specific to the nervous system (e.g., reflex testing, sensory testing). Neurodynamic mobility testing is covered in Chapter 11. UMNs are located in the white columns of the spinal cord and the cerebral hemispheres. A UMN lesion, also known as a central palsy, is a lesion of the neural pathway above the anterior horn cell or motor nuclei of the CNS. Signs and symptoms associated with a UMN lesion follow.

An examination of the transmission capability of the nervous system can be performed as part of the orthopaedic examination to detect the presence of either an upper motor neuron

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A UMN lesion is characterized by spastic paralysis or paresis, little or no muscle atrophy, hyper-reflexive muscle stretch (deep tendon) reflexes in a nonsegmental distribution, and the presence of pathologic signs and reflexes. Nystagmus. Nystagmus is characterized by an involuntary loss of control of the conjugate movement of the eyes (around one or more axes) involved with smooth pursuit or saccadic movement. When the eyes oscillate like a sine wave, it is called pendular nystagmus. If the nystagmus consists of drifts in one direction with corrective fast phases, it is called jerk nystagmus. The more benign types of nystagmus include the proprioceptive causes of spontaneous nystagmus, postural nystagmus, and nystagmus that is elicited with head positioning or induced by movement (vestibular nystagmus). A unidirectional nystagmus is related to the geometric relationship of the SSC, with a change in head position often exacerbating the nystagmus. On the other hand, a central vestibular nystagmus, which is caused by disease of the brain stem or the cerebellum, exhibits bidirectionality to the nystagmus (i.e., left beating on left gaze and right beating on right gaze).205 The more serious causes of nystagmus include, but are not limited to, vertebrobasilar ischemia, tumors of the posterior cranial fossa, intracranial bleeding, craniocervical malformations, and autonomic dysfunction. Differentiation between the benign and serious causes of nystagmus is obviously very important. ■■ Proprioceptive nystagmus occurs immediately upon turning the head (i.e., there is no latent period). ■■ The ischemic type of nystagmus has a latent period and is usually only evident when the patient’s neck is turned to a position and maintained there for a period of a few seconds up to 3 minutes. ▶▶ Dysphasia. Dysphasia is defined as a problem with vocabulary and results from a cerebral lesion in the speech areas of the frontal or temporal lobes. The temporal lobe receives most of its blood from the temporal branch of the cortical artery of the vertebrobasilar system and may become ischemic periodically, producing an inappropriate use of words. ▶▶ Wallenberg Syndrome. This is the result of a lateral medullary infarction.206 Classically, sensory dysfunction ▶▶

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Spasticity occurs because the reflex arc to the muscle remains anatomically intact, despite the loss of cerebral innervation and control via the long tracts. During spinal shock, the arc does not function, but as the spine recovers from the shock, the reflex arc begins to function without the inhibitory or regulatory impulses from the brain, creating local spasticity and clonus.

CLINICAL PEARL Medical etiologies for increased spasticity include a new or enlarged CNS lesion, genitourinary tract dysfunction (infection, obstruction, etc.), gastrointestinal disorders (bowel impaction, hemorrhoids, etc.), venous thrombosis, fracture, muscle strain, and pressure ulcers.209–212 ▶▶

Drop Attack. A drop attack is described as a loss of balance resulting in a fall, but with no loss of consciousness. Because it is the consequence of a loss of lower extremity control, it is never a good or benign sign. The patient, usually elderly, falls forward, with the precipitating factor being extension of the head. Recovery,

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providing nothing is injured in the fall, is usually immediate. Causes include213,214 ■■ a vestibular system impairment; ■■ neoplastic and other impairments of the cerebellum; ■■ vertebrobasilar compromise (see Chapter 24); ■■ sudden spinal cord compression; ■■ third ventricle cysts; ■■ epilepsy; and ■■ type 1 Chiari malformation. ▶▶ Wernicke encephalopathy. Wernicke encephalopathy (WE) is an acute life-threatening neurological condition caused by thiamine deficiency that is characterized by a clinical triad of ophthalmoparesis with nystagmus, ataxia, and confusion, and which primarily affects the peripheral and CNSs.215 ▶▶ Vertical diplopia. A history of “double vision” should alert the clinician to this condition. Patients with vertical diplopia complain of seeing two images, one atop or diagonally displaced from the other.

The Nervous System

in lateral medullary infarction is characterized by selective involvement of the spinothalamic sensory modalities with dissociated distribution (ipsilateral trigeminal and contralateral hemibody/limbs).207 However, various patterns of sensory disturbance have been observed in lateral medullary infarction that include contralateral or bilateral trigeminal sensory impairment, restricted sensory involvement, and a concomitant deficit of lemniscal sensations.207 ▶▶ Dysphonia. Dysphonia presents as a hoarseness of the voice. Usually, no pain is reported. Painless dysphonia is a common symptom of Wallenberg syndrome. ▶▶ Ataxia. Ataxia is often most marked in the extremities. In the lower extremities, it is characterized by the so-called drunken-sailor gait pattern, with the patient veering from one side to the other and having a tendency to fall toward the side of the lesion. Ataxia of the upper extremities is characterized by a loss of accuracy in reaching for, or placing, objects. Although ataxia can have a number of causes, it generally suggests CNS disturbance, specifically a cerebellar disorder, or a lesion of the posterior columns. ▶▶ Spasticity. Spasticity is defined as a motor disorder characterized by a velocity-dependent increase (resistance increases with velocity) in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex.208 The spinal cord experiences spinal shock immediately following any trauma causing tetraplegia or paraplegia, resulting in the loss of reflexes innervated by the portion of the cord below the site of the lesion. The direct result of this spinal shock is that the muscles innervated by the traumatized portion of the cord, the portion below the lesion, as well as the bladder, become flaccid. Spinal shock, which wears off between 24 hours and 3 months after injury, can be replaced by spasticity in some, or all of these muscles.209

Hemianopia. This finding, defined as a loss in half of the visual field, is always bilateral. A visual field defect describes sensory loss restricted to the visual field and arises from damage to the primary visual pathways linking the optic tract and striate cortex (see section “Supraspinal Reflexes”). ▶▶ Ptosis. Ptosis is defined as a pathologic depression of the superior eyelid such that it covers part of the pupil. It results from a palsy of the levator palpebrae and Müller’s muscle. ▶▶ Miosis. Miosis is defined as the inability to dilate the pupil (damage to sympathetic ganglia). It is one of the symptoms of Horner syndrome. ▶▶ Horner syndrome. Horner syndrome results from an interruption of the oculosympathetic pathway resulting from a lesion of (1) the reticular formation, (2) the descending sympathetic system, and (3) the oculomotor nerve caused by a sympathetic paralysis.216,217 The other clinical signs of Horner syndrome are ptosis, enophthalmos, facial reddening, and anhydrosis.217 If Horner syndrome is suspected, the patient should immediately be returned or referred to a physician for further examination. ▶▶ Dysarthria. Dysarthria is defined as an undiagnosed change in articulation. Dominant or nondominant hemispheric ischemia, as well as brain stem and cerebellar impairments, may result in altered articulation. ▶▶

The LMN begins at the α-motor neuron and includes the posterior (dorsal) and anterior (ventral) roots, spinal nerve, peripheral nerve, neuromuscular junction, and muscle–fiber complex.43 The LMN consists of a cell body located in the anterior gray column and its axon, which travels to a muscle by way of the cranial or peripheral nerve. Lesions to the LMN can occur in the cell body or anywhere along the axon. A LMN lesion is also known as a peripheral palsy. These lesions

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can be the result of direct trauma, toxins, infections, ischemia, or compression. The characteristics of a LMN lesion include muscle atrophy and hypotonus, diminished or absent muscle stretch (deep tendon) reflex of the areas served by a spinal nerve root or a peripheral nerve, and absence of pathologic signs or reflexes.



TABLE 3-11  

ANATOMY

The Scanning Examination

124

Designed by Cyriax,218 the upper (Table 3-12) and lower (Table 3-13) quarter scanning examinations are based on sound anatomic and pathologic principles. The clinician must choose which scanning examination to use, based on the presenting signs and symptoms. The purpose of the scanning examinations is to help rule out the possibility of symptom referral from other areas, to ensure that all possible causes of the symptoms are examined, and to ensure a correct diagnosis. The scanning examination is typically applied to patients presenting with neuromusculoskeletal complaints and differs from the five elements of patient/client management from The Guide in that the latter can be used as a system to approach virtually any type of patient, ranging from a pediatric patient with a permanent neurological condition to a patient with a serious injury to the integument, such as a burn patient.219 The other major difference between the two approaches is that the scanning examination is designed to identify a specific pathoanatomical dysfunction, while The Guide works within movement-based diagnostic categories.219 Thus, the tests used in the scanning examinations (Table 3-14) may produce a medical diagnosis (e.g., intervertebral disk protrusion, prolapse, or extrusion; acute arthritis; specific tendinopathy; muscle belly tear; spondylolisthesis; or lateral recess stenosis) rather than a physical therapy one. Often, the scanning examination does not generate enough signs and symptoms to formulate a working hypothesis or a diagnosis. A negative scanning examination does not imply that there were no findings; rather, the results of examination were insufficient to generate a diagnosis on which an intervention could be based. In this case, further testing with the tests and measures outlined in The Guide are required in order to proceed. The thoroughness of the scanning examination is influenced by both patient tolerance and professional judgment. A general guideline is that the examination must continue until the clinician is confident that the patient’s symptoms are not the result of a serious condition that demands medical attention.

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Upper Motor Neuron Lesion

Lower Motor Neuron Lesion

Location/ Structures

Cranial nerve nuclei/ Central nervous nerves and system—cortex, anterior horn brainstem, cell, spinal roots, corticospinal tracts, peripheral nerve spinal cord

Pathology examples

Stroke, traumatic brain Peripheral nerve injury, spinal cord neuropathy, injury radiculopathy, polio, Guillain Barre

Tone

Increased: Hypertonia, Decreased or absent: velocity dependent Hypotonia, flaccidity, non-velocity dependent

Reflexes

Decreased or absent: Increased: hyporeflexia, hyperreflexia, cutaneous clonus, exaggerated reflexes cutaneous and decreased/absent autonomic reflexes, +Babinski

Involuntary movements

Muscle spasms: flexor or extensor

Fasciculations: with denervation

Voluntary Movements

Impaired or absent: dyssynergic patterns, mass synergies

Weak or absent (if nerve integrity interrupted)

Strength

Weakness or paralysis: ipsilateral (stroke) or bilateral (SCI) Corticospinal: contralateral if above decussation in medulla; ipsilateral if below distribution: never focal

Ipsilateral weakness or paralysis in limited distribution: segmental/focal/ root pattern

Muscle appearance

Disuse atrophy: variable, widespread distribution, especially of antigravity muscles

Neurogenic atrophy

CLINICAL PEARL The differing symptoms between a UMN lesion and a LMN lesion (Table 3-11) are the result of injuries to different parts of the nervous system. LMN impairment involves damage to a neurologic structure distal to the anterior horn cell, whereas UMN impairment involves damage to a neurologic structure proximal to the anterior horn cell, namely, the spinal cord or CNS.

 ajor Differences Between UMN and LMN M Lesion Signs and Symptoms

The tests included in the scanning examination are strength testing, sensation testing (light touch and pinprick), muscle stretch reflexes, and the pathological reflexes (Table 3-14). The various tests of the scanning examinations specific to the cervical, thoracic, and lumbar spine are described in the relevant chapters. The scarcity of research to refute the work of Cyriax would suggest that its principles are sound and that its use should be continued.220,221

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TABLE 3-12

Upper-Quarter-Quadrant Scanning Motor Examination Muscle Tested

Root Level

Peripheral Nerve

Shoulder abduction

Deltoid

Primarily C5

Axillary

Elbow flexion

Biceps brachii

Primarily C6

Musculocutaneous

Elbow extension

Triceps brachii

Primarily C7

Radial

Wrist extension

Extensor carpi radialis longus, brevis, and extensor carpi ulnaris

Primarily C6

Radial

Wrist flexion

Flexor carpi radialis and flexor carpi ulnaris

Primarily C7

Median nerve for radialis and ulnar nerve for ulnaris

Finger flexion

Flexor digitorum superficialis, flexor digitorum profundus, and lumbricales

Primarily C8

Median nerve for superficialis and both median and ulnar nerves for profundus and lumbricales

Finger abduction

Posterior (dorsal) interossei

Primarily T1

Ulnar

Complaints of Dizziness Although most causes of dizziness can be relatively benign, dizziness may signal a more serious problem, especially if it is associated with trauma to the neck or the head or with motions of cervical rotation and extension (e.g., vertebral artery compromise). The clinician must ascertain whether the symptoms of dizziness result from vertigo, nausea, giddiness, unsteadiness, or fainting, among others. Nausea is an uneasiness of the stomach that often accompanies the urge to vomit but does not always lead to the forcible voluntary or involuntary emptying of stomach contents into the mouth (vomiting). If vertigo is suspected, the patient’s physician should be informed, for further investigation. However, in and of itself, vertigo is not usually a contraindication to the continuation of the examination. Differential diagnosis includes primary CNS diseases, vestibular and ocular involvement, and, more rarely, metabolic disorders.222 A patient complaining of dizziness can be classified into four subtypes (Table 3-15). Careful questioning can help in the differentiation of the cause.

TABLE 3-13

This differentiation is important, as certain types of dizziness are amenable to physical therapy interventions (Table 3-16); others produce contraindications to certain interventions, while still other causes of dizziness require medical referral.55 The presence of presyncope would suggest compromise of the function of the cerebral hemispheres or the brain stem. Different conditions can cause either a pancerebral hypoperfusion (Table 3-17) or a selective hypoperfusion of the brain stem, the latter of which includes vertebrobasilar insufficiency, vertebrobasilar infarction, and subclavian steal syndrome.55 The presence of vertigo, nystagmus, hearing loss or tinnitus, and brain stem signs can help the clinician differentiate between a central or a peripheral vestibular lesion (Table 3-18).55 Peripheral vertigo is manifested with general complaints such as unsteadiness and lightheadedness. Central vertigo is usually caused by a cerebellar disorder, an ischemic process, or a disturbance of the vestibular system (Table 3-19). Cervical vertigo, on the other hand, may be produced by localized muscle changes and receptor irritation.

Lower-Quarter-Quadrant Scanning Motor Examination

Muscle Action

Muscle Tested

Root Level

Peripheral Nerve

Hip flexion

Iliopsoas

L1–2

Femoral to iliacus and lumbar plexus to psoas

Knee extension

Quadriceps

L2–4

Femoral

Hamstrings

Biceps femoris, semimembranosus, and semitendinosus

L4–S3

Sciatic

Dorsiflexion with inversion

Tibialis anterior

Primarily L4

Deep fibular (peroneal)

Great toe extension

Extensor hallucis longus

Primarily L5

Deep fibular (peroneal)

Ankle eversion

Fibularis (peroneus) longus and brevis

Primarily S1

Superficial fibular (peroneal) nerve

Ankle plantarflexion

Gastrocnemius and soleus

Primarily S1

Tibial

Hip extension

Gluteus maximus

L5–S2

Inferior gluteal nerve

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The Nervous System

Muscle Action

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TABLE 3-14

 omponents of the Scanning C Examination and the Structures Tested

Component

Description

Active ROM

Willingness to move, ROM, integrity of contractile and inert tissues, pattern of restriction (capsular or noncapsular), quality of motion, and symptom reproduction

ANATOMY

Passive ROM

Integrity of inert and contractile tissues, ROM, end-feel, and sensitivity

Resisted

Integrity of contractile tissues (strength and sensitivity)

Stress

Integrity of inert tissues (ligamentous-disk stability)

Dural

Dural mobility

Neurologic

Nerve conduction

Dermatome

Afferent (sensation)

Myotome

Efferent (strength and fatigability)

Reflexes

Afferent–efferent and central nervous systems

ROM, range of motion.

TABLE 3-15 Subtype

Description

Vertigo

A false sensation of movement of either the body or the environment, usually described as spinning, which suggests vestibular system dysfunction Usually episodic with an abrupt onset and often associated with nausea or vomiting The dysfunction can be located in the peripheral or central vestibular system Often accompanied by other signs and symptoms including impulsion (the sensation that the body is being hurled or pulled in space), oscillopsia (the visual illusion of moving back and forth or up and down), nystagmus, gait ataxia, nausea, and vomiting

     

Presyncope

   

 

Dizziness provoked by head movements or head positions could indicate an inner ear dysfunction. Dizziness provoked by certain cervical motions, particularly extension or rotation, also may indicate vertebral artery compromise. Dizziness resulting from vertebral artery compromise should be associated with other signs and symptoms, which could include neck pain and nausea. The pain associated with vertebral artery compromise develops on one side of the neck in one-fourth of patients and usually is confined to the upper anterolateral cervical region (see Chapter 24). Persistent, isolated neck pain may mimic idiopathic carotidynia, especially if it is associated with local tenderness. Pain is also usually the initial manifestation of a carotid artery dissection. ▶▶ Dizziness associated with tinnitus or a hearing loss could indicate a tumor of CN VIII. ▶▶ Dizziness can occur if the calcareous deposits that lie on the vestibular receptors are displaced to new and sensitive regions of the ampulla of the posterior canal, evoking a hypersensitive response to stimulation with certain head positions or movements. The Dix–Hallpike test can be used to help determine if the cause of the patient’s dizziness is a vestibular impairment (benign paroxysmal positional vertigo, or BPPV—see Chapter 23), resulting from an accumulation of utricle debris (otoconia), which can move within the posterior SCC and stimulate the vestibular sense organ (cupula). This test usually is performed only if the vertebral artery test and cervical instability tests do not provoke symptoms. The test involves having the clinician move the patient rapidly from a sitting to a supine position with the head turned so that the affected ear (provocative position) is 30–45 degrees below the horizontal to stimulate the ▶▶

126

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The Four Subtypes of Dizziness

Disequilibrium

 

 

Other dizziness

 

 

Described as a sensation of an impending faint or loss of consciousness, which is not associated with an illusion of movement May begin with diminished vision or a roaring sensation in the ears May be accompanied by transient neurological signs, e.g., dysarthria, visual disturbances, and extremity weakness Results from conditions that compromise the brain’s supply of blood, oxygen, or glucose A sense of imbalance without vertigo, or a sense that a fall is imminent, which is generally attributed to neuromuscular problems The unsteadiness or imbalance occurs only when erect and disappears when lying or sitting May result from visual impairment, peripheral neuropathy, musculoskeletal disturbances and may include ataxia Described as a vague or floating sensation with the patient having difficulty relating to specific feeling to the clinician Includes descriptions of lightheadedness, heavy headedness, or wooziness that cannot be classified as any of the three previous subtypes The main causes of this subtype are psychiatric disorders including anxiety, depression, and hyperventilation

Data from Baloh RW. Approach to the dizzy patient. Baillieres Clin Neurol. 1994;3:453–465; Drachman DA, Hart CW. An approach to the dizzy patient. Neurology. 1972;22:323–334; Hanson MR. The dizzy patient. A practical approach to management. Postgrad Med. 1989;85:99–102, 107–108; Eaton DA, Roland PS. Dizziness in the older adult, Part 2. Treatments for causes of the four most common symptoms. Geriatrics. 2003;58:46, 49–52; Eaton DA, Roland PS. Dizziness in the older adult, Part 1. Evaluation and general treatment strategies. Geriatrics. 2003;58:28–30, 33–36; Huijbregts P, Vidal P. Dizziness in orthopaedic physical therapy practice: classification and pathophysiology. J Man Manip Ther. 2004;12:199–214; Simon RP, Aminoff MJ, Greenberg DA. Clinical Neurology. 4th ed. Stanford, CT: Appleton and Lange, 1999.

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TABLE 3-16

Signs and Symptoms Indicative of Pathologies Amenable to Sole Physical Therapy Management Precipitated by positioning, movement, or other stimuli (see below) Short latency: 1–5 seconds Brief duration: 16 = Unlikely to respond to therapy procedures

CLINICAL PEARL

174

Sensitivity and specificity are accuracy properties used for both screening and diagnostic accuracy tests (see Clinical Decision Making later)30: ▶▶ The closer the sensitivity is to 100% in the presence of a test with a negative result, the stronger the ability of that clinical measure to rule out the potential for a particular diagnosis. ▶▶ The closer the specificity is to 100% in the presence of a test with a positive result, the stronger the ability of that clinical measure to rule in the potential for a particular diagnosis.

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Based on the history, there may be times when the extent of the remainder of the examination may have to be limited. The decision to limit the examination is based on the presence of any subjective features that indicate the need for caution (see Systems Review).

Observation Observational information forms the basis of the early clinical impression. It is, in essence, the beginning of the clinical search for patient consistency and reliability. Observation of the patient begins when the patient enters the clinic. As the clinician greets the patient and takes him or her to the treatment room,

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an initial observation is made. This early observation can provide the clinician with information that includes, but is not limited to, how the patient holds the extremity, whether an antalgic gait is present, and how much discomfort appears to be present. The more formal observation of each body area is included in each of the relevant chapters. Much can be learned from thorough observation31:

In the case of a child, is there any unexplained or excessive bruising, and does the parent or guardian appear to be answering for the child? These findings could indicate some form of abuse occurring at home. ▶▶ Does the patient require assistance in ambulation, transferring, or changing of clothing? ▶▶ Do the observation findings match the findings from the history? ▶▶

Throughout the history, systems review, and tests and measures, collective observations form the basis for diagnostic deductions. Some of the observations made may be very subtle. For example, hoarseness of the voice could suggest laryngeal cancer, whereas a weakened, thickened, and lowered voice may indicate hypothyroidism. Warm, moist hands felt during a handshake may indicate hyperthyroidism. Cold, moist hands may indicate an anxious patient. Patients react differently to injury. Some patients may exaggerate the symptoms through facial expressions and gestures whereas others remain stoic. Patients may appear calm and pleasant, defensive, angry, apprehensive, or depressed. Anxious patients, or patients in severe pain, often appear restless. Clinicians must learn to adopt their approaches to these different reactions. For example, an anxious or apprehensive patient may require more reassurance than a calm and pleasant patient. Much of the observation involves assessment of posture (see Chapter 6). Postural deviations negatively affecting the location of the center of gravity or center of mass in relation to the base of support may result in a patient complaining of pain and/or dysfunction when in sustained positions. Changes in the contours of the body shape or posture can be so specific that it often is possible to isolate the single muscle involved, the movements affected, and the related joint dysfunction from observation alone. For example, a change in a soft tissue contour as compared to the other side could indicate muscle

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Structural: Those deformities present at rest. For example, torticollis and kyphosis. ▶▶ Functional: Deformities that are the result of assumed postures and which disappear when the posture is changed. For example, functional scoliosis is due to a leg length discrepancy that disappears when the patient bends forward (see Chapter 27). ▶▶

The patient’s position of comfort can provide the clinician with valuable information. For example, patients with lateral recess spinal stenosis of the lumbar spine, congestive heart failure, or pulmonary disease often prefer the sitting position, whereas patients with pericarditis often sit and lean forward. Patients with a posterior–lateral lumbar disk herniation often prefer to stand or lie rather than sit.

Systems Review The information from the history and the systems review serves as a guide for the clinician in determining which structures and systems require further investigation. The systems review is the part of the examination that identifies possible health problems that require consultation with, or referral to, another healthcare provider (Table 4-9).3 The systems review consists of a limited examination of the anatomic and physiologic status of all systems (i.e., musculoskeletal, neurological, cardiovascular, pulmonary, integumentary, GI, urinary system, and genitoreproductive).3 The systems review includes the following components3: For the cardiovascular/pulmonary system, the assessment of heart rate, respiratory rate, blood pressure, and edema. There are four so-called vital signs that are standard in most medical settings: temperature, heart rate, blood pressure, and respiratory rate. Pain is considered by many to be a fifth vital sign. The clinician should monitor at least heart rate and blood pressure in any person with a history of cardiovascular disease or pulmonary disease, or those at risk for heart disease.32 ▶▶ Temperature. Body temperature is one indication of the metabolic state of an individual; measurements provide information concerning basal metabolic state, possible presence or absence of infection, and metabolic response to exercise.33 “Normal” body temperature of the adult is 98.4°F (37°C). However, a temperature in the range of 96.5–99.4°F (35.8–37.4°C) is not at all uncommon. Fever or pyrexia is a temperature exceeding 100°F (37.7°C). Hyperpyrexia refers to an extreme elevation of temperature above 41.1°C (or 106°F).33 Hypothermia refers to an abnormally low temperature (below 35°C or 95°F). The temperature is generally taken by placing the bulb of a thermometer under the patient’s tongue for 1–3 minutes, depending on the device. In most individuals, there is a diurnal (occurring everyday) variation in body temperature of 0.5–2°F. The lowest ebb

Patient/Client Management

How does the patient arise from a seated position to greet the clinician, easily or in a guarded manner? ▶▶ Does the patient look directly into the eyes of the clinician or look away? Is there a nervousness or fear present? ▶▶ Is there an exaggerated pain response, as demonstrated by facial expression and/or voiced complaints? ▶▶ Does the patient sit to the side with the majority of weight on one buttock while the opposite leg is extended, a position associated with a lumbar spinal nerve root syndrome? ▶▶ In the case of an adult, is a spouse, or significant other, in attendance and does such a presence seem appropriate? If the presence appears inappropriate (signs of fear, questions always answered by the spouse/significant other, overly attentive spouse/significant other, etc.), some form of abuse occurring at home should be suspected. ▶▶

atrophy. These deviations and changes prompt a further musculoskeletal examination to determine the cause and potential management strategies. If there are any obvious deformities, the clinician must determine whether they are structural or functional:

▶▶

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TABLE 4-9

EXAMINATION AND EVALUATION

Signs/Symptoms

Common Cause

Angina pain not relieved in 20 minutes

Myocardial infarction

Angina pain with nausea, sweating, and profuse sweating

Myocardial infarction

Bowel or bladder incontinence and/or saddle anesthesia

Cauda equina lesion

Anaphylactic shock

Immunological allergy or disorder

Signs/symptoms of inadequate ventilation

Cardiopulmonary failure

Patient with diabetes who is confused, lethargic, or exhibits changes in mental function

Diabetic coma

Patient with positive McBurney’s point or rebound tenderness

Appendicitis or peritonitis

Sudden worsening of intermittent claudication

Thromboembolism

Throbbing chest, back, or abdominal pain that increases with exertion accompanied by a sensation of a heartbeat when lying down and palpable pulsating abdominal mass

Aortic aneurysm or abdominal aortic aneurysm

Data from Goodman CC, Snyder TEK. Differential Diagnosis in Physical Therapy. Philadelphia, PA: WB Saunders, 1990; Stowell T, Cioffredi W, Greiner A, et al. Abdominal differential diagnosis in a patient referred to a physical therapy clinic for low back pain. J Orthop Sports Phys Ther. 2005;35:755–764.

176

is reached during sleep. Menstruating women have a wellknown temperature pattern that reflects the effects of ovulation, with the temperature dropping slightly before menstruation, and then dropping further 24–36 hours prior to ovulation. Coincident with ovulation, the temperature rises and remains at a somewhat higher level until just before the next menses. It is also worth noting that in women or men older than 75 years of age, and in those who are immunocompromised (e.g., transplant recipients, corticosteroid users, persons with chronic renal insufficiency, or anyone taking excessive antipyretic medications), the fever response may be blunted or absent.33 ▶▶ Heart rate. In most people, the pulse is an accurate measure of heart rate. The heart rate or pulse is taken to obtain information about the resting state of the cardiovascular system and the system’s response to activity or exercise and recovery.33 It is also used to assess patency of the specific arteries palpated and the presence of any irregularities in the rhythm.33 When the heart muscle contracts, blood is ejected into the aorta, and the aorta stretches. At this point, the wave of distention (pulse wave) is most pronounced, but relatively slow moving (3–5 m/s). As it travels toward the peripheral blood vessels, it gradually diminishes and becomes faster.

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In the large arterial branches, its velocity is 7–10 m/s; in the small arteries, it is 15–35 m/s. When taking a pulse, the fingers must be placed near the artery and pressed gently against a firm structure, usually a bone. The pulse can be taken at a number of points. The most accessible is usually the radial pulse, at the distal aspect of the radius. Sometimes, the pulse cannot be taken at the wrist and is taken at the elbow (brachial artery), at the neck against the carotid artery (carotid pulse), behind the knee (popliteal artery), or in the foot using the dorsalis pedis or posterior tibial arteries. The pulse rate can also be measured by listening directly to the heart beat, using a stethoscope. One should avoid using the thumb when taking a pulse, as it has its own pulse that can interfere with detecting the patient’s pulse. The normal adult heart rate is 70 beats per minute (bpm), with a range of 60–80 bpm. A rate of greater than 100 bpm is referred to as tachycardia. Normal causes of tachycardia include anxiety, stress, pain, caffeine, dehydration, or exercise. A rate of less than 60 bpm is referred to as bradycardia. Athletes may normally have a resting heart rate lower than 60. The normal range of resting heart rate in children is between 80 and 120 bpm. The rate for a newborn is 120 bpm (normal range 70–170 bpm).

 igns and Symptoms Requiring S Immediate Medical Referral

CLINICAL PEARL There is normally a transient increase in pulse rate with inspiration, followed by a slowing down with expiration.22

▶▶

Respiratory rate. The normal chest expansion difference between the resting position and the fully inhaled position is 2–4 cm (females > males). The clinician should compare measurements of both the anterior–posterior diameter and the transverse diameter during rest and at full inhalation. Normal respiratory rate is between 8 and 14 per minute in adults and slightly quicker in children. The following breathing patterns are characteristic of disease: ■■ Cheyne–Stokes respiration, characterized by a periodic, regular, sequentially increasing depth of respiration, occurs with serious cardiopulmonary or cerebral disorders. ■■ Biot’s respiration, characterized by irregular spasmodic breathing and periods of apnea, is almost always associated with hypoventilation due to central nervous system (CNS) disease. ■■ Kussmaul’s respiration, characterized by deep, slow breathing, indicates acidosis, as the body attempts to blow off carbon dioxide. ■■ Apneustic breathing is an abnormal pattern of breathing characterized by a post-inspiratory pause. The usual cause of apneustic breathing is a pontine lesion. ■■ Paradoxical respiration is an abnormal pattern of breathing, in which the abdominal wall is sucked in during inspiration (it is usually pushed out). Paradoxical respiration is due to paralysis of the diaphragm.

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▶▶

stage 2 hypertension: systolic blood pressure ≥160 mm Hg or diastolic blood pressure ≥100 mm Hg. The normal values for resting blood pressure in children are ■■

systolic: birth to 1 month, 60–90 mm Hg; up to 3 years of age, 75–130 mm Hg; and over 3 years of age, 90–140 mm Hg; and ▶▶ diastolic: birth to 1 month, 30–60 mm Hg; up to 3 years of age, 45–90 mm Hg; and over 3 years of age, 50–80 mm Hg. ▶▶

Orthostatic hypotension is defined as a drop in systolic blood pressure when assuming an upright position. Orthostatic hypotension can occur as a side effect of antihypertensive medications (see Chapter 9), and in cases of low blood volume in patients who are postoperative or dehydrated, and in those with dysfunction of the autonomic nervous system, such as that which occurs with a spinal cord injury or postcerebrovascular accident.33 Activities that may increase the chance of orthostatic hypotension, such as application of heat modalities, hydrotherapy, pool therapy, moderate-to-vigorous exercise using the large muscles, sudden changes of position, and stationary standing, should be avoided in susceptible patients.33 The normal systolic range generally increases with age. The pressure should be determined in both the arms. Causes of marked asymmetry in blood pressure of the arms include the following: errors in measurements, marked difference in arm size, thoracic outlet syndromes, dissection of an aorta, external arterial occlusion, and atheromatous occlusion. ▶▶

Edema. Edema is an observable swelling from fluid accumulation in certain body tissues. Edema most commonly occurs in the feet and legs, where it is also referred to as peripheral edema. Swelling or edema may be localized at the site of the injury or diffused over a larger area. In general, the amount of swelling is related to the severity of the injury. However, in some cases, serious injuries produce very limited swelling, whereas, in others, minor injuries cause significant swelling. Edema occurs as a result of changes in the local circulation and an inability of the lymphatic system to maintain equilibrium. The

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swelling is the result of the accumulation of excess fluid under the skin, in the interstitial spaces or compartments within the tissues that are outside of the blood vessels. Most of the body’s fluids that are found outside of the cells are normally stored in two spaces: the blood vessels (referred to as blood volume) and the interstitial spaces (referred to as interstitial fluid). Generally, the size of lymph nodes is dependent on the size of the drainage area. Usually, the closer the lymph node is to the spinal cord, the greater the size of the lymph node. The neck is the exception to the rule. In various diseases, excess fluid can accumulate in either one or both of the interstitial spaces or blood vessels. An edematous limb indicates a poor venous return. Pitting edema is characterized by an indentation of the skin after the pressure has been removed. A report of rapid joint swelling (within 2–4 hours) following a traumatic event may indicate bleeding into the joint. Swelling of a joint that is more gradual, occurring 8–24 hours following the trauma, is likely caused by an inflammatory process or synovial swelling. The more serious reasons for swelling include fracture, tumor, congestive heart failure, and deep vein thrombosis. For the integumentary system, the assessment of skin integrity, skin color, and the presence of scar formation. The integumentary system includes the skin, the hair, and the nails. The examination of the integumentary system may reveal manifestations of systemic disorders. The overall color of the skin should be noted. Cyanosis in the nails, the hands, and the feet may be a sign of a central (advanced lung disease, pulmonary edema, congenital heart disease, or low hemoglobin level) or peripheral (pulmonary edema, venous obstruction, or congestive heart failure) dysfunction.33 Palpation of the skin, in general, should include assessment of temperature, texture, moistness, mobility, and turgor.33 Skin temperature is best felt over large areas using the back of the clinician’s hand. An assessment should be made as to whether this is localized or generalized warmth33: ■■ Localized. May be seen in areas of the underlying inflammation or infection. ■■ Generalized. May indicate fever or hyperthyroidism. Skin texture is described as smooth or rough (coarse). Skin mobility may be decreased in areas of edema or in scleroderma. ▶▶

For the musculoskeletal system, the gross assessment of symmetry, the range of motion, strength, weight, and height. ▶▶ For the neuromuscular system, a general assessment of gross coordinated movement (e.g., balance, locomotion, transfers, and transitions). In addition, the clinician observes for peripheral and cranial nerve integrity and notes any indication of neurological compromises such as tremors or facial tics. ▶▶ For communication ability, affect, cognition, language, and learning style, the clinician notes whether the patient’s communication level is age appropriate; whether the patient is oriented to person, place, and time; and whether the emotional and behavioral responses appear to be

Patient/Client Management

Blood pressure. Blood pressure is a measure of vascular resistance to blood flow.33 The normal adult blood pressure can vary over a wide range. The assessment of blood pressure provides information about the effectiveness of the heart as a pump and the resistance to blood flow. It is measured in mm Hg and is recorded in two numbers. The systolic pressure is the pressure that is exerted on the brachial artery when the heart is contracting, and the diastolic pressure is the pressure exerted on the artery during the relaxation phase of the cardiac cycle.33 The JNC 7 report released in May 2003 added a new category of prehypertension and established more aggressive guidelines for medical intervention of hypertension. The normal values for resting blood pressure in adults are ■■ normal: systolic blood pressure internal rotation (3:2:1)

Acromioclavicular

No true capsular pattern; possible loss of horizontal adduction and pain (and sometimes slight loss of end range) with each motion

Sternoclavicular

See acromioclavicular joint

Humeroulnar

Flexion > extension (±4:1)

Humeroradial

No true capsular pattern; possible equal limitation of pronation and supination

Superior radioulnar

No true capsular pattern; possible equal limitation of pronation and supination with pain at end ranges

Inferior radioulnar

No true capsular pattern; possible equal limitation of pronation and supination with pain at end ranges

Wrist (carpus)

Flexion = extension

Radiocarpal

See wrist (carpus)

Carpometacarpal

Flexion = extension

Midcarpal

Flexion = extension

Carpometacarpal 1

Retroposition

Carpometacarpals 2–5

Fan > fold

Metacarpophalangeal 2–5

Flexion > extension (±2:1)

Interphalangeal 2–5 Proximal (PIP) Distal (DIP)

  Flexion > extension (±2:1) Flexion > extension (±2:1)

Hip

Internal rotation > flexion > abduction = extension > other motions

Tibiofemoral

Flexion > extension (±5:1)

Superior tibiofibular

No capsular pattern; pain at end range of translatory movements

Talocrural

Plantar flexion > dorsiflexion

Talocalcaneal (subtalar)

Varus > valgus

Midtarsal

Inversion (plantar flexion, adduction, and supination)

Talonavicular calcaneocuboid

> Dorsiflexion

Metatarsophalangeal 1

Extension > flexion (±2:1)

Metatarsophalangeals 2–5

Flexion ≥ extension

Interphalangeals 2–5 Proximal Distal

  Flexion ≥ extension Flexion ≥ extension

Data from Cyriax J. Textbook of Orthopaedic Medicine: Diagnosis of Soft Tissue Lesions. 8th ed. London: Bailliere Tindall; 1982.

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erroneously classified as normal motion. To help determine whether the motion is normal or excessive, passive range of motion (PROM), in the form of passive overpressure, and the end-feel are assessed.

CLINICAL PEARL Apprehension from the patient during AROM that limits a movement at near or full range suggests instability, whereas apprehension in the early part of the range suggests anxiety caused by pain.

Active physiologic intervertebral mobility, or active mobility, tests of the spine were originally designed by osteopaths to assess the ability of each spinal joint to move actively through its normal range of motion, by palpating over the transverse processes of a joint during the motion (see also Position Testing of the Spine). Theoretically, by palpating over the transverse processes, the clinician can indirectly assess the motions occurring at the zygapophyseal joints on either side of the intervertebral disk. However, the clinician must remember that, although it is convenient to describe the various motions of the spine occurring in a certain direction, these involve the integration of movements of a multi-joint complex (see Chapter 22). The human zygapophyseal joints are capable of only two major motions: gliding upward and gliding downward. If these movements occur in the same direction, flexion or extension of the spine occurs, while if the movements occur in opposite directions, side flexion occurs. Osteopaths use the terms opening and closing to describe flexion and extension motions, respectively, at the zygapophyseal joint. Under normal circumstances, an equal amount of gliding occurs at each zygapophyseal joint with these motions. During flexion, both zygapophyseal joints glide superiorly (open). ▶▶ During extension, both zygapophyseal joints glide inferiorly (close). ▶▶ During side flexion, one joint is gliding inferiorly (closing), while the other joint is gliding superiorly (opening). For example, during right side flexion, the right joint is gliding inferiorly (closing), while the left joint is gliding superiorly (opening). ▶▶

By combining flexion or extension movements with side flexion, a joint can be “opened” or “closed” to its limits. Thus, flexion and right-side flexion of a segment assesses the ability of the left joint to open maximally (flex), whereas extension and left-side flexion of a segment assesses the ability of the left joint to close maximally (extend). There is a point that may be considered as the center of segmental rotation, about which all segmental motion must occur. In the case of a zygapophyseal joint impairment (hypermobility or hypomobility), it is presumed that this center of rotation will be altered. If one zygapophyseal joint is rendered hypomobile (i.e., the superior facet cannot move to the extreme of superior

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CLINICAL PEARL

Patient/Client Management

Active Physiological Range of Motion of the Spine

or inferior motion), then the pure motions of flexion and extension cannot occur. This results in a relative asymmetric motion of the two superior facets, as the end of the range of flexion or extension is approached (i.e., a side-flexion motion will occur). However, this side-flexion motion will not be about the normal center of segmental rotation. The structure responsible for the loss of zygapophyseal joint motion, whether it is a muscle, disk protrusion, or the zygapophyseal joint itself, will become the new axis of vertebral motion, and a new component of rotation about a vertical axis, normally unattainable, will be introduced into the segmental motion. The degree of this rotational deviation is dependent on the distance of the impairment from the original center of rotation. Because the zygapophyseal joints in the spine are posterior to the axis of rotation, an obvious rotational change occurring between full flexion and full extension (in the position of a vertebral segment) is indicative of zygapophyseal joint motion impairment. By observing any marked and obvious rotation of a vertebral segment occurring between the positions of full flexion and full extension, one may deduce the probable pathologic impairment.

Active motion induced by the contraction of the muscles determines the so-called physiologic range of motion, whereas passively performed movement causes stretching of noncontractile elements, such as ligaments, and determines the anatomic range of motion. The active mobility tests of the spine are described in the appropriate chapters.

Passive Physiological Range of Motion of the Spine The passive physiologic intervertebral mobility, or passive mobility, tests use the same principles as the active physiologic intervertebral mobility tests to assess the ability of each joint in the spine to be moved passively through its normal range of motion. During extension the spinous processes should approximate, whereas during flexion they should separate. If the pain is reproduced, it is useful to associate the pain with the onset of tissue resistance to gain an appreciation of the acuteness of the problem. The passive mobility tests of the spine are described in the appropriate chapters.

Mobility Mobility can be viewed as a factor of range of motion, flexibility, and accessory joint motion (see Chapter 13): The term range of motion refers to the distance and direction a joint can move, and it is measured using a goniometer. ▶▶ Flexibility refers to the passive extensibility of connective tissue that provides the ability to move a joint or series ▶▶

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of joints through a full, nonrestricted, injury, and painfree ROM. The extensibility and habitual length of connective tissue are factors of the demands placed upon it (see Chapter 2). These demands produce changes in the viscoelastic properties and, thus, the length–tension relationship of a muscle or muscle group, resulting in an increase or a decrease in the length of those structures. A decrease in the length of the soft-tissue structures, or adaptive shortening, is very common in postural dysfunctions. Although some types of flexibility (e.g., straight leg raise) can be measured using a goniometer, most types are assessed using specific tests. A more subjective test for flexibility includes an examination of the end-feel, which can detect a loss of motion resulting from the excessive tension of the agonist muscle. ▶▶ Accessory joint motion. Accessory joint motion is the amount of the arthrokinematic glide that occurs at the joint surfaces, termed joint play (see Chapter 1). The examination of mobility is performed to determine if a particular structure or group of structures has sufficient movement to perform a desired activity. Decreased mobility can be produced by restricted accessory joint motion; ▶▶ tissue damage secondary to trauma; ▶▶ prolonged immobilization; ▶▶ disease; and ▶▶ hypertonia. Hypertonic muscles that are superficial can be identified through observation and palpation. Observation will reveal the muscle to be raised, and light palpation will provide information about tension, as the muscle will feel hard and may stand out from those around it. ▶▶

Joint Integrity

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Joint integrity testing can provide valuable information about the status of each joint and its capsule. Kaltenborn49 introduced the concept of motion restriction of a joint based on its arthrokinematics. In order for a joint to function completely, both the osteokinematic and arthrokinematic motions have to occur normally (see Chapter 1). It, therefore, follows that if a joint is not functioning completely, either the physiologic range of motion is limited compared with the expected norm, or there is no PROM available between the physiologic barrier and the anatomic barrier. As previously mentioned, the assessment of the end-feel can help determine the cause of the restriction. In general, the physiologic motion is controlled by the contractile tissues, whereas the accessory motion is controlled by the integrity of the joint surfaces and the noncontractile (inert) tissues. This guideline may change in the case of a joint that has undergone degenerative changes, which can result in a decrease in the physiologic motions (capsular pattern of restriction). It is important that the intervention to restore the complete function of the joint is aimed at the specific cause. Joint pain and dysfunction do not occur in isolation. Various different measurement scales have been proposed for judging the amount of accessory joint motion present between two joint surfaces (see Chapter 10), most of which are based on a

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comparison with a comparable contralateral joint, using manually applied forces in a logical and precise manner. In the extremities, these tests are referred to as passive articular mobility or joint glide tests. In the spine, these tests are referred to as the passive physiologic accessory intervertebral motion testing.

CLINICAL PEARL In general, if the concave-on-convex glide of the joint surfaces is restricted, there is a contracture of the trailing portion of the capsule, whereas if the convex-on-concave glide of the joint surfaces is restricted, there is an inability of the moving surface to glide into the contracted portion of the capsule. The passive articular mobility tests involve the clinician assessing the arthrokinematic, or accessory, motions using joint glides, and determining whether the glide is hypomobile, normal, or hypermobile (see Chapters 2 and 10). Accessory motions are involuntary motions. With few exceptions, muscles cannot restrict the glides of a joint, especially if the glides are tested in the open-packed position of a peripheral joint and, at the end of available range, in the spinal joints. Thus, if the clinician assesses the accessory motion of the joint by performing a joint glide, information about the integrity of the inert structures will be given. There are two scenarios: 1. The joint glide is unrestricted. An unrestricted joint glide indicates two differing conclusions: a. The integrity of both the joint surface and the periarticular tissue is good. If the joint surface and the periarticular structures are intact, the patient’s loss of motion must be the result of a contractile tissue. The intervention for this type involves soft-tissue mobilization techniques designed to change the length of a contractile tissue. b. The joint glide is unrestricted but excessive. This is very difficult to detect, but if present, may indicate a pathological hypermobility or instability, or it may be normal for the individual. In these cases, the end-feel can provide some useful information. The intervention for this type concentrates on stabilizing techniques designed to give secondary support to the joint through muscle action. 2. The joint glide is restricted. If the joint glide is restricted, the joint surface and the periarticular tissues are implicated as the cause of the patient’s loss of motion, although as previously mentioned, the contractile tissues cannot definitively be ruled out. The intervention for this type of finding initially involves a specific joint mobilization to restore the glide. Once the joint glide is restored following these mobilizations, the osteokinematic motion can be assessed again. If it is still reduced, the contractile tissues are likely to be at fault. Distraction and compression can be used to help differentiate the cause of the restriction. a. Distraction. Distraction is a force imparted passively by the clinician that results in a distraction of the

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cause of a limitation in a joint’s physiologic range of motion; ▶▶ the end-feel response of the tissues; ▶▶ stage of healing; and ▶▶

▶▶

the integrity of the support structures (e.g., ligaments) of a joint (e.g., the integrity of the anterior cruciate ligament is tested with the Lachman test).

Based on the information gleaned from the joint glide/ accessory motion assessment, the clinician can make a clinical decision as to which intervention to use. If the joint glide is felt to be restricted, and there is no indication of a bony end-feel or severe irritability, joint mobilization techniques are used. If the joint glide is found to be unrestricted, the clinician may decide to employ a technique that increases the extensibility of the surrounding connective tissues, such as muscle energy, because abnormal shortness of these connective tissues, including the ligaments, the joint capsule, and the periarticular tissues, can restrict joint mobility.

CLINICAL PEARL Caution must be used when basing clinical judgments solely on the results of accessory motion testing, because few studies have examined the validity and reliability of accessory motion testing of the spine or extremities, and little is known about the validity of these tests for most inferences.

TABLE 4-18

Position Testing in the Spine The position tests are osteopathic screening tests used to compare the relative position of a specific zygapophyseal joint(s) with the joint(s) below (see appropriate chapters). As with all screening tests, position testing is valuable in focusing the attention of the clinician to a specific area but is not appropriate for making a definitive statement concerning the movement status of the segment. However, when combined with the results of the passive and active movement testing, position tests help to form a working hypothesis.

Muscle Performance: Strength, Power, and Endurance Strength is a measure of the power with which musculotendinous units act across a bone-joint lever-arm system to actively generate motion or passively resist movement against gravity and variable resistance.48 According to Cyriax, pain with a contraction generally indicates an injury to the contractile tissue or joint.34 This suspicion can be confirmed by combining the findings from the type of symptom, the symptom duration, the symptom distribution, and the end-feel (Table 4-18). Cyriax reasoned that if you isolate and then apply tension to a structure, you can make a conclusion as to the integrity of that structure.34 His work also introduced the concept of tissue reactivity. Tissue reactivity is the manner in which different stresses and movements can alter the clinical signs and symptoms. This knowledge can be used to gauge any subtle changes to the patient’s condition. In addition to examining the integrity of the contractile and inert structures, strength testing may be used to examine the integrity of the key muscles (see Chapter 3). Pain with muscle testing may indicate a muscle injury, a joint injury, or a combination of both. Pain that occurs consistently with resistance, at whatever the length of the muscle, may indicate a tear of the muscle belly. The weakness elicited with muscle testing must be differentiated between weakness throughout the range of motion (pathological weakness) and weakness that only occurs in certain positions (positional weakness). According to Cyriax,34,50 strength testing can provide the clinician with the following findings: ▶▶

A weak and painless contraction may indicate palsy or a complete rupture of the muscle–tendon unit. The motor disorder associated with peripheral neuropathy is first

Differential Diagnosis of Contractile, Inert, and Neural Tissue Injury

 

Contractile Tissue

Inert Tissue

Neural Tissue

Pain

Cramping, dull, and ache

Dull–sharp

Burning and lancinating

Paresthesia

No

No

Yes

Duration

Intermittent

Intermittent

Intermittent–constant

Dermatomal distribution

No

No

Yes

Peripheral nerve sensory distribution

No

No

Yes (if peripheral nerve involved)

End-feel

Muscle spasm

Boggy and hard capsular

Stretch

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joint surfaces. It is not synonymous with traction (see Chapter 1). If the distraction is limited, a contracture of connective tissue should be suspected.   If the distraction increases the pain, it may indicate a tear of connective tissue (e.g., joint capsule) and may be associated with increased range.   If the distraction eases the pain, it may indicate an involvement of the joint surface. b. Compression. Compression is the opposite force to distraction and involves an approximation of the joint surfaces (see Chapter 1).   If the compression increases the pain, a loose body or an internal derangement of the joint may be present. If the compression decreases the pain, it may implicate the joint capsule. Thus, by assessing these joint motions, the clinician can determine the

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manifested by weakness and a diminished or absent tendon reflex (see Chapter 3). ▶▶ A strong and painless contraction indicates a normal finding. ▶▶ A weak and painful contraction. A study indicated that the conditions related to this finding needed to include not only serious pathology, such as a significant muscle tear or a tumor, but relatively minor muscle damage and inflammation such as that induced by eccentric isokinetic exercise.45 ▶▶ A strong and painful contraction indicates a grade I contractile lesion. Pain that does not occur during the test, but occurs upon the release of the contraction, is thought to have an articular source, produced by the joint glide that occurs following the release of tension.

CLINICAL PEARL Pain that occurs with resistance, accompanied by pain at the opposite end of the passive range, indicates muscle impairment.

The degree of certainty regarding the findings just described depends on a combination of the length of the muscle tested and the force applied. To fully test the integrity of the muscle–tendon unit, a maximum contraction must be performed in the fully lengthened position of the muscle–tendon unit. Although this position fully tests the muscle–tendon unit, there are some problems with testing in this manner: The joint and its surrounding inert tissues are in a more vulnerable position and could be the source of the pain. ▶▶ It is difficult to differentiate between damage to the contractile tissue of varying severity. The degree of significance with the findings in resistive testing depends on the position of the muscle and the force applied (Table 4-19). For example, pain reproduced with a ▶▶

TABLE 4-19

 trength Testing Related to Joint Position S and Muscle Length

minimal contraction in the rest position for the muscle is more strongly suggestive of a contractile lesion than pain reproduced with a maximal contraction in the lengthened position for the muscle. ▶▶ As a muscle lengthens, it reaches a point of passive insufficiency, where it is not capable of generating its maximum force output (see Chapter 1). If the same muscle is tested on the opposite side, using the same testing procedure, the concern about the length of the muscle is removed, because the focus of the test is to provide a comparison with the same muscle on the opposite side, rather than to assess the absolute force output. To assess strength, strength values using manual muscle testing (MMT) have traditionally been used between similar muscle groups on opposite extremities or antagonistic ratios. This information is then used to determine whether a patient was fully rehabilitated. It should be noted that there is considerable variability in the amount of resistance that normal muscles can hold against. The application of resistance throughout the arc of motion (make test or active resistance test) in addition to resistance applied at only one point in the arc of motion (break test), which is used more often, can help in judging the strength of a muscle.45 The various techniques for assessing muscle strength using MMT are described in Chapter 12.

CLINICAL PEARL Perhaps the most obvious problem of using the “break” test method during manual muscle testing is that the tests may demonstrate substantial ceiling effects that depend on the characteristics of the clinician. For example, small clinicians may find it difficult to “break” muscle contractions, so they may tend to underestimate weakness when compared to large clinicians.

During all testing, stabilization of the body part on which the muscle originates, in addition to careful avoidance of substitution by other muscle groups, is emphasized. Substitute motions are compensatory movement patterns caused by muscle action of a stronger adjacent agonist muscle, or a muscle group that normally serves as a stabilizer. Substitutions by other muscle groups during testing indicate the presence of weakness. It does not, however, tell the clinician the cause of the weakness. Proper alignment is determined by the direction of the muscle fibers and the line of pull of the muscle to be tested (see Chapter 12). The alignment or position of the patient or the limb with respect to gravity may also be important based on the grade anticipated.

Muscle Length

Rationale

Fully lengthened    

Muscle in position of passive insufficiency Tightens the inert component of the muscle Tests for muscle tears (tenoperiosteal tears) while using minimal force

Mid-range  

Muscle in strongest position Tests overall power of muscle

CLINICAL PEARL

Fully shortened  

Muscle in its weakest position Used for the detection of palsies, especially if coupled with an eccentric contraction

Manual muscle testing has been shown to be less sensitive in detecting strength deficits in stronger muscles than in weaker muscles.45

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Several scales have been devised to assess muscle strength. For example, Janda51 used a 0–5 scale with the following descriptions:

Grade 3: F (fair). A muscle that can move through its complete range of movement against gravity but only if no additional resistance is applied. If the muscle strength is less than grade 3, then the methods advocated in muscle testing manuals must be used.45 ▶▶ Grade 2: P (poor). A very weak muscle that is only able to move through its complete range of motion if the force of gravity is eliminated. ▶▶ Grade 1: T (trace). A muscle with evidence of slight contractility but demonstrates no effective movement. ▶▶ Grade 0. A muscle with no evidence of any contractility. ▶▶

The grading systems for MMT produce ordinal data with unequal rankings between grades. For example, the grades 5 (normal) and 4 (good) typically encompass a large range of a muscle’s strength, while the grades of 3 (fair), 2 (poor), and 1 (trace) include a much narrower range.45 If the popular methods to grade muscles are analyzed, the frailties and similarities become obvious. If the muscle strength is less than grade 3, these testing grades are useful, but it is the grades of 3 and higher that produce the most confusion. Some of the confusion arises from the descriptions of maximal, moderate, and minimal, or considerable, which removes much of the objectivity from the tests. Strength testing must elicit a maximum contraction of the muscle being tested if it is to be deemed a valid test. The following strategies ensure that this occurs: 1. Placing the joint that the muscle to be tested crosses, in (or close to) its open-packed position. This strategy helps protect the joint from excessive compressive forces and the surrounding inert structures from excessive tension. 2. Placing the muscle to be tested in a shortened position. This puts the muscle in an ineffective physiologic position and has the effect of increasing motor neuron activity. 3. Using gravity-minimized positions. This strategy avoids the effect of the weight of the moving body segment on force measurements. For example, to test the strength of

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Grade 5: N (normal). A normal, very strong muscle with a full range of movement and one that is able to overcome considerable resistance. This does not mean that the muscle is normal in all circumstances (e.g., when at the onset of fatigue or in a state of exhaustion). If the clinician is having difficulty differentiating between a grade 4 and a grade 5, the eccentric “break” method of muscle testing may be used. This procedure starts as an isometric contraction, but then the clinician applies sufficient force to cause an eccentric contraction or a “break” in the patient’s isometric contraction. ▶▶ Grade 4: G (good). A muscle with good strength and a full range of movement, and one that is able to overcome moderate resistance. The subjectivity involved in a grade 4 score is one of the major criticisms of MMT as the grading requires the clinician to assign an ordinal number to a subjective evaluation of resistance offered by the patient. ▶▶

the hip abductors, the patient is positioned in supine so that the muscle action pulls in a horizontal plane relative to the ground.45 4. Having the patient perform an eccentric muscle contraction by using the command “Don’t let me move you.” Because the tension at each cross-bridge and the number of active cross-bridges is greater during an eccentric contraction (see Chapter 1), the maximum eccentric muscle tension developed is greater with an eccentric contraction than with a concentric one. 5. Breaking the contraction. It is important to break the patient’s muscle contraction, in order to ensure that the patient is making a maximal effort and that the full power of the muscle is being tested. 6. Holding the contraction for at least 5 seconds. Weakness resulting from nerve palsy has a distinct fatigability. The muscle demonstrates poor endurance because usually it is only able to sustain a maximum muscle contraction for about 2–3 seconds before complete failure occurs. This strategy is based on the theories behind muscle recruitment, wherein a normal muscle, while performing a maximum contraction, uses only a portion of its motor units, keeping the remainder in reserve to help maintain the contraction (see Chapter 1). A palsied muscle, with its fewer functioning motor units, has very few, if any, motor units in reserve. If a muscle appears to be weaker than normal, further investigation is required, as follows: a. The test is repeated three times. Muscle weakness resulting from disuse will be consistently weak and should not become weaker with several repeated contractions. In contrast, a palsied muscle becomes weaker with each contraction. b. Another muscle that shares the same innervation is tested. Knowledge of both spinal and peripheral nerve innervation will aid the clinician in determining which muscle to select (see Chapter 3). 7. Comparing findings with the uninvolved side. As always, these tests cannot be evaluated in isolation but have to be integrated into a total clinical profile, before drawing any conclusion about the patient’s condition.

CLINICAL PEARL MMT is an ordinal level of measurement and has been found to have both inter- and intrarater reliability, especially when the scale is expanded to include plus or minus a half or a full grade. Although the grading of muscle strength has its role in the clinic, and the ability to isolate the various muscles is very important in determining the source of nerve palsy, specific grading of individual muscles does not give the clinician much information on the ability of the structure to perform functional tasks. In addition, measurements of isometric muscle force are specific to a point or small range in the joint range excursion and, thus, cannot be used to predict dynamic force capabilities.

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EXAMINATION AND EVALUATION

Muscle function testing should address the production and control of motion in functional activities. Although there is general agreement about the role of the trunk and pelvic musculature in normal functioning of the vertebral column, protection against pain, and recurrence of low back disorders, more research is needed to determine the role of functional strength in the extremities. Part of the functional assessment includes an assessment of those muscles that are prone to weakness, which can provide the clinician with the following information: ▶▶ The strength of individual muscles or muscle groups that form a functional unit. ▶▶ Nature, range, and quality of simple movement patterns. ▶▶ The relationship between the strength and the flexibility of a muscle or muscle group. ▶▶ The ability of the whole body to perform a task. More recently, the use of quantitative muscle testing (QMT) has been recommended to assess strength, as it produces interval data that describe force production. QMT methods include the following: The use of handheld dynamometers. Although more costly and time consuming than MMT, handheld dynamometry can be used to improve objectivity and sensitivity. Patients are typically asked to push against the dynamometer with a maximal isometric contraction (make test), or hold a position until the clinician and the dynamometer overpower the muscle producing an eccentric contraction (break test).45 Normative force values for particular muscle groups by patient age and gender have been reported, with some authors including regression equations that take into account body weight and height.52 ▶▶ The use of an isokinetic dynamometer. This is a stationary, electromechanical device that controls the velocity of the moving body segment by resisting and measuring the patient’s effort so that the body segment cannot accelerate beyond a preset angular velocity.45 Isokinetic dynamometers measure torque and range of motion as a function of time and can provide an analysis of the ratio between the eccentric contraction and concentric contraction of a muscle at various positions and speeds. This ratio is aptly named the eccentric/concentric ratio. The ratio is calculated by dividing the eccentric strength value by the concentric strength value. Various authors have demonstrated that the upper limit of this ratio is 2.0 and that lower ratios indicate pathology. ▶▶

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One of the major criticisms of muscle testing is the over estimation of strength when a muscle is weak as identified by QMT, compared to the same muscle being graded as normal by MMT, such that a theoretical percentage score based on MMT is likely to grossly overestimate the strength of a patient.53 Although MMT results are more consistent, the variation produced by QMT can appreciate differences in strength undetectable in MMT.53

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Regardless of the type of muscle testing used, the procedure is innately subjective and depends on the subject’s ability to exert a maximal contraction. This ability can be negatively impacted by such factors as pain, poor comprehension, motivation, cooperation, fatigue, and fear.

CLINICAL PEARL Voluntary muscle strength testing will remain somewhat subjective until a precise way of measuring muscle contraction is generally available.48 This is particularly true when determining normal and good values.

Functional Screening In physical therapy, musculoskeletal screening can be used as a method to identify potential risk factors for people without symptoms to prevent a loss of function as well as providing guidance with a view of preventing or reducing recurrence. A number of variables affect function. These include age, gender, physical capacity (strength, power, flexibility, dexterity, agility, speed, muscular endurance, cardiovascular endurance, coordination, and skill), healing status (phase of healing, weight-bearing status, precautions/contraindications, and comorbidities), and psychological profile (motivation, fear, and coping mechanisms).54 Functional testing is a complex and multifactorial process in which the clinician makes a determination about the patient’s level of functional independence based on principles of physiology, biomechanics, and motor behavior54: Physiology. Relevant physiological issues include the functions of body structures and systems, the extent of the injury, and the patient’s healing status, energy systems, adaptation, and overall fitness level. ▶▶ Biomechanics. Biomechanical considerations include functional anatomy, direction/planes of motion and stress, kinematics (time, distance, position, displacement, velocity), and kinetics (force, torque, mass, acceleration, inertia, momentum). ▶▶ Motor behavior. Motor behavior issues include proprioception, perception, transfer, practice, learning, control, coordination, and performance. ▶▶

Function-based measurements, often referred to as functional performance measures, measure the ability to demonstrate the skillful and efficient assumption, maintenance, modification, and control of voluntary postures and movement patterns.3 Functional performance measures, which typically involve a set of proxy movements that mimic a certain function, or the critical elements of that function, have often been criticized, as detailed testing of their measurement properties has not been extensively reported.55 Preparticipation screens are functional performance measures for athletes who are planning to return to their sport. Clearly, it is unrealistic to identify individual tests to predict every musculoskeletal injury in all population types and to design a screening test for each potential intrinsic and extrinsic risk factor that might be present at the moment of an injury event.56–60 It is true that many nonmodifiable risk

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factors, such as age, gender, height, race, previous history, sport, and climate, have been implicated in altering the risk of musculoskeletal injury.61–65 There are, however, a number of risk factors with predictive validity and known reliability for injury risk. These include the following61:

Ideally, a screening protocol should be highly relevant to a specific individual and their specific roles as well as being reliable, simple, financially viable, easy to administer, and not involve complicated tests or expensive equipment.61 The Musculoskeletal Readiness Screening Tool (MRST), Functional Movement ScreenTM, and the Lower Quarter Y Balance TestTM are examples of reliable, field expedient screening protocols that use grading of movement to develop an injury risk profile for an individual. Musculoskeletal Readiness Screening Tool.66  The MRST was developed to predict injury. Tests include the weightbearing forward lunge, modified deep squat, closed kinetic chain upper extremity stability test (while in the push-up position, the subject leans over to touch one hand on the other and then return the hand to the starting position), forward step down with eyes closed, stationary tuck jump, unilateral wall sit hold, the Feagin hop (the subject, standing on a line with the uninvolved lower extremity held in slight knee flexion, performs a maximum effort vertical hop and attempts to land in the same position), individual perceived level of risk for injury, and self-reported history of injury. A score of 2 indicates the subject was able to perform the movement correctly and without pain. A score of 1 indicates that only part of the movement was complete and the subject performed the movement without pain. A score of 0 indicates that the subject had pain with the movement or had a bilateral deficiency on the weight-bearing lunge forward lunge. This scoring system allows for a cumulative score ranging from 0 to 12, with lower scores thought to indicate higher risk for future injury. The Functional Movements Screen (FMS).  The FMS is an assessment tool that attempts to address the quality of multiple movement factors, including balance, with the goal of predicting general risk of musculoskeletal conditions and injuries.58,67–69 The original intent of the FMS was to identify functional movement deficits and asymmetries that may be

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Inline lunge (Fig. 4.2) Hurdle step (Fig. 4.3) ▶▶ Deep squat (Fig. 4.4) ▶▶ Quadruped rotary stability (Fig. 4.5) ▶▶ Active straight leg raise (Fig. 4.6) ▶▶ Shoulder mobility (Fig. 4.7) ▶▶ Trunk stability push-up (Fig. 4.8) ▶▶ ▶▶

For the component tests that are scored for both the right and left sides, the lowest score is used when calculating the FMS composite score. Each of these movement component tests is scored on a scale of 0–3, with the sum creating a component score ranging from 0 to 21 points. It has been suggested that a composite score that is less than or equal to 14 on the FMS may suggest higher injury risk, but that a score greater than 14 does not rule out future injury risk.56 Unfortunately, as yet, interpretation of FMS scores is limited by the scant evidence in widely accessible journals. For example, Hartigan et al.71 concluded that one of the components of the FMS, the inline lunge, was not related to balance, power, or speed. However, other studies have advocated its use.57,59,72 Lower Quarter Y Balance Test.  This test, developed from the Star Excursion Balance Test (SEBT) (see Chapter 3), is a portion of the FMS used to evaluate dynamic balance and functional symmetry during single-leg balance with reaching in the anterior, posterior medial, and posterior lateral directions.

Patient/Client Management

Prone passive hip internal rotation. Reduced hip internal rotation on the ipsilateral leg is an independent predictor for lower limit/back injury. ▶▶ Modified Thomas test (quadriceps flexibility). Reduced quadriceps flexibility (90

Reasonable agreement for clinical measurements

Data from Portney LG, Watkins MP. Foundations of Clinical Research: Applications to Practice. Norwalk, CT: Appleton & Lange; 1993.

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▶▶

Standard error of measurement (SEm). The SEm estimates how repeated measures of an individual on the same instrument tend to be distributed around his or her “true” score, and it is an indication of how much change there might be when the test is repeated. The SEm can be used to differentiate between real change and random measurement error.128 The smaller the SEm, the more precise the measurement capacity of the instrument.

Validity

▶▶

Construct validity. This type of validity represents the level of agreement between a measurement and the idea it purports to measure. To establish adequate construct validity of a measurement, the measurement should provide similar results as other measurements that are intended to measure the same variable. In addition, the measurement should provide different results from other measurements of theoretically different ideas. Convergent validity is the agreement between two different measurements of the same variable. Divergent validity is the extent to which two measurements of theoretically separate ideas are unrelated.

Content validity. This type of validity is the extent to which a measurement reflects the idea (content) that it purports to measure. Measurements with high content validity demonstrate a more accurate representation of the variable being measured. ▶▶ Criterion-related validity. This type of validity is an estimate of the extent to which the test can substitute for another test, which may be a gold-standard test or a test of a related variable. Criterion-related validity is commonly assessed as concurrent validity and predicted validity where concurrent validity is the measure of association between two measurements taken at the same time, and where predictability is an estimate of the ability of a measurement to forecast a future measurement or outcome. ▶▶ Face validity. This type of validity is an approximation that a measurement appears to reflect the variable that the measurement is intended to estimate. For example, palpation of the hand and wrist is considered to have high face validity, because locations for palpation reflect the typical locations of anatomical structures. ▶▶

In order to determine if a test is both reliable and valid, the test must be examined in a research study and, preferably, multiple studies. Validity is directly related to the notion of sensitivity and specificity. Sensitivity is the ability of the test to pick up what it is testing for, and specificity is the ability of the test to reject what it is not testing for. The sensitivity and specificity of any test must be considered together and not as one component in isolation.9

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Patient/Client Management

The validity of a test is defined as the degree to which the test measures what it purports to be measuring and how well it correctly classifies individuals with or without a particular disease. There are several types of test validity that should be considered when evaluating for inclusion in the physical therapy examination2:

Sensitivity represents the proportion of patients with a disorder who test positive. A test that can correctly identify every person who has the disorder has a sensitivity of 1.0. SnNout is an acronym for when the sensitivity of a symptom or sign is high, a negative response rules out the target disorder. Thus, a so-called highly sensitive test helps rule out a disorder. The positive predictive value is the proportion of patients with positive test results who are correctly diagnosed. Responsiveness is the characteristic of sensitivity to true change or difference between measurements. Measurement changes may be relevant within the same patient over time; measurement differences may be clinically important between subjects with and without a certain pathology.2 ▶▶ Specificity is the proportion of the study population without the disorder that test negative.129 A test that can correctly identify every person who does not have the target disorder has a specificity of 1.0. SpPin is an acronym for when specificity is extremely high, a positive test result rules in the target disorder. Thus, a so-called highly specific test helps rule in a disorder or condition. The negative predictive value is the proportion of patients with negative test results who are correctly diagnosed. ▶▶

Interpretation of sensitivity and specificity values is easiest when their values are high.91 A test with a very high sensitivity, but low specificity, and vice versa, is of little value, and the acceptable levels are generally set at between 50% (unacceptable test) and 100% (perfect test), with an arbitrary cutoff at about 80%.129 Once the specificity and sensitivity of the test are established, the predictive value of a positive test versus a negative test can be determined if the prevalence of the disease/dysfunction is known. For example, when the prevalence of the disease increases, a patient with a positive test is more likely to have the disease (a false-negative is less likely). A negative result of a highly sensitive test will probably rule out a common disease, whereas if the disease is rare, the test must be much more specific for it to be clinically useful.

CLINICAL PEARL Collectively, estimates of validity, reliability, and responsiveness may be called psychometric properties.2 The likelihood ratio (LR) is the index measurement that combines sensitivity and specificity values into one number and can be used to gauge the performance of a diagnostic test, as it indicates how much a given diagnostic test result will lower or raise the pretest probability of the target disorder.130

CLINICAL PEARL Sensitivity, specificity, and positive and negative LRs are the most robust metrics in determining diagnostic accuracy.9

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TABLE 4-25

2 × 2 Table

 

Disease/Outcome

  Test  

Positive (+) Negative (−)

Present

Absent

a (true +ve) c (false −ve)

b (false +ve) d (true −ve)

Four measures contribute to sensitivity and specificity (Table 4-25):

EXAMINATION AND EVALUATION

True positive. The test indicates that the patient has the disease or the dysfunction, and this is confirmed by the gold standard test. ▶▶ False positive. The clinical test indicates that the disease or the dysfunction is present, but this is not confirmed by the gold standard test. ▶▶ False negative. The clinical test indicates the absence of the disorder, but the gold standard test shows that the disease or dysfunction is present. ▶▶ True negative. The clinical and the gold standard test agree that the disease or dysfunction is absent.

Another way to summarize diagnostic test performance using Table 4-25 is via the diagnostic odds ratio (DOR): DOR = true/false = (a*d)/(b*c). The DOR of a test is the ratio of the odds of positivity in disease relative to the odds of positivity in the nondiseased. The value of a DOR ranges from 0 to infinity, with higher values indicating better discriminatory test performance. A value of 1 means that a test does not discriminate between those patients with the disorder and those without.

CLINICAL PEARL

▶▶

These values are used to calculate the statistical measures of accuracy, sensitivity, specificity, negative and positive predictive values, and negative and positive LRs, as indicated in Table 4-26. A test with a strong LR+ value moves the clinician closer to a diagnosis and a test with a strong LR− value moves the clinician further away from a diagnosis. An LR+ value of 5.0 or greater and an LR− value of 0.20 or less are moderately to highly valuable in modifying the baseline probability to the extent of ruling in or ruling out the pathology, respectively.9 Also, as either the LR+ or LR− approaches a value of 1.0, the value of the diagnostic test diminishes to the point where it insignificantly modifies the baseline probability.9 TABLE 4-26

The DOR value rises steeply when sensitivity or specificity becomes near perfect. The quality assessment of studies of diagnostic accuracy (QUADAS)131 is an evidence-based quality assessment tool currently recommended for use in systematic reviews of diagnostic accuracy studies (DASs). The aim of DAS is to determine how good a particular test is at detecting the target condition. DAS allows the calculation of various statistics that provide an indication of “test performance”—how good the index test is at detecting the target condition. These statistics include sensitivity, specificity, positive and negative predictive values, positive and negative LRs, and diagnostics odd ratios. The QUADAS tool is a list of 14 questions which should each be answered “yes,” “no,” or “unclear” (Table 4-27). A score of 10 or greater of “yes” answers is indicative of a higher quality study, whereas a score of less than 10 “yes” answers suggests a poorly designed study. Throughout this text, the QUADAS score is used (if known) to evaluate the various physical therapy examination tests. Whenever considering outcomes and outcome measurements, it is important to remember that there is now good evidence showing that in musculoskeletal health, psychological

Definition and Calculation of Statistical Measures

Statistical Measure

Definition

Calculation

Accuracy

The proportion of people who were correctly identified as either having or not having the disease or dysfunction

(TP + TN)/(TP + FP + FN + TN)

Sensitivity

The proportion of people who have the disease or dysfunction and who test positive

TP/(TP + FN)

Specificity

The proportion of people who do not have the disease or dysfunction and who test TN/(FP + TN) negative

Positive predictive value

The proportion of people who test positive and who have the disease or dysfunction

TP/(TP + FP)

Negative predictive value

The proportion of people who test negative and who do not have the disease or dysfunction

TN/(FN + TN)

Positive LR

How likely a positive test result is in people who have the disease or dysfunction as Sensitivity/(1 − specificity) compared to how likely it is in those who do not have the disease or dysfunction

Negative LR

How likely a negative test result is in people who have the disease or dysfunction as (1 − sensitivity)/specificity compared to how likely it is in those who do not have the disease or dysfunction

FN, false negative; FP, false positive; TN, true negative; TP, true positive.

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Reproduced with permission from Powell JW, Huijbregts PA. Concurrent criterion-related validity of acromioclavicular joint physical examination tests: a systematic review. J Man Manip Ther. 2006;14(2):E19–E29.

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TABLE 4-27

The QUADAS Tool

 

Yes

No

Unclear

 1.

Was the spectrum of patients representative of the patients who will receive the test?

( )

( )

( )

 2.

Were selection criteria clearly described?

( )

( )

( )

 3.

Is the reference standard likely to correctly classify the target condition?

( )

( )

( )

 4.

Is the time period between reference standard and index test short enough to be reasonably sure that the target condition did not change between the two tests?

( )

( )

( )

 5.

Did the whole sample or a random selection of the sample, receive verification using a reference standard of diagnosis?

( )

( )

( )

 6.

Did patients receive the same reference standard regardless of the index test result?

( )

( )

( )

 7.

Was the reference standard independent of the index test (i.e., the index test did not form part of the reference standard)?

( )

( )

( )

 8.

Was the execution of the index test described in sufficient detail to permit replication of the test?

( )

( )

( )

 9.

Was the execution of the reference standard described in sufficient detail to permit its replication?

( )

( )

( )

10.

Were the index test results interpreted without knowledge of the results of the reference standard?

( )

( )

( )

11.

Were the reference standard results interpreted without knowledge of the results of the index test?

( )

( )

( )

12.

Were the same clinical data available when test results were interpreted as would be available when the test is used in practice?

( )

( )

( )

13.

Were uninterpretable/intermediate test results reported?

( )

( )

( )

14.

Were withdrawals from the study explained?

( )

( )

( )

Patient/Client Management

Item

Reproduced with permission from Whiting P, Rutjes AW, Reitsma JB, et al. The development of QUADAS: a tool for the quality assessment of studies of diagnostic accuracy included in systematic reviews. BMC Med Res Methodol. 2003 Nov 10;3:25.

factors (such as fear avoidance beliefs, anxiety, depression, poor coping strategies, poor self-efficacy, and preexisting somatization) are important predictors of poor outcomes, and likely play a more significant role in the transition from acute to persistent pain and disability than biomedical factors.5,110,132–135 Similarly, social factors (social arrangements, health and disability structures, and local cultural beliefs) have been shown to influence outcomes, such as disability, beyond the factors operating at the level of individuals.110,136

Prognosis and Plan of Care The prognosis is the predicted optimal level of function that the patient will attain within a certain time frame. This information helps guide the intensity, duration, and frequency of the intervention and aids in justifying the intervention. Prognostic studies have become identified as a research priority as healthcare providers attempt to differentiate between patients with a more favorable prognosis and those with a poor prognosis.137 The goal is to either identify baseline characteristics that are associated with a specific outcome at a given point or determine those characteristics that tend to have a good prognosis regardless of treatment provided.138,139 These determinations will allow for a more intensive approach to patients with a poor

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general prognosis, and a less intensive approach to those who are inclined to improve regardless of intervention.138 The prognosis represents a synthesis, based on an understanding of the extent of pathology, premorbid conditions, the ability of surrounding tissue structures to compensate in the short- or long-term, the healing processes of the various tissues, the patient’s age, foundational knowledge, theory, evidence, experience, and examination findings, and takes into account the patient’s social, emotional, and motivational status.99,105 A number of studies have demonstrated a significant relationship between patient expectations and outcomes,140–145 including one by Bishop et al.146 which reported that more than 80% of patients expected that manual therapy to the cervical spine would provide relief of symptoms, prevention of disability, and improvement of activity level and sleep. Another study140 noted that low or negative expectations before treatment affected outcome 6 months after treatment. It would seem apparent that a physical therapist can consciously or unconsciously shape patient expectations, and thus influence outcomes, through placebo (positive) or nocebo (negative) pathways.123 The patient’s aspirations and patient-identified problems, together with those problems identified by the clinician, determine the focus of the goals (Table 4-28).99 The patient

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TABLE 4-28

Patient-Specific Functional Scale (PSFS)

Clinicians should read to the patient and fill in Functional Goal and Outcome Worksheet. Note: Complete this at the end of the history and prior to the physical examination. Read at Baseline Assessment I’m going to ask you to identify 3 to 5 important activities that you are unable to do or are having difficulty with as a result of your ______________________ problem. Today, are there any activities that you are unable to do or have difficulty with because of your _______________________ problem? (Clinician: show scale)

EXAMINATION AND EVALUATION

Read at Follow-up Visits When I assessed you on (state previous assessment date), you told me that you had difficulty with (read all activities from list one at a time). Today, do you still have difficulty with 1 (have patient score each item); 2 (have patient score each item); 3 (have patient score each item); etc. Patient-Specific Activity Scoring Scheme (Point to one number): Activity 1

Unable to perform activity

0 1

2

3

4

5

6

7

8

9

10

 

 

 

 

 

 

 

 

 

Able to perform activity at same level as before injury or problem

0 1

2

3

4

5

6

7

8

9

10

 

 

 

 

 

 

 

 

 

Able to perform activity at same level as before injury or problem

0 1

2

3

4

5

6

7

8

9

10

 

 

 

 

 

 

 

 

 

Able to perform activity at same level as before injury or problem

0 1

2

3

4

5

6

7

8

9

10

 

 

 

 

 

 

 

 

 

Able to perform activity at same level as before injury or problem

0 1

2

3

4

5

6

7

8

9

10

 

 

 

 

 

 

 

 

 

Able to perform activity at same level as before injury or problem

Activity 2

Unable to perform activity Activity 3

Unable to perform activity Activity 4

Unable to perform activity Activity 5

Unable to perform activity

206

and clinician should come to an agreement regarding the most important problems, around which care should be focused, and together establish relevant goals.99 Ideally, in each patient encounter, the clinician should strive to discover the patient’s expectation and then deliver and exceed it to the extent that it does not cause more harm.123 Patient education and patient responsibility become extremely important in determining the prognosis. Typically the goal of a rehabilitation program is to return the patient/ athlete to the preinjury level using the patient’s uninjured side as the gold standard. This may sometimes be inadequate as in most cases the clinician does not know what the preinjury level actually was. Instead, the goal of every rehabilitation program should be to obtain an enhanced and improved level of whole body functional ability.147 In addition, the rehabilitation program should identify, address, and correct all specific predisposing factors that may lead to another injury by addressing the physical, biomechanical, environmental, and psychological factors of the whole person during the rehabilitation process.147

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The POC is organized around the patient’s goals. The physical therapist’s POC consists of consultation, education, and intervention. Procedural interventions are covered in Chapter 8.

Patient Participation in Planning. The patient’s aspirations and patient-identified problems, together with those problems identified by the clinician, determine the focus of the goals.99 The patient and clinician should come to an agreement regarding the most important problems, around which care should be focused, and together establish relevant goals.99 Patient education and patient responsibility become extremely important in determining the prognosis.

Anticipated Goals and Expected Outcomes This includes the predicted positive effects on the disorder or condition; dysfunction; ▶▶ functional limitations and disabilities; ▶▶ prevention of future occurrences; ▶▶ ▶▶

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health, fitness and wellness of the patient; and ▶▶ patient/client satisfaction. ▶▶

▶▶

The intervention is typically guided by short-term (anticipated goals) and long-term (expected outcomes) goals, which are dynamic in nature, being altered as the patient’s condition changes, and strategies with which to achieve those goals based on the stages of healing.

CLINICAL PEARL

The following information must be included within the POC based on the anticipated goals. Frequency of treatments, including how often the patient will be seen per day or per week. ▶▶ What interventions the patient will receive, including the use of any modalities, therapeutic exercise, and any specialized equipment. ▶▶

▶▶

Plans for discharge, including patient and family education, equipment needs, and referral to other services as appropriate.

The documented goals should be listed in order of priority with the most important or more vital functional activities listed first. Short-Term (Anticipated) Goals.  Short-term goals are the interim steps along the way to achieving the long-term goals. The purposes of the short-term goals include the following: ■■ To set the priorities of the intervention. ■■ To direct the intervention based on the specific needs and problems of the patient. ■■ To provide a mechanism to measure the effectiveness of the intervention. ■■ To communicate with other healthcare professionals. ■■ To provide an explanation of the rationale behind the goal to third-party payers. The time frame for short-term goals can be based on the next time the patient will be seen. ▶▶

CLINICAL PEARL Examples of short-term goals based on the facility (with and without using abbreviations): ▶▶ Acute-care: Indep. walker amb. on level surfaces 50% PWB on R LE for 50 ft w/i 3 days. The patient will ambulate independently with a walker for 50 ft with 50% partial weight bearing of the right lower extremity within 3 days. ▶▶ Outpatient orthopaedic clinic: Pt. will ↑ R knee √ AROM to 0–90 degrees within 2 days to assist with ambulation. The patient will increase right knee flexion AROM to 0–90 degrees within 2 days to assist with ambulation.

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Coordination, Communication, and Documentation Coordination The physical therapist is responsible for the coordination of physical therapy care and services.

Communication Communication with all of the individuals involved in a patient’s care is typically provided either verbally or through written documentation. Much about becoming a clinician relates to an ability to communicate with the patient, the patient’s family, and the other members of the healthcare team. It is important to remember that listening is often more critical than speaking. Special attention needs to be paid to cultural diversity and to nonverbal communication such as:

Patient/Client Management

The most successful intervention programs are those that are custom designed from a blend of clinical experience and scientific data, with the level of improvement achieved being related to goal setting and the attainment of those goals.

Long-Term (Expected Outcomes) Goals.  Long-term goals are the final product of a therapeutic intervention. The purposes of long-term goals are the same as those for short-term goals. Long-term goals typically use functional terms rather than such items as degrees of range of motion or grades of muscle strength. Examples of typical long-term goals would include: ■■ The patient will be independent with transfers on/off toilet, supine-sit, and sit-stand and with ambulation for 100 ft using an assistive device at time of discharge. ■■ The patient will be independent with ambulation on level and uneven surfaces and stair negotiation without assistive device at time of discharge.

Facial expression. The facial expression should be one of interest and concern. ▶▶ Voice volume. The voice volume should be at a level that is sufficient for the patient to hear. Avoid speaking loudly when possible, especially to those who are hard of hearing. ▶▶ Posture. An upright and attentive posture is preferable. ▶▶ Touch. Any touch used, based on respect for the patient’s cultural preferences and personal boundaries, should be confident and firm. ▶▶ Gestures. Gestures should be limited to those describing a particular activity. ▶▶ Physical closeness. Comfort with physical closeness varies according to culture. In the United States, a distance of 18 in to 4 ft is considered normal for a professional distance. ▶▶ Eye contact. Maintaining eye contact enhances trust and demonstrates attentiveness. ▶▶ Eye level. Whenever possible, the clinician should alter his or her position so that the eye level between patient and clinician is the same. For example, if the patient is sitting, the clinician should assume a sitting position. ▶▶

The appearance of the clinician can convey an air of professionalism. Most institutions have a dress code that should be adhered to.

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CLINICAL PEARL

EXAMINATION AND EVALUATION

Learn to be a good listener by ▶▶ Looking at the person who is talking and give him or her your full attention ▶▶ Making appropriate eye contact ▶▶ Showing understanding by summarizing and asking for confirmation ▶▶ Letting the speaker finish the point they were making ▶▶ Showing interest ▶▶ Being respectful Communication between the clinician and the patient begins when the clinician first meets the patient and continues throughout any future sessions. Communication involves interacting with the patient using terms he or she can understand. The introduction to the patient should be handled in a professional yet empathetic tone. Listening with empathy involves understanding the ideas being communicated and the emotion behind the ideas. In essence, empathy is seeing another person’s viewpoint, so that a deep and true understanding of what the person is experiencing can be obtained. Particularly important aspects of empathy are the recognition of patients’ rights, potential cultural differences, typical responses to loss, and the perceived role of spirituality in health and wellness to the patient.

CLINICAL PEARL A patient’s privacy and dignity should be maintained at all times. Privacy includes the patient’s personal space. Whenever appropriate, the clinician should ask permission from the patient before carrying out an action (moving the patient’s belongings off the bedside table, sitting down, etc.)

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Given the nature of the physical therapy profession, physical therapists interact frequently with people with disabilities. When writing or speaking about people with disabilities, it is important to put the person first. Group designations such as “the blind” or “the disabled” are inappropriate because they do not reflect the individuality, equality or dignity of people with disabilities. Similarly, words like “normal person” imply that the person with a disability is not normal, whereas “person without a disability” is descriptive but not negative. Etiquette considered appropriate when interacting with people with disabilities is based primarily on respect and courtesy. Outlined below are tips to help when communicating with persons with disabilities provided by the Office of Disability Employment Policy; the Media Project, Research and Training Center on Independent Living, University of Kansas, Lawrence, KS; and the National Center for Access Unlimited, Chicago, IL. General Tips.  When introduced to a person with a disability, it is appropriate to offer to shake hands. People with limited hand use or who wear an artificial limb can usually shake hands (shaking hands with the left hand is an acceptable

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greeting). If you offer assistance to a person with a disability, wait until the offer is accepted, then listen to or ask for instructions. Address people who have disabilities by their first names only when extending the same familiarity to all others. Communicating with Individuals Who are Blind or Visually Impaired.  The clinician should speak to the individual when he or she is approached, and speak in a normal tone of voice. When conversing in a group, the clinician should remember to identify themselves and the person to whom he or she is speaking. The clinician should not attempt to lead the individual without first asking; allow the person to hold your arm and control her or his own movements. Direct action should be given using descriptive words giving the person verbal information that is visually obvious to individuals who can see. For example, if you are approaching a series of steps, mention how many steps. If you are offering a seat, gently place the individual’s hand on the back or arm of the chair so that the person can locate the seat. At the end of the session, the clinician should tell the individual that he or she is leaving. Communicating with Individuals Who are Deaf or Hard of Hearing.  The clinician should gain the patient’s attention before starting a conversation (e.g., tap the person gently on the shoulder or arm), and then look directly at the individual, face the light, speak clearly, in a normal tone of voice, and keep the hands from obstructing the mouth. Short, simple sentences should be used. If the patient uses a sign language interpreter, the clinician should speak directly to the person, not the interpreter. If the clinician places a phone call, he or she should let the phone ring longer than usual. If a Text Telephone (TTY) is not available, the clinician should dial 711 to reach the national telecommunications relay service, which will facilitate the call. Communicating with Individuals with Mobility Impairments.  Whenever possible, the clinician should position himself or herself at the wheelchair user’s eye level without leaning on the wheelchair or any other assistive device. Never patronize people who use wheelchairs by patting them on the head or shoulder. Do not assume that an individual in a wheelchair wants to be pushed—ask first. Communicating with Individuals with Speech Impairments.  If the clinician does not understand something the patient said, he or she should not pretend that they did but should ask the individual to repeat what he or she said and then repeat it back. To help the patient, the clinician should try to ask questions which require only short answers or a nod of the head. The clinician should not speak for the individual or attempt to finish her or his sentences. If the clinician is having difficulty understanding the individual, writing should be considered as an alternative means of communicating, but only after asking the individual if this is acceptable. Communicating with Individuals with Cognitive Disabilities.  Whenever possible, the clinician and patient should communicate in a quiet or private location, and should be prepared to repeat what is said, orally or in writing. It is important that the clinician be patient, flexible and supportive, and the clinician should wait for the individual to accept the offer of assistance; do not “over-assist” or be patronizing.

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At the end of the first visit and at subsequent visits, the clinician should ask if there are any questions. Each session should have closure, which may include a handshake if appropriate.

Documentation

Subjective: Information about the condition from the patient or family member. ▶▶ Objective: Measurement a clinician obtains during the physical examination. ▶▶ Assessment: Analysis of problems including the long- and short-term goals. ▶▶ Plan: A specific intervention plan for the identified problem(s). ▶▶

The purposes of documentation are as follows148: To document what the clinician does to manage the individual patient’s case. ▶▶ To record examination findings, patient status, intervention provided, and the patient’s response to treatment. ▶▶ To communicate with all other members of the healthcare team—this helps provide consistency among the services provided. This includes communication between physical therapists and physical therapist assistants. ▶▶ To provide information to third-party payers, such as Medicare and other insurance companies who make decisions about reimbursement based on the quality and completeness of the physical therapy note. ▶▶ To help the physical therapist organize his/her thought processes involved in patient care. ▶▶ To be used for quality assurance and improvement purposes and for issues such as discharge planning. ▶▶ To serve as a source of data for quality assurance, peer and utilization review, and research. ▶▶

Patient-Related Instruction Patient education is an important component of the POC. There are probably as many ways to teach as there are to learn. The clinician needs to be aware that people may have very different preferences for how, when, where, and how often they learn (see Chapter 8).

Outcomes The assessment of change in a patient’s symptoms and function over time is essential to both clinical practice and research.149 Outcome measures (OMs) are integral to improving quality of treatment and thus we usually expect outcome instruments to evaluate the effectiveness of physical therapy

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Patient/Client Management

Documentation in health care includes any entry into the patient/client record. This documentation, considered a legal document, becomes a part of the patient’s medical record. The SOAP (Subjective, Objective, Assessment, Plan) note format has traditionally been used to document the examination and intervention process.

interventions. Outcomes measurement is a process that describes a systematic method to gauge the effectiveness and efficiency of an intervention. However, OMs are more than just tools with which treatment is evaluated and the quality of care is monitored. Indeed, they are involved in guiding clinicians whether or not to refer someone for treatment or to enable patients to self-track their own health outline.150 The efficiency of an intervention is a factor of utilization (e.g., number of outpatient visits, length of inpatient stay) with the costs of care and outcome. The trend in using outcome measures in the decision-making process is consistent with the evidence-based approach (EBP) and represents the final step in the evaluation of clinical performance.3,151 In such cases, reliability (consistent scores in the absence of change) and responsiveness (ability to detect clinically important changes) are critical measurement properties.152 Clinically, we want to know that stable or untreated patients tested by different physical therapists (interrater reliability) or assessed at different times (test-retest reliability) would demonstrate a consistent score so that when change occurs it is more likely to reflect a true change.152 A health outcome measure is an instrument that enables an observer to objectively evaluate an intended goal (typically an improvement in health status) from a healthcare activity (treatment).150 As outcomes exist for a wide range of purposes, the clinician should be able to evaluate and choose the appropriate outcome measure for a specific patient population. Measurement properties cannot be considered in isolation, and selecting optimal measures requires balancing competing priorities.152 Measurement instruments must be able to detect a change when it has occurred and to remain stable when a change has not occurred.153 The better the sophistication, predictability, and accuracy of the measurement tool, the less chance there is for errors in measurement that make it difficult to ascertain whether true progress has occurred. In an effort to counteract the potential for these measurement errors, the term minimal detectable change (MDC) has been introduced. The MDC is defined as the minimal amount of change that exceeds measurement error.153 The MDC is a statistical measure of meaningful change and is related to an instrument’s reliability.153 Although various methods for calculating the MDC have been proposed; a consensus has yet to be reached as to what is the optimal method. Unfortunately, statistically significant change using the MDC may not indicate that the change is clinically relevant. The minimally clinically important difference (MCID) is a measure of clinical relevance and indicates the amount of change in scale points that must occur before the change may be considered meaningful.154 MCIDs in performance measures have become commonly used outcome measures. Responsiveness, as investigated with the MCID, indicates whether a patient experiences a beneficial change following treatment that would mandate a change in patient management, in the absence of troublesome side effects, excessive costs, and inconveniences.55,155 The sensitivity of the MCID is represented by the number of patients the outcome measure correctly identifies as having changed an important amount divided by all of the patients who truly changed an important amount.156 The specificity of the MCID is represented by the number of patients the outcome measure correctly identifies as not having changed an important

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TABLE 4-29

Types of Outcome Measures

EXAMINATION AND EVALUATION

Measure

Description

Notes

EQ-5D

One of the most commonly used generic instruments The EQ-5D is known to lack responsiveness to change in musculoskeletal conditions and has therefore and captures quality-of-life from five health been superseded by the EQ-5D-5L, which offers domains: mobility, self-care, usual activities, pain/ five rather than three levels within each domain discomfort, and anxiety/depression. making it more sensitive to changes in health.

Musculoskeletal Patient Reported Outcome Measures (MSK-PROM)

A tool that enables clinicians to quickly evaluate and The MSK-PROM is designed to complement the EQ-5D-5L with six additional items that monitor musculoskeletal health status using single considerably increase the responsiveness of the questions for each health domain (independence EQ-5D-5L items when used alone. from others, physical function, pain intensity, work interference, limitations in activities and roles that matter, quality-of-life, understanding about how to deal with the condition, anxiety/depression, overall impact on the patient, and a generated item about the severity of their worst symptom).

International Classification The ICF provides a standard classification framework of Functioning, Disability based on a biopsychosocial model and suggest and Health (ICF) the following categories: body functions and structures, activity and participation restriction, environmental factors, and personal factors.

Common domains across conditions include symptom severity (pain intensity), function (physical function, social function, work function), general well-being/quality of life, global improvement, emotional functioning, participation restriction, and environmental factors such as levels of support needed, independence, relationships with family/others and patient satisfaction.

Patient-Specific Function Scale

Allows goal setting and monitoring of progress at a completely individual level, which tends to make it more sensitive to change than conventional measures.

Less useful for group level comparisons.

Orebro Musculoskeletal Pain Screening Tool

A tool designed specifically to facilitate clinical decision making.

Has established cutoff thresholds for the provision of cognitive behavioral approaches alongside manual therapy to prevent work absence.

Data from Jull G, Moore A, Falla D, et al. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. London, England: Elsevier; 2015.

210

amount divided by all of the patients who truly did not change an important amount.156 It is theorized that the reporting of MCID provides a more definite response of improvement thereby reducing the chance for error potentially associated with minimal improvement scores.157 Measures of responsiveness have commonly been reported as statistically significant changes in scores, which are useful in establishing the threshold of change needed beyond measurement error.55 Although it is tempting to make the assumption that the minimum level of statistical change (MDC) would be less than or equal to the MCID, the relationship between the MDC and the MCID scores is yet to be determined.154 Part of the problem in designing an outcome measurement tool is that function is highly individual, with multiple levels of difficulty and a high degree of specificity. For example, high-level or complex tasks may not be appropriate for severely injured older patients or those with certain comorbidities. To the payers of healthcare, a successful outcome is likely viewed as one that involved cost-efficient patient management.153 The most commonly used outcomes in musculoskeletal practice are patient reported outcome measures (Table 4-29). Anthropometric instruments (e.g., grip strength) and

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examiner completed observation lists (e.g., Berg balance scale) are also used.

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CHAPTER OBJECTIVES

CHAPTER 5

▶▶

Quality. The physical therapy profession will commit to establishing and adopting best practice standards across the domains of practice, education, and research as the individuals in these domains strive to be flexible, prepared, and responsive in a dynamic and ever-changing world. As independent practitioners, doctors of physical therapy in clinical practice will embrace best practice standards in the examination, diagnosis/classification, intervention, and outcome measurement.”

▶▶

Collaboration. The physical therapy profession will demonstrate the value of collaboration with other healthcare providers, consumers, community organizations, and other disciplines to solve the health-related challenges that society faces. In clinical practice, doctors of physical therapy, who collaborate across the continuum of care, will ensure that services are coordinated, of value, and consumer-centered by referring, comanaging, engaging consultants, and directing and supervising care.

At the completion of this chapter, the reader will be able to: 1. Understand the importance of differential diagnosis. 2. Recognize some of the signs and symptoms that indicate the presence of a serious pathology. 3. Discuss the concept of malingering. 4. Describe why certain signs and symptoms (red flags) require medical referral. 5. Describe the various infective diseases and inflammatory disorders that the orthopaedic clinician may encounter. 6. Describe the various neoplastic and metabolic diseases that can impact the orthopaedic patient. 7. Discuss the differences between fibromyalgia (FM) and myofascial pain syndrome (MPS). 8. List the various systemic or medical pathologies that can mimic musculoskeletal pathology in the various body regions.

OVERVIEW The American Physical Therapy Association Vision Statement for the American Physical Therapy Association (APTA) is “transforming society by optimizing movement to improve the human experience.”1 With the majority of US states now permitting direct access to physical therapists, many physical therapists now have the primary responsibility for being the gatekeepers of health care and for making medical referrals. In light of the APTA’s movement toward realizing “Vision 2020,” the APTA’s Board provides the following guiding principles: ▶▶

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Identity. The physical therapy profession will define and promote the movement system as the foundation for optimizing movement to improve the health of society. Recognition and validation of the movement system are essential to understand the structure, function, and potential of the human body.

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Through the history and physical examination, physical therapists diagnose and classify different types of information for use in their clinical reasoning and intervention.2 The Guide clearly articulates the physical therapist’s responsibility to recognize when a consultation with, or referral to, another healthcare provider is necessary.3 This responsibility requires that the clinician have a high level of knowledge, including an understanding of the concepts of medical screening and differential diagnosis. This is because a patient can present with multiple symptomatic areas that can pose a diagnostic challenge for the physical therapist. Though musculoskeletal and nonmusculoskeletal symptoms typically present separately, they can occur together, mimicking each other, making the ability to differentiate between musculoskeletal and nonmusculoskeletal symptoms a critical skill for the physical therapist. Thus, when a patient is referred to physical therapy, the primary objective of the examination process is to determine whether (1) the patient can be treated primarily and independently by the physical therapist, (2) the patient needs multidisciplinary management that includes physical therapy intervention, or (3) the patient requires referral to another healthcare practitioner to obtain optimal care.4 The results of a number of studies have demonstrated that physical therapists can provide safe and effective care for

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Yellow-flag findings are potential confounding variables that may be cautionary warnings regarding the patient’s condition, and that require further investigation. Examples include negative coping mechanisms, anxiety, depression, kinesiophobia, dizziness, abnormal sensation patterns, fainting, progressive weakness, and circulatory or skin changes. ▶▶ Red-flag findings are symptoms or conditions that may require immediate attention and supersede physical therapy being the primary provider of service (Table 5-1), as they are typically indicative of nonmechanical (nonneuromusculoskeletal) conditions or pathologies of visceral origin. Common red-flags are reports of trauma, fever or chills, unremitting night pain, bilateral symptoms and unintentional, substantial weight loss. An affirmative response to a single red-flag question may not be a reason for an immediate referral but a cluster typically would be.9−11 The presence of any of the following findings during the patient history, systems review, and/or scanning examination (see Chapters 3 and 4) may indicate serious pathology requiring medical referral: ▶▶ Fevers, chills, or night sweats.  These signs and symptoms are almost always associated with a systemic disorder such as an infection.12 ▶▶ Recent unexplained weight changes.  An unexplained weight gain could be caused by congestive heart failure, ▶▶

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hypothyroidism, or cancer.13 An unexplained weight loss could be the result of a gastrointestinal disorder, hyperthyroidism, cancer, or diabetes.13 ▶▶ Malaise or fatigue.  These complaints, which can help determine the general health of the patient, may be associated with a systemic disease.12 ▶▶ Unexplained nausea or vomiting.  This is never a good symptom or sign.12 ▶▶ Unilateral, bilateral, or quadrilateral paresthesias.  The distribution of neurologic symptoms can give the clinician clues as to the structures involved. Quadrilateral paresthesia always indicates the presence of central nervous system (CNS) involvement. ▶▶ Shortness of breath.  Shortness of breath can indicate a myriad of conditions. These can range from anxiety and asthma to a serious cardiac or pulmonary dysfunction.12 ▶▶ Dizziness.  The differential diagnosis of dizziness can be quite challenging. Patients often use the word “dizziness” to refer to feelings of lightheadedness, various sensations of body orientation, blurry vision, or weakness in the legs. ▶▶ Nystagmus.  Nystagmus is characterized by a rhythmic movement of the eyes, with an abnormal shifting away from fixation and rapid return.14 Failure of any one of the main control mechanisms for maintaining steady gaze fixation (the vestibuloocular reflex and a gaze-holding system) results in a disruption of steady fixation (see Chapter 3). ▶▶ Bowel or bladder dysfunction.  Bowel and bladder dysfunction may indicate compromise of the cauda equina. Cauda equina syndrome is associated with compression of the spinal nerve roots that supply neurologic function to the bladder and bowel. A massive disk herniation may cause spinal cord or cauda equina compression. One of the early signs of cauda equina compromise is the inability to urinate while sitting down, because of the increased levels of pressure. The most common sensory deficit occurs over the buttocks, posterior–superior thighs, and perianal regions (the so-called saddle anesthesia). Rapid diagnosis and surgical decompression of this abnormality are essential to prevent permanent neurologic dysfunction. ▶▶ Severe pain.  An insidious onset of severe pain with no specific mechanism of injury. ▶▶ Pain at night that awakens the patient from a deep sleep, usually at the same time every night, and which is unrelated to a movement. This finding may indicate the presence of a tumor. ▶▶ Painful weakness. The presence of a painful weakness almost always indicates serious pathology, including but not limited to a complete rupture of contractile tissue or nerve palsy. ▶▶ A gradual increase in the intensity of the pain. This symptom typically indicates that the condition is worsening, especially if it continues during rest. ▶▶ Radiculopathy.  Neurologic symptoms associated with more than two lumbar levels or more than one cervical level. With the exception of central protrusions or a disk

Differential Diagnosis

patients with musculoskeletal conditions in a direct access setting. Indeed, in a study by Childs et al.,5 physical therapists demonstrated higher levels of knowledge in managing musculoskeletal conditions than medical students, physician interns and residents, and most physician specialists except for orthopaedists. In addition, physical therapist students enrolled in educational programs conferring the doctoral degree achieved higher scores than their peers enrolled in programs conferring the master’s degree.5 Furthermore, licensed physical therapists who were board certified achieved higher scores and pass rates than their colleagues who were not board certified.5 During the patient interview, the physical therapist gains vital clues to the patient’s condition by inquiring about the patient’s symptoms, including their behavior, duration, location, and quality. Self-report outcome measures further enhance patient history by detailing the effects of the injury or illness on the patient’s quality of life, including function.6 The information gained from the interview guides the decision-making process and can help the therapist detect potentially serious pathology, choose which diagnostic tests or measures to use during the examination, and select the most appropriate intervention for the patient’s current condition.4 Although it is not within the scope of physical therapy practice to diagnose systemic pathology, it is important for the physical therapist to recognize possible signs and symptoms consistent with systemic pathology, which may mimic or be obscured by musculoskeletal symptoms.4,7 In those cases of nonmusculoskeletal symptoms, to aid the differential diagnosis of musculoskeletal conditions commonly encountered by physical therapists, screening tools have been designed to help recognize potential serious disorders (yellow or red flags).8

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TABLE 5-1

Red-Flag Findings

EXAMINATION AND EVALUATION

History

Possible Condition

Constant and severe pain, especially at night

Neoplasm and acute neuromusculoskeletal injury

Unexplained weight loss

Neoplasm

Loss of appetite

Neoplasm

Unusual fatigue

Neoplasm and thyroid dysfunction

Visual disturbances (blurriness or loss of vision)

Neoplasm

Frequent or severe headaches

Neoplasm

Arm pain lasting >2–3 months

Neoplasm or neurologic dysfunction

Persistent root pain

Neoplasm or neurologic dysfunction

Radicular pain with coughing

Neoplasm or neurologic dysfunction

Pain worsening after 1 month

Neoplasm

Paralysis

Neoplasm or neurologic dysfunction

Trunk and limb paresthesia

Neoplasm or neurologic dysfunction

Bilateral nerve root signs and symptoms

Neoplasm, spinal cord compression, and vertebrobasilar ischemia

Signs worse than symptoms

Neoplasm

Difficulty with balance and coordination

Spinal cord or CNS lesion

Fever or night sweats

Common findings in systemic infection and many diseases

Frequent nausea or vomiting

Common findings in many diseases, particularly of the gastrointestinal system

Dizziness

Upper cervical impairment, vertebrobasilar ischemia, craniovertebral ligament tear, inner ear dysfunction, CNS involvement, and cardiovascular dysfunction

Shortness of breath

Cardiovascular and/or pulmonary dysfunction and asthma

Quadrilateral paresthesia

Spinal cord compression (cervical myelopathy) and vertebrobasilar ischemia

CNS, central nervous system. Data from Meadows J. A Rationale and Complete Approach to the Sub-Acute Post-MVA Cervical Patient. Calgary, AB: Swodeam Consulting; 1995.

lesion at L4 through L5, disk protrusions typically only affect one spinal nerve root. Multiple-level involvement could suggest the presence of a tumor or other growth, or it may indicate symptom magnification. The presence or absence of objective findings should help determine the cause.

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Performing a medical screen is an inherent step in making a diagnosis for the purpose of deciding whether a patient referral is warranted, but the medical screen performed by the physical therapist is not synonymous with differential diagnosis. Differential diagnosis involves the ability to quickly differentiate problems of a serious nature from those that are not, using the history and physical examination. Problems of a serious nature include, but are not limited to, visceral diseases, cancer, infections, fractures, and vascular disorders. The purpose of the medical screen is to confirm (or rule out) the need for physical therapy intervention; the appropriateness of the referral; whether there are any red-flag findings, red-flag risk factors, or clusters of red-flag signs and/or symptoms; and whether the patient’s condition falls into one of the categories of conditions outlined in the Guide.15 Screening

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for medical disease includes communicating with a physician regarding a list or pattern of signs and symptoms that have caused concern but not to suggest the presence of a specific disease.2 In clinical practice, physical therapists commonly use a combination of red-flag findings, the scanning examination, and the systems review to detect medical diseases. The combined results provide the physical therapist with a method to gather and evaluate examination data, pose and solve problems, infer, hypothesize, and make clinical judgments, such as the need for a patient/client referral.15 Systemic dysfunction or disease can present with seemingly bizarre symptoms. These symptoms can prove to be very confusing to the inexperienced clinician. Complicating the scenario is that certain patients who are pursuing litigation can also present with equally bizarre symptoms. These patients may be subdivided into two groups: 1. Those patients with a legitimate injury and cause for litigation who genuinely want to improve. 2. Those patients who are merely motivated by the lure of the litigation settlement and who have no intention of

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showing signs of improvement until their case is settled. Termed malingerers, these patients are a frustrating group for clinicians to deal with, because, like the nonorganic patient type, they display exaggerated complaints of pain, tenderness, and suffering.

subjective complaints of paresthesia with only stockingglove anesthesia (conditions including diabetic neuropathy and the T4 syndrome must be ruled out); ▶▶ inappropriate scoring on the Oswestry Low Back Disability Questionnaire (Table 5-2), Neck Disability Index (Table 5-3), and McGill Pain Questionnaire (see Chapter 4); ▶▶ muscle stretch reflexes inconsistent with the presenting problem or symptoms; ▶▶ cogwheel motion of muscles during strength testing for weakness; and ▶▶ the ability of the patient to complete a straight-leg raise in a supine position, but demonstrating difficulty in performing the equivalent range (knee extension) in a seated position. ▶▶

CLINICAL PEARL Whatever the reasoning or motivation behind the malingering patient, the success rate from the clinician’s viewpoint will be low, and so it is well worth recognizing these individuals from the outset.

In contrast to the malingering patient, is the patient with psychogenic symptoms. This type of patient tends to exhibit an exaggeration of the symptoms in the absence of objective findings. Psychogenic symptoms are common in patients with anxiety, depression, or hysteria, making it important for the clinician to determine the level of psychological stress in a patient who demonstrates symptom magnification. A number of characteristics of this illness behavior have been proposed (Table 5-4).

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Ehlers-Danlos Syndrome Ehlers-Danlos syndrome (EDS) is an inherited heterogeneous connective tissue disorder characterized by varying degrees of skin hyperextensibility, joint hypomobility, joint dislocations, musculoskeletal pain, and vascular fragility.16 Inheritance is autosomal dominant, autosomal recessive, or X-linked. There are six major types16 Classical. This type is characterized by the presence of skin hyperextensibility with atrophic scars in individuals with joint hypomobility. ▶▶ Hypermobility. This type is characterized by hypermobile joints and some degree of skin hyperextensibility. This type is associated with the most debilitating musculoskeletal manifestations, and joint pain is reported by 100% of patients. If this type occurs in conjunction with pregnancy, the normal levels of hypermobility due to the hormone-induced ligamentous changes can have a profound impact (see Chapter 30). Generalized joint hypermobility is also found in Marfan syndrome and osteogenesis imperfecta which are also heritable disorders of connective tissue. ▶▶ Vascular. This type is characterized by fragile viscera and, therefore, has the most serious consequences. ▶▶ Kyphoscoliosis. This type is characterized by severe hypotonia and scoliosis. ▶▶ Arthrochalasia. This type is characterized by severe hypermobility and joint dislocations. ▶▶ Dermatosparaxis. This type is characterized by fragile, sagging, and redundant skin. ▶▶

Differential Diagnosis

Malingering is defined as the intentional production of false symptoms or the exaggeration of symptoms that truly exist. These symptoms may be physical or psychological but have, in common, the intention of achieving a certain goal. With very few exceptions, patients in significant pain look and feel miserable, move extremely slowly, and present with consistent findings during the examination. In contrast, malingerers present with severe symptoms and exaggerated responses during the examination, but can often be observed to be in no apparent distress at other times. This is particularly true if the malingering patient is observed in an environment outside of the clinic. However, it cannot be stressed enough that all patients should be given the benefit of the doubt until the clinician, with a high degree of confidence, can rule out an organic cause for the pain. A number of clinical signs and symptoms can alert the clinician to the possibility of a patient who is malingering. These include:

INHERITED DISEASES

The diagnosis of this condition begins with a complete history. The typical history with EDS includes reports of joint dislocations, subluxations, pain, easy bruising, easy bleeding, or poor wound healing.16 The physical examination includes an evaluation of range of motion (ROM). Joint hypermobility is assessed using the Beighton criteria scale (Table 5-5), where a maximum score of 9 points is possible, and a score of >4 defines hypermobility. The skin is assessed for its consistency, presence of dystrophic scars, striae, brown discoloration (secondary to hemosiderin deposition at areas of repetitive trauma and bruising), and hyperextensibility.16 Physical therapy can be used to enhance musculotendinous strength, neuromuscular coordination, and joint proprioception to maximize function, minimize symptoms, and improve joint stability.16

VASCULAR DISEASES Peripheral Artery Disease17 Peripheral artery disease (PAD) is the term used to describe partial or complete atherosclerotic occlusive disease involving one or more arteries, usually involving the lower extremities. PAD is an important consideration in the differential diagnosis of lower extremity pain as it may mimic or coexist with

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TABLE 5-2

Oswestry Low Back Disability Questionnaire

PLEASE READ: This questionnaire is designed to enable us to understand how much your low back pain has affected your ability to manage your everyday activities. Please answer each section by marking the ONE BOX that most applies to you. We realize that you feel that more than one statement may relate to your problem, but please just mark the one box that most closely describes your problem at this point in time. Name: Date:

EXAMINATION AND EVALUATION

Section 1—Pain Intensity •  The pain comes and goes and is very mild •  The pain is mild and does not vary much •  The pain comes and goes and is moderate •  The pain is moderate and does not vary much •  The pain comes and goes and is severe •  The pain is severe and does not vary much Section 2—Personal Care •  I have no pain when I wash or dress • I do not normally change my way of washing and dressing even though it causes some pain • I have had to change the way I wash and dress because these activities increase my pain • Because of pain I am unable to do some washing and dressing without help • Because of pain I am unable to do most washing and dressing without help • Because of pain I am unable to do any washing and dressing without help Section 3—Lifting (Skip if you have not attempted lifting since the onset of your back pain.) •  Can lift heavy weights without increasing my pain •  Can lift heavy weights but it increases my pain •  Pain prevents me from lifting heavy weights off the floor • Pain prevents me from lifting heavy weights off the floor but I can manage if they are conveniently positioned, e.g., on a table • Pain prevents me from lifting heavy weights but I can manage light to medium weights if they are conveniently positioned •  I can only lift very light weight at the most Section 4—Walking •  I have no pain when I walk •  I have some pain when I walk but it does not prevent me from walking normal distances •  Pain prevents me from walking long distances •  Pain prevents me from walking intermediate distances •  Pain prevents me from walking short distances •  Pain prevents me from walking at all Section 5—Sitting •  Sitting does not cause me any pain •  I can sit as long as I need to, provided I have my choice of chair •  Pain prevents me from sitting more than 1 hour •  Pain prevents me from sitting more than ½ hour •  Pain prevents me from sitting more than 10 minutes •  Pain prevents me from sitting at all

Section 6—Standing •  Standing does not cause me any pain • I have some pain when I stand but it does not increase with time •  Pain prevents me from standing more than 1 hour •  Pain prevents me from standing more than ½ hour •  Pain prevents me from standing more than 10 minutes •  Pain prevents me from standing at all Section 7—Sleeping •  I have no pain when I lie in bed • I have some pain when I lie in bed but it does not prevent me from sleeping well •  Because of pain my sleep is reduced by 25% •  Because of pain my sleep is reduced by 50% •  Because of pain my sleep is reduced by 75% •  Pain prevents me from sleeping at all Section 8—Sex Life (if applicable) •  My sex life is normal and causes no pain •  My sex life is normal but increases my pain •  My sex life is nearly normal but is very painful •  My sex life is severely restricted •  My sex life is nearly absent because of pain •  Pain prevents any sex life at all Section 9—Social Life •  My social life is normal and causes no pain •  My social life is normal but increases my pain • Pain has no significant effect on my social life, apart from limiting my more energetic interests (sports, etc.) •  Pain has restricted my social life and I do not go out often •  Pain has restricted social life to my home •  I have no social life because of pain Section 10—Traveling •  I have no pain when I travel • I have some pain when I travel but none of my usual forms of travel make it worse • Traveling increases my pain but has not required that I seek alternative forms of travel • I have had to change the way I travel because my usual form of travel increases my pain •  Pain has restricted all forms of travel •  I can only travel while lying down

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TABLE 5-3

Neck Disability Index

This questionnaire has been designed to give the doctor information as to how your neck pain has affected your ability to manage in everyday life. Please answer every section and mark in each section only the ONE BOX that applies to you. We realize you may consider that two of the statements in any one section relate to you, but please just mark the box that most closely describes your problem. Section 1—Pain Intensity

•  I have no pain at the moment

•  The pain is very mild at the moment

•  The pain is moderate at the moment

•  The pain is fairly severe at the moment

Section 2—Personal Care (Washing, Dressing, etc.) •  I can look after myself normally without causing extra pain •  I can look after myself normally but it causes extra pain •  It is painful to look after myself and I am slow and careful •  I need some help but manage most of my personal care •  I need help every day in most aspects of self-care •  I do not get dressed, I wash with difficulty and stay in bed Section 3—Lifting •  I can lift heavy weights without extra pain •  I can lift heavy weights but it gives extra pain • Pain prevents me from lifting heavy weights off the floor, but I can manage if they are conveniently positioned, for example, on a table • Pain prevents me from lifting heavy weights, but I can manage light to medium weights if they are conveniently positioned •  I can lift very light weights •  I cannot lift or carry anything at all Section 4—Reading •  I can read as much as I want to with no pain in my neck •  I can read as much as I want to with slight pain in my neck •  I can read as much as I want with moderate pain in my neck •  I can’t read as much as I want because of moderate pain in my neck •  I can hardly read at all because of severe pain in my neck •  I cannot read at all Section 5—Headaches •  I have no headaches at all •  I have slight headaches which come infrequently •  I have moderate headaches which come infrequently •  I have moderate headaches which come frequently •  I have severe headaches which come frequently •  I have headaches almost all the time

Section 8—Driving •  I can drive my car without any neck pain • I can drive my car as long as I want with slight pain in my neck • I can drive my car as long as I want because of moderate pain in my neck • I can’t drive my car as long as I want because of moderate pain in my neck •  I can hardly drive at all because of severe pain in my neck •  I can’t drive my car at all

Differential Diagnosis

•  The pain is the worst imaginable at the moment

Section 7—Work •  I can do as much work as I want to •  I can only do my usual work, but no more •  I can do most of my usual work, but no more •  I cannot do my usual work •  I can hardly do any work at all •  I can’t do any work at all

Section 9—Sleeping •  I have no trouble sleeping •  My sleep is slightly disturbed (less than 1 hour sleepless) •  My sleep is mildly disturbed (1–2 hours sleepless) •  My sleep is moderately disturbed (2–3 hours sleepless) •  My sleep is greatly disturbed (3–5 hours sleepless) •  My sleep is completely disturbed (5–7 hours sleepless) Section 10—Recreation • I am able to engage in all my recreation activities with no neck pain at all • I am able to engage in all my recreation activities, with some pain in my neck • I am able to engage in most, but not all of my usual recreation activities because of pain in my neck • I am able to engage in a few of my usual recreation activities because of pain in my neck • I can hardly do any recreation activities because of pain in my neck •  I can’t do any recreation activities at all   

Section 6—Concentration •  I can concentrate fully when I want to with no difficulty •  I can concentrate fully when I want to with slight difficulty •  I have a fair degree of difficulty in concentrating when I want to •  I have a lot of difficulty in concentrating when I want to •  I have a great deal of difficulty in concentrating when I want to •  I cannot concentrate at all Data from Vernon H, Mior S. The neck disability index: a study of reliability and validity. J Manipulative Physiol Ther. 1991 Sep;14(7):409–415.

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TABLE 5-4

 addell Test for Nonorganic W Physical Signs

Test

Inappropriate Response

Tenderness

Superficial, nonanatomic to light touch

Simulation   Axial loading  Rotation

EXAMINATION AND EVALUATION

 Distraction

CLINICAL PEARL Axial loading on a standing patient’s skull produces low back pain Passive, simultaneous rotation of shoulders and pelvis produces low back pain Discrepancy between findings on supine and seated straight leg raising

Regional disturbances  Weakness Giving way (Cogwheel) weakness  Sensory Nondermatomal sensory loss  Overreaction Disproportionate facial expression, verbalization, or tremor during examination Data from Waddell G, McCulloch JA, Kummel E, et al. Nonorganic physical signs in low-back pain. Spine (Phila Pa 1976). 1980 Mar-Apr;5(2):117–125.

neuromusculoskeletal conditions especially in patients over 50 years of age. For example, any neuromusculoskeletal entity that causes pain into the buttock, thigh, calf, or foot may share a differential diagnosis with PAD. Perhaps the most common differential diagnosis is “neurogenic claudication” from lumbar spinal stenosis (see Chapter 28).

CLINICAL PEARL Although PAD is uncommon before age 50, the incidence rises sharply thereafter, such that 15–20% of persons over age 70 have PAD.17 Patients with PAD typically have claudication that begins slowly and progresses over time. The typical symptoms, which are usually absent at rest but occur with lower extremity

TABLE 5-5

 eighton Criteria for Generalized B Joint Hypermobility

Finding

Score (Points)

Forward flexion of the trunk with knees fully extended so that the palms of the hand rest flat on the floor

1 point

Hyperextension of the elbows beyond 10 degrees

1 point for each elbow

Hyperextension of the knees beyond 10 degrees

1 point for each knee

Passive apposition of the thumbs to the flexor aspect of the forearm

1 point for each hand

Passive dorsiflexion of the little fingers 1 point for each hand beyond 90 degrees

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Data from Beighton P, Solomon L, Soskolne CL. Articular mobility in an African population. Ann Rheum Dis. 1973 Sep;32(5):413–418.

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exercise, may occur in the thighs, hips, buttocks, or foot arch of one or both legs. Pain at rest represents a critical turning point in the progression of the disease process and indicates a high-risk situation for limb loss.

The location of the claudication symptoms can often be an indicator of the location of the arterial blockage, with the symptoms typically occurring distal to the blockage. For example18,19: ▶▶ Calf claudication may indicate occlusive disease in the popliteal or superficial femoral arteries, ▶▶ Thigh symptoms suggest involvement of the iliac or proximal femoral arteries, ▶▶ Buttock symptoms suggest involvement in the aorta or proximal iliac arteries. Observation of the patient should seek evidence of tissue loss (ulcers or wounds) or other signs of decreased blood flow, pallor or cyanotic discoloration, and slow capillary refill (5 seconds or longer). Although not specific to PAD, trophic changes, including shiny skin, loss of hair, and thick nails, may suggest PAD. Palpation of the involved extremity may demonstrate coolness of the skin. An examination of the pulses is essential when evaluating a patient for PAD, beginning with the pedal pulses (dorsalis pedis and posterior tibial arteries). Pulses may also be examined at the more proximal locations (the popliteal, femoral, and iliac arteries, and the aorta). Additionally, stethoscopic auscultation for bruits, suggesting turbulent flow, can be performed.20 The ankle-brachial index (ABI) (see Chapter 4), also known as the ankle-arm index, can prove diagnostic for PAD—patients with an ABI of 0.90 or less can be diagnosed with PAD with 79–95% sensitivity and 96–100% specificity.21

CLINICAL PEARL Patients with suspected PAD should be referred to their physician for risk factor modification (tobacco cessation, as well as lifestyle and pharmacologic measures for management of dyslipidemia, hypertension, and diabetes), and potential further evaluation of cerebrovascular disease and CAD.17 There is substantial evidence to support supervised exercise training as a major component in the treatment of claudication.22,23

INFECTIVE DISEASES Osteomyelitis Osteomyelitis is an acute or chronic inflammatory process of the bone and its marrow secondary to infection with pyogenic organisms or other sources of infection, such as tuberculosis,

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or specific fungal infections (mycotic osteomyelitis), parasitic infections (Hydatid disease), viral infections, or syphilitic infections (Charcot arthropathy). The following are the two primary categories of acute osteomyelitis: Hematogenous osteomyelitis.  It is an infection caused by bacterial seeding from the blood. The most common site is the rapidly growing and highly vascular metaphysis of growing bones. ▶▶ Direct or contiguous inoculation.  This type of osteomyelitis is caused by direct contact between the tissue and bacteria during surgery, a penetrating wound, or as a result of poor dental hygiene.

Respiratory weakness due to high cervical (phrenic nerve, C4) and thoracic spinal cord involvement is the most common cause of death in ALS, often in conjunction with aspiration pneumonia.24

▶▶

CLINICAL PEARL The most common clinical finding in patients with osteomyelitis is a constant pain with marked tenderness over the involved bone.

NEUROLOGIC DISORDERS Amyotrophic Lateral Sclerosis Amyotrophic lateral sclerosis (ALS), commonly referred to as Lou Gehrig’s disease, is a neurodegenerative progressive disorder that causes rapid loss of motor neurons in the brain and spinal cord, leading to paralysis and death. Diagnosis is based solely on clinical data. The diagnosis of ALS depends upon the recognition of a characteristic constellation of symptoms and signs and supportive electrophysiological findings. For clinically definite ALS diagnosis, upper motor neuron (UMN) and lower motor neuron (LMN) signs in bulbar and two spinal regions or in three spinal regions are required. The LMN weakness and muscle atrophy involves both peripheral nerve and myotomal distributions. The clinical hallmark of ALS is the coexistence of muscle atrophy, weakness, fasciculations, and cramps (caused by LMN degeneration), together with hyperactive or inappropriately brisk muscle stretch reflexes, pyramidal tract signs, and increased muscle tone (due to corticospinal tract involvement).24 Muscle cramps are often already present before other symptoms develop. Most patients present with asymmetrical, distal weakness of the arm or leg. The symptoms usually progress first in the affected extremity and then gradually spread to adjacent muscle groups and remote ipsilateral or contralateral regions. Although disability is usually limited in the early stages, ALS progresses relentlessly. Most patients are ultimately unable to walk, care for themselves, speak, and swallow.24 However, there is usually no clinical involvement of parts of the CNS other than the motor pathways.24

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Guillain–Barré syndrome (GBS) is challenging to identify because of its multitude of presentations and manifestations. GBS may be defined as a postinfectious, acute, paralytic peripheral neuropathy. It can affect any age group although there is a peak incidence in young adults. GBS appears to be an inflammatory or immune-mediated condition. The majority of patients describe an antecedent febrile illness. Upper respiratory infections are seen in 50% of cases and are caused by a variety of viruses.25 The illness is usually an acute respiratory or gastrointestinal condition that lasts for several days and then resolves. This is followed in 1–2 weeks by the development of a progressive ascending weakness or paralysis, which is usually symmetric. The progression of the weakness or paralysis can be gradual (1–3 weeks) or rapid (1–2 days).25 The patient reports difficulty or instability with walking, arising from a chair, and ascending or descending stairs. Associated signs and symptoms include cranial nerve involvement (facial weakness), paresthesias, sensory deficits, difficulty in breathing, diminished muscle stretch reflexes, autonomic dysfunction (tachycardia and vasomotor symptoms), oropharyngeal weakness, and ocular involvement.25 The differential diagnosis of GBS is quite large and includes the spectrum of illnesses causing acute or subacute paralysis. These include spinal cord compression (myelopathy), UMN disorders, poliomyelitis, transverse myelitis, polyneuropathy, SLE, polyarteritis nodosa, myasthenia gravis, and sarcoidosis.25 All patients with suspected GBS are typically hospitalized for vigilant monitoring because of the high risk of respiratory failure, which occurs in approximately one-third of patients.25

Differential Diagnosis

Disease states known to predispose patients to osteomyelitis include diabetes mellitus, sickle-cell disease, acquired immune deficiency syndrome, IV drug abuse, alcoholism, chronic steroid use, immunosuppression, and chronic joint disease. Clinical signs and symptoms associated with osteomyelitis include fever (approximately 50% of cases), fatigue, edema, erythema, tenderness, and reduction in the use of the extremity.

Guillain–Barré Syndrome

Syringomyelia Syringomyelia is a disease that produces fluid-containing cysts (syrinx) within the spinal cord, often associated with stenosis of the foramen magnum. The syrinx can occur within the spinal cord (syringomyelia) or brain stem (syringobulbia). Syringomyelia has been found in association with various disorders, including spinal column or brain stem abnormalities (scoliosis, Klippel–Feil syndrome, Chiari I malformation), intramedullary tumors, and traumatic degeneration of the spinal cord.26,27 Chiari I malformation is the most common condition in patients with syringomyelia. Painful dysesthesias, which have been described variously as burning pain, pins-and-needles sensations, and stretching or pressure of the skin, occur in up to 40% of patients with syringomyelia.26,27 The pain tends to arise in a dermatomal pattern and is accompanied, in most cases, by hyperesthesia. Radiologic features that suggest syringomyelia include an increase in the width and depth of the cervical canal, bony abnormalities at the craniovertebral junction, diastematomyelia, and occipitalization of the atlas.26,27

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INFLAMMATORY DISORDERS Perhaps, the most common inflammatory disorders of the musculoskeletal system are the rheumatoid diseases.

Rheumatoid Arthritis

EXAMINATION AND EVALUATION 222

Rheumatoid arthritis (RA) can be defined as a chronic, progressive, systemic, inflammatory disease of connective tissue, characterized by spontaneous remissions and exacerbations (flare-ups). It is the second most common rheumatic disease after osteoarthritis (OA), but it is the most destructive to synovial joints. Unlike OA, RA involves primary tissue inflammation rather than joint degeneration. Although most individuals who develop RA do so in their early-to-middle adulthood, some experience it either earlier (Juvenile RA— see Chapter 30) or later. Although the exact etiology of RA is unclear, it is considered one of many autoimmune disorders. Abnormal immunoglobulin (Ig) G and IgM antibodies develop in response to IgG antigens, to form circulating immune complexes. These complexes lodge in connective tissue, especially synovium, and create an inflammatory response. Inflammatory mediators, including cytokines (e.g., tumor necrosis factor), chemokines, and proteases, activate and attract neutrophils and other inflammatory cells. The synovium thickens, fluid accumulates in the joint space, and a pannus forms, eroding joint cartilage and bone. Bony ankylosis, calcifications, and loss of bone density follow. RA typically begins in the joints of the arm or hand. The individual complains of joint stiffness lasting longer than 30 minutes on awakening, pain, swelling, and heat (synovitis). Unlike with OA, the distal interphalangeal joints of the fingers usually are not involved in RA. The signs and symptoms of RA vary among individuals, depending on the rate of progress of the disease. A complete musculoskeletal examination helps diagnose the disease. Clinical manifestations include both joint involvement and systemic problems; some are associated with the early stages of RA, whereas others are seen later in advanced disease. Complaints of fatigue, anorexia, low-grade fever, and mild weight loss are commonly associated with RA. As the disease worsens, joints become deformed, and secondary osteoporosis (see “Metabolic Disease”) can result in fractures, especially in older adults. Hand and finger deformities are typical in the advanced stages of the disease. Palpable subcutaneous nodules, often appearing on the ulnar surface of the arm, are associated with a severe, destructive disease pattern. As the disease progresses over years, systemic manifestations increase and potentially life-threatening organ involvement begins. Cardiac problems, such as pericarditis and myocarditis, and respiratory complications, such as pleurisy, pulmonary fibrosis, and pneumonitis, are common. RA can affect body image, self-esteem, and sexuality in older adults. The person with RA loses control over body changes, is chronically fatigued, and eventually may lose independence in activities of daily living (ADLs). As a reaction to these losses, individuals may display the phases of the grieving process,

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such as anger or denial. Some people become depressed, feeling helpless and hopeless because no cure presently exists for the condition. Chronic pain and suffering interfere with quality of life. The physical therapy examination of the patient with RA involves: measurement of independence with functional activities; measurement of joint inflammation; ▶▶ measurement of joint ROM; and ▶▶ determination of limiting factors including pain, weakness, and fatigue. ▶▶ ▶▶

Because RA affects multiple body systems, lessens the quality of life, and affects functional ability; the approach to managing the patient with this condition must be interdisciplinary. Management typically includes drug therapy, physical and/or occupational therapy, and recreational therapy. Some clients also need psychologic counseling to help cope with the disease. Rest and energy conservation are crucial for managing RA (Table 5-6). Pacing activities, obtaining assistance, and allowing rest periods help conserve energy. Positioning joints in their optimal functional position help to prevent deformities. Ambulatory and adaptive devices can help individuals maintain independence in ADLs. For example, a long-handled shoehorn may help in putting on shoes. Velcro attachments on shoes often are a better option than laces. Styrofoam or paper cups may collapse or bend, whereas a hard plastic or china cup may be easier to handle. The clinician should also review principles of joint protection with the patient and family and provide adaptive equipment as needed to perform ADLs independently. Strengthening exercises and pain-relief measures, such as the use of ice and heat, can be prescribed. Ice application is used for hot, inflamed joints. Heat is used for painful joints that are not acutely inflamed. Showers, hot packs (not too heavy), and paraffin dips are ideal for heat application. Some RA patients have associated syndromes. Two such syndromes are Sjogren and Felty syndromes. Sjogren syndrome is characterized by dryness of the eyes (keratoconjunctivitis), mouth (xerostomia), and other mucous membranes. Felty syndrome is characterized by leukopenia and hepatosplenomegaly, often leading to recurrent infections. It encompasses a diverse group of pathogenic mechanisms in RA, all of which result in decreased levels of circulating neutrophils. No single test or group of laboratory tests can confirm a diagnosis of RA, but they can support the findings from the patient’s history and the physical findings. A number of immunologic tests, such as the rheumatoid factor and antinuclear antibody titer, are available to aid diagnosis. Normal values differ, depending on the precise laboratory technique used.

Gout Gout is the most common form of inflammatory arthritis in men older than 40 years and appears to be on the rise. The rising prevalence of gout is thought to stem from dietary changes (high-purine diet, and habitual alcohol ingestion),

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TABLE 5-6

Intervention Strategies for Rheumatoid Arthritis Intervention

Example

Pain control            

Therapeutic heat to decrease rigidity of joints, increase the flexibility of fibrous tissue, and decrease pain and muscle spasm Massage, usually applied with heat treatment and before stretching, can be used to relieve pain and prevent adhesions Therapeutic cold can be used for analgesic and vasoconstriction purposes in inflamed joints during the acute period. Care must be taken to avoid adverse effects

Heat applications: Aquatic therapy Instructions on the wearing of warm pajamas, sleeping bag, and electric blanket Paraffin for hands Ultrasound Heating pads—moist heat better than dry heat

Minimizing the effects of inflammation            

Joint protection strategies Splinting Rest from abuse Body mechanics education  

As needed—balance rest with activity by using splinting (articular resting) Resting splints are used to rest the joint in the appropriate position in the acute period Dynamic splints are used to exert adequate force that the tissue can tolerate and provide sufficient joint volume Functional splints are used to protect the joint in the course of activity Stabilizer splints are used in cases of permanent contractures. Gradual casting can be used to apply a stretch to the contracture

Preventing limitation ROM and stretching exercises and restoring   ROM in affected joints

Acute stage: passive and active assisted to avoid joint compression Subacute/chronic stages: active exercises, passive stretching or contract–relax techniques

Maintaining and improving strength              

Resistive exercises Endurance exercises Electrical stimulation

Acute and subacute stages: isometric exercises progressing cautiously to resistive Subacute/chronic stages: strengthening exercises that avoid substitutions and minimize instability, atrophy, deformity, pain, and injury Chronic stage: judicious use of concentric exercise Provision of encouragement to exercise—fun and recreational activities of moderate intensity and 30 minutes duration per day Swimming Tai Chi Short-term electrical stimulation is useful in cases of excessive muscle atrophy and in those who cannot exercise

Ensuring normal growth and development  

Posture and positioning Mobility and assistive devices    

To maintain joint ROM, patients should spend 20 min/day in prone to stretch the hip flexors and quadriceps; assess leg length discrepancy in standing and avoid scoliosis Extended comb handles, thicker spoons, shoehorns Clothes with easy openings and/or Velcro

obesity, environmental factors, increasing longevity, subclinical renal impairment, and the increased use of drugs causing hyperuricemia, particularly diuretics.28 High blood levels of uric acid lead to inflammation, joint swelling, and severe pain. Symptoms are caused by deposits of sodium urate or calcium pyrophosphate crystals in joints and periarticular tissues. Onset is usually sudden, often during the night or early morning. The classic finding of gouty arthritis (gout) is warmth, swelling, cutaneous erythema, and severe pain of the

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Differential Diagnosis

Objective

first metatarsophalangeal (MTP) joint (podagra).28 However, other joints may also be involved. These include the shoulder, knee, wrist, ankle, elbow, or fingers. Fever, chills, and malaise accompany an episode of gout.28 As the condition becomes chronic, the patient may report morning stiffness and joint deformity, progressive loss of function, or disability. Chronic gouty nephropathy may occur. Differential diagnosis includes cellulitis, septic arthritis, RA, bursitis related to a bunion, sarcoidosis, multiple myeloma, and hyperparathyroidism.

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Treatment is geared toward pharmacologic control of serum uric acid levels.

Ankylosing Spondylitis

EXAMINATION AND EVALUATION

Ankylosing spondylitis (AS, also known as Bekhterev or Marie–Strümpell disease) is a chronic rheumatoid disorder. The patient is usually between 15 and 40 years.29 There is a 10–20% risk that offspring of patients with the disease will later develop it.29 Although males are affected more frequently than females, mild courses of AS are more common in the latter.29 A human leukocyte antigen (HLA) haplotype association (HLA-B27) has been found with AS and remains one of the strongest known associations of disease with HLAB27, but other diseases are also associated with the antigen.30 C-reactive protein has only 53% sensitivity and 70% specificity in spondyloarthropathies (X20).31 Thoracic involvement in AS occurs almost universally. The disease includes involvement of the anterior longitudinal ligament and ossification of the intervertebral disk, thoracic zygapophyseal joints, costovertebral joints, and manubriosternal joint. This multijoint involvement of the thoracic spine makes the checking of chest expansion measurements a required test in this region. In time, AS progresses to involve the whole spine and results in spinal deformities, including flattening of the lumbar lordosis, kyphosis of the thoracic spine, and hyperextension of the cervical spine. These changes, in turn, result in flexion contractures of the hips and knees, with significant morbidity and disability. The most characteristic feature of the back pain associated with AS is pain at night.30 Patients often awaken in the early morning (between 2 and 5 AM) with back pain and stiffness and usually either take a shower or exercise before returning to sleep. Back ache during the day is typically intermittent, irrespective of exertion or rest. Five screening questions for AS have been described29: 1. Is there morning stiffness? 2. Is there an improvement in discomfort with exercise? 3. Was the onset of back pain before age 40 years? 4. Did the problem begin slowly? 5. Has the pain persisted for at least 3 months?

224

Peripheral arthritis is uncommon in AS, but when it occurs, it is usually late in the course of the condition.32 Peripheral arthritis developing early in the course of the disease is a predictor of disease progression. The arthritis usually occurs in the lower extremities in an asymmetric distribution. The inspection usually reveals a flat lumbar spine and gross limitation of extension, and side bending in both directions (capsular pattern). In addition, the glides of the costotransverse joints and distraction of the sternoclavicular joints are decreased. Mobility loss tends to be bilateral and symmetric. There is loss of spinal elongation on flexion in the McRae’s modification of the Schober test,33,34 although this can occur in patients with chronic low back pain (LBP), or spinal tumors, and is thus not specific for inflammatory spondylopathies. The McRae’s modified Schober test is performed with the patient standing upright. The clinician marks the spinous

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process of L5 with a pen, and then creates a mark 10 cm above the L5 and 5 cm below L5 in the midline. The patient is then asked to bend forward maximally, and the distance between the upper and lower marks is measured. Patients with normal mobility of the spine have an increase of at least 5 cm in the measured distance from upright (15 cm) to maximal flexion (should be >20 cm).33,34 The patient may relate a history of costochondritis, and, upon examination, rib springing may give a hard end-feel. Basal rib expansion often is decreased with the chest expansion test. The chest expansion test is performed with the patient’s hands elevated and folded behind the head. The clinician takes a circumferential measurement of the patient’s chest at the level of the fourth intercostal space, or just below the breast in females. Chest circumference is measured after a maximal forced expiration and again after a maximal inspiration. The expansion should be more than 5 cm. Expansion of less than 2.5 cm is abnormal.33,34 As the disease progresses, the pain and stiffness can spread up the entire spine, pulling it into forward flexion, so that the patient adopts the typical stooped-over position. The patient gazes downward, the entire back is rounded, the hips and knees are semiflexed, and the arms cannot be raised beyond a limited amount at the shoulders.29 An exercise program is particularly important for these patients to maintain functional spinal outcomes.29 The goal of exercise therapy is to maintain the mobility of the spine and involved joints for as long as possible and to prevent the spine from stiffening in an unacceptable kyphotic position. A strict regimen of daily exercises, which include positioning, spinal extension exercises, breathing exercises, and exercises for the peripheral joints, must be followed. Several times a day, patients should lie prone for 5 minutes, and they should be encouraged to sleep prone or supine on a hard mattress and avoid the side-lying position. Swimming is the best routine sport.

Psoriatic Arthritis Psoriatic arthritis, which is an inflammatory form of arthritis associated with a chronic skin condition called psoriasis, affects men and women with equal frequency, with its peak onset in the fourth decade of life, although it may occur in children and in older adults.35 Psoriatic arthritis can manifest in one of a number of patterns, including distal joint disease (affecting the distal interphalangeal joints of the hands and feet), asymmetric oligoarthritis, polyarthritis (which tends to be asymmetric in half the cases), and arthritis mutilans (a severe destructive form of arthritis and a spondyloarthropathy that occurs in 40% of patients, but most commonly in the presence of one of the peripheral patterns).36 Patients with psoriatic arthritis have less tenderness over both affected joints and tender points than patients with the classic RA.37 The spondyloarthropathy of psoriatic arthritis may be distinguished from AS by the pattern of the sacroiliitis.36,37 Whereas sacroiliitis in AS tends to be symmetric, affecting both sacroiliac joints to the same degree, it tends to be asymmetric in psoriatic arthritis, and patients with psoriatic arthritis do not have as severe a spondyloarthropathy as patients with AS.36

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NEOPLASTIC DISEASE Benign Tumors: Osteoblastoma and Osteoid Osteoma Osteoblastoma and osteoid osteoma are benign bone-forming tumors with similar clinical findings. Osteoblastoma is a solitary bone neoplasm. It is most common in the vertebrae of children and young adults. Short and flat bones are more commonly affected than the long bones. ▶▶ Osteoid osteoma is a benign osteoblastic tumor of unknown etiology. It occurs most often in the long bones. ▶▶

Painful scoliosis is a well-recognized presentation of spinal osteoid osteoma and osteoblastoma and is thought to be caused by pain-provoked muscle spasm on the side of the lesion.

Malignant Tumors Metastatic disease of the spine is the most frequent neoplastic disorder of the axial skeleton. Malignant tumors can be primary or secondary. 1. Primary. Primary tumors include the following: a. Multiple myeloma. Myeloma is a plasma cell tumor. It is the most common malignant primary bone tumor. Early in its course, it can easily be overlooked as the cause of back pain. Common presentations of myeloma include bone pain, recurrent or persistent infection, anemia, renal impairment, or a combination of these. Some patients are asymptomatic. Presenting features, which require urgent specialist referral, include: (1) persistent, unexplained backache associated with loss of height and osteoporosis; and (2) symptoms suggestive of spinal cord or nerve root compression. b. Chordoma. Chordomas are rare tumors of notochordal origin. They typically are slow-growing,

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locally aggressive tumors. Chordomas usually are diagnosed in patients with pain or symptoms caused by compression of the surrounding structures. The clinical presentation initially may be mild in nature, leading to considerable delay in seeking medical attention. Vertebral chordomas involve the spinal cord and nerve roots progressively, resulting in pain, numbness, motor weakness, and, eventually, paralysis. c. Osteosarcoma. Osteosarcoma is a relatively uncommon malignancy. The peak incidence of osteosarcoma occurs in the second decade, with an additional smaller peak after the age of 50 years.42,43 These tumors typically arise in the metaphyseal regions of long bones, with the rib, distal femur, proximal tibia, and proximal humerus representing the four most common sites. The metaphysis of the vertebra is also predilected.44−46 Osteosarcomas frequently penetrate and destroy the cortex of the bone and extend into the surrounding soft tissues.   The initial clinical symptom of a malignant tumor is frequently pain in the affected area, which may also be associated with localized soft-tissue swelling or limitation of motion in the adjacent joint.

Differential Diagnosis

Another articular feature of psoriatic arthritis is the presence of dactylitis, tenosynovitis (often digital, in flexor and extensor tendons and in the Achilles tendon), and enthesitis.35 The presence of erosive disease in the distal interphalangeal joints is typical. Nail lesions occur in more than 80% of the patients with psoriatic arthritis and have been found to be the only clinical feature distinguishing patients with psoriatic arthritis from patients with uncomplicated psoriasis.38,39 Other extra-articular features include iritis, urethritis, and cardiac impairments similar to those seen in AS, although less frequently.36,40,41 Treatment for psoriatic arthritis is directed at reducing and controlling inflammation, with milder cases of psoriatic arthritis often being treated with nonsteroidal antiinflammatory drugs (NSAIDs) alone. More severe cases are treated using disease-modifying antirheumatic drugs or biological response modifiers to help prevent irreversible joint destruction and disability.

2. Secondary. Metastases to the spine most commonly arise from breast and lung cancer and from lymphoma. The clinical findings for a secondary spinal tumor are similar to those of a primary tumor.

METABOLIC DISEASE Osteoporosis More than 10 million adults in the United States have osteoporosis, 80% of which are women, but almost 3 million males are affected as well.47 Osteoporosis or osteopenia can result from an insufficient bone formation (low bone mass), excessive bone resorption, or a combination of these two phenomena (see Chapter 1). The result is decreased bone mineral density (BMD) and a progressive loss of trabecular connectivity that is irreversible and diminishes the bone quality in terms of its mechanical resistance to deformity underloading.48 In addition to the loss of bone mass, there is also narrowing of the bone shaft and widening of the medullary canal. Osteoporosis causes pathological (fragility) fractures of the vertebrae and fractures of other bones such as the ribs, proximal humerus, distal forearm, proximal femur (hip), and pelvis. However, with appropriate care, osteoporosis, fractures, and resultant disability can be prevented. Osteoporosis has been classified into two broad general types: type 1 (postmenopausal) and type 2 (involutional).49 Type 2 osteoporosis generally is seen in the older age population and has been referred to as senile osteoporosis.49

CLINICAL PEARL Women are more prone to develop osteoporosis because of the contribution of the loss of estrogen to accelerated bone loss in the postmenopausal female population.

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EXAMINATION AND EVALUATION 226

Numerous risk factors have been identified as contributing to the likelihood that an individual will develop bone loss. Genetics plays a major role, and female gender, positive family history, and racial characteristics associated with Caucasian, Asian, or Hispanic background increase the risk of osteoporosis.47 Low body weight (1 mm) Tenderness over the posterior (dorsal) wrist over the scapholunate ligament Scaphoid shift test produces abnormal popping and reproduces the patient’s pain

Mallet finger    

Flexed or dropped posture of the finger at the DIP joint History of jamming injury (impact of a thrown ball) Inability to actively extend or straighten the DIP joint

Jersey finger (FDP avulsion)

Mechanism is hyperextension stress applied to a flexed finger (e.g., grabbing a player’s jersey) Patient lacks active flexion at the DIP joint (FDP function lost) Swollen finger often assumes a position of relative extension compared to the other more flexed fingers

The Forearm, Wrist, and Hand

Flexor tendon sheath infection        

Degenerative arthritis of the fingers Heberden nodes (most common) Bouchard nodes (common) Mucous cysts (occasional) Decreased motion at involved IP joints Instability of involved joints (occasional) Modified with permission from Reider B. The Orthopaedic Physical Examination. Philadelphia, PA: WB Saunders; 1999.

Improve patient comfort by controlling and then decreasing pain and inflammation. ▶▶ Control and then eliminate edema. ▶▶ Restoration of a full pain-free range of motion in the entire kinetic chain. ▶▶ Restoration of proprioception as appropriate. ▶▶ Retard muscle atrophy. ▶▶ Minimize detrimental effects of immobilization and activity restriction. ▶▶ Scar management if appropriate. ▶▶ Maintain general fitness. ▶▶ Patient to be independent with a home exercise program. ▶▶

Pain and inflammation control is the major focus of the intervention program in the acute phase. This may be accomplished using the principles of POLICE (protection, optimal loading, ice, compression, and elevation). Icing for

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20–30 minutes, three to four times a day, concurrent with nonsteroidal antiinflammatory drugs (NSAIDs), or aspirin, can aid in reducing pain and swelling. One of the most significant problems a clinician faces with a hand-injured patient is the control and the elimination of edema. Edema can increase the risk of infection, increase stiffness, decrease motion, and inhibit arterial, venous, and lymphatic flow. Methods to control edema include elevation of the upper extremity and hand above the level of the heart, cryotherapy, active exercise, retrograde massage, intermittent compression, continuous compression wrapping, and contrast baths. Scar tissue management focuses on the control of stresses placed on healing tissues. Early active and passive motion provides controlled stress, encouraging optimal remodeling of scar tissue. Methods to control scarring include the use of thermal agents, transverse friction massage (TFM) (see Chapter 11), mechanical vibration, compressive techniques, and splinting. Silicone gel sheets are available commercially,

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THE EXTREMITIES

and patients are instructed to wear them if appropriate at night for up to 3 months following surgery.9 Dynamic wrist stability is influenced by proprioceptive and neuromuscular activity.26 The dart-throwing motion (DTM) has been advocated in the rehabilitation of the wrist and hand, particularly following carpal ligament injuries and repairs.7,27–29 The DTM is defined as a plane in which the wrist functional oblique motion occurs from radial extension to ulnar flexion.30 DTM occurs mostly at the midcarpal joint with minimal involvement of the radiocarpal joint.30 It is also considered one of the most natural rotations of the wrist that can be performed with minimal muscle force.30 Functional activities, such as twisting the lid of a jar, pouring from a jug, drinking from a glass, hammering a nail, throwing a ball, are all performed within this path of motion.7,31–33 The DTM is initially performed without resistance and then weight is added as tolerated. Proprioceptive awareness can be enhanced using mirror therapy, an evidence-based treatment widely used in cases of chronic pain, CRPS, phantom limb, musculoskeletal conditions, and patients poststroke.7 The patient observes the reflection of the uninvolved hand in different wrist positions and mimics the positions with the involved hand, which is positioned behind the mirror. The Sports Pro Gyro Exerciser (DFX Sport and Fitness, Anaheim, CA) can be used to improve unconscious neuromuscular control by generating forces in multiple directions, which forces the muscles of the forearm to react in an unpredictable way and promotes reactive muscle activation (see later).7,34 Therapeutic exercises are performed with the goal of regaining adequate soft-tissue rebalancing of the wrist by restoring the alignment of the extensor and the flexor tendons as near to normal as possible, and to prevent scarring or softtissue contractures by influencing the physiologic process of collagen formation. Movement is necessary to maintain joint mobility and gliding tendon function. Range-of-motion exercises are introduced as early as tolerated. These may be passive, active assisted, or active, as appropriate. If protected motion is necessary, it can be provided with taping, bracing, or in extreme cases, casting. PROM exercises are performed through the available range of motion to maintain joint and soft-tissue mobility, or a passive stretch can be applied to the end range of motion to lengthen pathologically shortened soft-tissue structures, thereby increasing motion. Depending on the focus of the intervention, the PROM exercises may include

FIGURE 18-72  Isolated MCP flexion.

FIGURE 18-73  Isolated PIP and DIP flexion and extension.

MCP flexion and extension (Fig. 18-72); and ▶▶ PIP and DIP flexion and extension (Fig. 18-73) and combined flexion and extension (Fig. 18-74). ▶▶

AROM exercises should include specific and composite exercises. Composite exercises, which include fisting and thumb opposition to each digit in addition to exercises involving the wrist, elbow, and shoulder, are designed to reproduce normal functional activities. Fast ballistic movements are discouraged if the goal is to restore mobility in the presence of increasing tissue resistance. Examples of AROM exercises include the following: ▶▶

798

Active wrist and finger flexion and extension, wrist ulnar and radial deviation, finger adduction and abduction,

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FIGURE 18-74  MCP, PIP, and DIP flexion and extension.

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Control/modify scar formation.  ▶▶ Substitute for a dysfunctional tissue.  ▶▶ Provide exercise.  Dynamic splints are used to provide active resistance in the direction opposite their line of pull to increase muscle strength, as well as to apply a corrective passive stretch to tendon adhesions and joint contractures. Drop-out splints, which are commonly used with elbow flexion contractures, block joint motion in one direction but allow motion in another. Articulated splints contain at least two static components and are designed in such a way as to allow motion in one plane at a joint. Staticprogressive splints involve the use of inelastic components to allow progressive changes in joint position as PROM changes without changing the structure of the splint. Serial static splints differ from static progressive splints in that they require the clinician to remold the splint to accommodate changes in the range of motion. ▶▶

and thumb opposition (Fig. 18-75), flexion, extension, abduction, and adduction. The wrist and hand muscles are usually exercised as a group if their strength is similar. Weaker muscles should be isolated in a similar fashion as that used when isolating the muscle for manual muscle testing. Protected range-of-motion exercises are performed to selectively mobilize joints and tendons while minimizing stress on repairing structures. As their name suggests, protected range-of-motion exercises are accomplished by placing the repaired structure in a protected position while adjacent tissues are carefully mobilized. An example of protective exercise can be seen following a radial nerve injury, where tendon transfers of the pronator teres, FCU, and FDS may be performed. Following the surgery the hand is immobilized with the wrist, MCP joints, and thumb in extension. At approximately 4 weeks, protective active motion exercises are introduced. These include MCP joint flexion and then PIP and DIP joint flexion with the MCP joint maintained in extension. ▶▶ ▶▶

Active exercises of forearm pronation and supination. Active exercises of elbow flexion and extension.

The AROM exercises are progressed to submaximal isometrics and muscle co-contractions. These early strengthening exercises are performed initially in the available pain-free ranges and, as the pain subsides, are gradually progressed so that they are performed throughout the entire range. Splinting of the wrist and hand may be necessary. It is not within the scope of this chapter to provide comprehensive detail with regard to splinting. Entire texts are devoted to the subject. However, splinting can often be an integral part of the rehabilitation program, and creative splinting can provide a useful adjunct to exercise. The general purposes of a splint are as follows: Prevent or correct deformity or dysfunction.  Maintain or reestablish normal tissue length, balance, and excursion. ▶▶ Immobilize/stabilize.  To stabilize a mobile joint so the corrective exercise force can be directed to the stiff joint or adherent tendon. ▶▶ Protect.  Static splints have no moveable parts and maintain joints in one position to promote healing and minimize stress. ▶▶

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Functional Phase The functional phase of rehabilitation is usually initiated when normal wrist positions and co-contractions of the wrist flexors and extensors can be performed. The goals of the functional phase include the following: Attain full range of pain-free motion. Restore normal joint kinematics. ▶▶ Improve muscle strength to within normal limits. ▶▶ Improve neuromuscular control. ▶▶ Restore normal muscle force couple relationships. ▶▶

The Forearm, Wrist, and Hand

FIGURE 18-75  Thumb opposition.

▶▶

The AROM exercises, initiated during the acute phase, are progressed until the patient demonstrates they have achieved the maximum range anticipated. Normal joint kinematics are restored using joint mobilization techniques. Joint mobilization techniques refer to passive traction and/or gliding movements to joint surfaces that maintain or restore the joint play normally allowed by the capsule. The joint mobilization techniques for the forearm, wrist, and hand are described in “Therapeutic Techniques” at the end of this chapter. Resistive exercises not only increase muscle strength and endurance but also improve the ability of the patient to actively mobilize stiff joints. Resistance exercises for the hand and wrist can be classified as either static (isometric) or dynamic (concentric, eccentric, or isokinetic). Strengthening of the muscles of the wrist and hand begins with specific exercises and progress to exercises that involve the entire upper kinetic chain, including the trunk. Isometric exercises may be continued from the acute phase when the available range of motion remains restricted. Wherever possible, resistance exercises that strengthen functional muscle groups rather than individual muscles should be selected. Specific exercises for the wrist and hand include the following: Resisted exercises into pronation (Fig. 18-76) and supination (Fig. 18-77). ▶▶ Hand and finger dexterity exercises including the ninepeg board (Fig. 18-78) or stroking exercises. ▶▶

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THE EXTREMITIES

FIGURE 18-76  Resisted pronation.

FIGURE 18-78  Nine-peg board.

Manually resisted exercises (Fig. 18-79). These are performed by the clinician initially, before becoming part of the patient’s home exercise routine using elastic bands (Fig. 18-80). ▶▶ Resisted exercises can be performed using gripping with light resistive putty (Fig. 18-81) or a hand exerciser (Fig. 18-82). Care must be taken with gripping or squeezing exercises because they typically restrict the use of the full range of motion.

▶▶

▶▶

Resisted exercises can also be performed using elastic resistance (Fig. 18-83), dumbbells (Fig. 18-84), or using a device called the TheraBand FlexBar, which is a flexible, durable resistance device with a ridged surface for enhanced grip during use that can be used to improve grip strength and upper extremity stabilization. The twisting techniques depicted in Figs. 17-72 through 17-75 can be used to include eccentric loading of the wrist extensors moving from a position of wrist extension to wrist flexion. Alternately, the techniques depicted Figs. 17-76 through 17-79 include eccentric loading of the wrist flexors moving from a position of wrist flexion to wrist extension. ▶▶ Wrist extension should be done in pronation to work against gravity or in neutral forearm rotation to eliminate gravity. This exercise encourages the involvement of the ECRL, ECRB, and ECU. MCP flexion can be employed to eliminate any contribution from the ECU, thereby isolating the wrist musculature. ▶▶

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FIGURE 18-77  Resisted supination.

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Wrist flexion should be done in supination to work against gravity or in neutral forearm rotation to eliminate gravity. Wrist flexion works the FCU and FCR. ▶▶ Proprioceptive neuromuscular facilitation (PNF) patterns of the upper extremity are performed actively and then with resistance. These patterns incorporate the conjunct rotations involved with finger, hand, and wrist motions. Wall push-ups encourage full wrist extension, while full push-ups require full, or close to full, wrist extension. ▶▶ Wrist flexion ball flips.  Holding a small weighted ball, the patient leans forward over a treatment table so that the forearm is resting on the table, but the hand and wrist are over the end, palm facing upward. The patient is asked to toss the ball into the air and then to catch it while keeping the elbow on the table. ▶▶

FIGURE 18-79  Manually resisted exercises.

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▶▶

FIGURE 18-80  Resistance using elastic bands.

FIGURE 18-81  Putty exercises.

FIGURE 18-82  Hand exerciser.

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Gyroball exercises.  A number of tools can be used to add variety to the wrist, hand, and forearm exercise program. One such tool is a gyroball, which is a ball in which a rotor is encased. Manipulating the ball causes the rotor to spin, which creates torque. Depending on the model of gyroball, approximately 25–40 lb of torque can be created. The patient holds the ball in one hand with the palm facing upward and the fingers wrapped around the ball. The patient flicks the rotor using the thumb and then immediately rotates the wrist to get the rotor spinning. Faster rotations of the wrist create a faster spin of the rotor (VIDEO). Once the rotor is spinning at an adequate speed, the patient attempts to maintain the speed for about 30– 60 seconds. Once the patient has completed an exercise with the rotor turning in one direction, the exercise is repeated by rotating the rotor in the opposite direction (VIDEO). As the patient masters the technique, exercises involving the entire upper extremity can be incorporated. For example, to exercise the elbow flexors, the ball is initially held by the patient with the arm by the side and the elbow flexed to 90 degrees. Once the ball is spinning, the patient then extends and flexes the elbow repeatedly (VIDEO). To exercise the muscles of the shoulder girdle, the patient initiates the rotation of the rotor with their arm by

FIGURE 18-84  Resisted wrist extension with dumbbell.

The Forearm, Wrist, and Hand

FIGURE 18-83  Resisted wrist flexion with elastic resistance.

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the side, and then gradually moves the arm into shoulder forward flexion (VIDEO), or shoulder abduction.

A

The exercises for the other joints of the upper extremity are outlined in Chapters 16 and 17.

THE EXTREMITIES

PRACTICE PATTERN 4D: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, RANGE OF MOTION ASSOCIATED WITH CONNECTIVE TISSUE DYSFUNCTION Rheumatoid Arthritis RA is a disease that affects the entire body and the whole person (see Chapter 5). It is a lifelong disease, which in the majority of people is only modified somewhat by intervention. The acute stage is characterized by pain, swelling, warmth, and limited motion from synovitis and tissue proliferation, most commonly in the MCP, PIP, and wrist joints bilaterally. The cycle of stretching, healing, and scarring that occurs as a result of the inflammatory process seen in patients with RA causes significant damage to the soft tissues and periarticular structures. This damage includes progressive muscle weakness and imbalances in length and strength between agonists and antagonists and between intrinsic and extrinsic muscles. As a consequence, these events may lead to pain, stiffness, joint damage, instability, and ultimately deformity. In the advanced stages, there are joint instabilities, subluxations, and deformities. Many common hand and wrist deformities can be seen, such as ulnar deviation of the MCP joints, boutonnière deformity, and swan-neck deformities of the digits.

Ulnar Drift The deformity of the ulnar drift and anterior (palmar) subluxation (Fig. 18-85A) is a result of a complex interaction of forces and damage to collateral ligaments and extensor mechanisms. Clinically, an ulnar drift of the MCP articulations often precedes the wrist deformities. The ulnar drift results in an imbalance that has the resultant effect of pulling the fingers into ulnar deviation, pronation, and anterior (palmar) subluxation. The list of causes includes the following: Subcollateral synovitis and weakening of the radial collateral ligament. ▶▶ Distortion and attenuation of the sagittal fibers of the extensor hood. ▶▶ A natural displacement of the extensor tendons to the ulnar side. ▶▶ Radial deviation of the wrist. ▶▶ Secondary contracture of the ulnar side intrinsic muscles. ▶▶ Dysfunction of the radial side intrinsics. ▶▶ Displacement of the flexor tendons to the ulnar side. ▶▶ Appositional pinch (i.e., key pinch). ▶▶ Gravity. ▶▶ The natural anatomic shape of the metacarpal head. ▶▶

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B

C

FIGURE 18-85  Finger deformities.

Normally, in the flexed position, minimal lateral movement occurs at the MCP joint, but with increased laxity of the collateral ligaments, up to 45 degrees of lateral deviation occurs in this position.

Boutonnière Deformity The boutonnière, or buttonhole deformity (Fig. 18-85B), occurs when the common extensor tendon that inserts on the base of the middle phalanx is damaged. In sports, the mechanism of injury is either a severe flexing force to the PIP joint or a direct blow to the posterior (dorsal) aspect of the PIP joint, which results in damage to the common extensor tendon. Damage to the central slip insertion on the dorsum of the PIP joint requires extra effort to extend the joint, causing hyperextension at the DIP joint. The failure of the lateral bands to be connected to the central slip allows these bands to drift forward. Eventually, they pass the axis of rotation of the PIP joint, and instead of extending this joint, they act as flexors while still hyperextending the DIP joint. Such destruction also results in the loss of the influence of the interosseous muscles, ED longus, and lumbrical muscles on the PIP joints. Simultaneous with the loss of this muscle influence, the lateral bands of the extensor mechanism slide anteriorly. The realignment of the extensor mechanism, coupled with the loss of certain muscle influence, produces a deformity of extension of the MCP and DIP joints and flexion of the PIP joint. Patients presenting with this condition should be treated conservatively with 4 weeks in a splint that holds the PIP joint in full extension, while allowing the DIP joint to flex. Subsequently, they can be managed with a Capener splint35 that takes the extension load off the PIP joint and allows the joint

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to move through a protective range of flexion.9 Gentle AROM exercises can begin for flexion and extension of the PIP joint at 4–8 weeks, with the splint being reapplied between exercises. General strengthening usually begins at 10–12 weeks. For a return to competition, an additional 2 months is required.

recurrent effusion, is progressively aggravated. Eventually, the individual cannot cope with the resulting difficulties with doing activities of daily living. This is the characteristic end point of this progressive disease.

Swan-Neck (Recurvatum) Deformity

Because pain and instability of the wrist prevent much of the power from the forearm muscles from being transmitted from the wrist to the hand, some stabilization at the wrist level is necessary. The assessment of the thumb and finger problems involves careful evaluation of grasp and pinch. Based on the pathomechanics of the rheumatoid process, the following concepts form the foundation of any intervention to manage RA of the hand:

Other Deformities Produced by RA Radial Deviation of the CMC Block.  This deformity is the result of the predominant action of the radial tendons (i.e., the FCR and the extensors carpi radialis longus and brevis), which radially deviate the CMC block. This deviation increases the angle between the radial border of the second metacarpal and the lower border of the distal radius, resulting in an important loss of muscular power in the flexors. The deviation of the wrist can involve an opposite deviation of the MCP joint when the stabilizing elements of these joints (lateral ligament and volar plate) are weakened. The radial deviation of the CMC block may produce an ulnar deviation of the MCP joints because of the interdependence of various articulations in the longitudinal chains.

Effects of RA The end result of the above-mentioned deformities is a reduction in the function of the hand and upper limb. Although humans are capable of significant compromise and adaptation, the loss of function that occurs with RA progressively accumulates to a point at which simple tasks become more difficult. The decreased excursion of tendons, weakness of muscles, and reduction of the range of motion in joints multiply the overall effects. Even when the muscle power is available, it may not be applied in the most effective direction. Joint laxity, which has been precipitated by synovitis and

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1. Control the inflammation. 2. Focus on joint systems rather than isolated joints. 3. Consider the status of all tissues in the hand. 4. Consider the type of rheumatoid disease. The intervention is related to the type of rheumatoid disease: a. The type in which scarring outweighs the articular damage. Patients with stiff joints because of scarring do poorly after soft-tissue surgery. Patients in this group require aggressive and sustained therapy, often for 3–4 months.

The Forearm, Wrist, and Hand

The swan-neck deformity is characterized by a flexion deformity at the DIP and hyperextension of the PIP joint. This deformity is the least functional of all of the deformities that exist within the hand. Destruction of the oblique retinacular ligament of the extensor mechanism leads to posterior (dorsal) displacement of the lateral bands of the extensor mechanism. This rearrangement leads to an increased extensor force across the PIP joint with a resulting hyperextension of the PIP joint and chronic injury to the volar plate. The extended position of the PIP joint stretches the FDS and FDP tendons. The pull on the FDP tendon causes a passive flexion of the DIP joint. The resultant loss of function makes it difficult to flex at the PIP joint during grasping activities. The hypertrophy of rheumatoid synovitis displaces the tendon of the ECU forward. An alteration in posture at one joint leads to the reverse posture of the adjacent joint. In addition to rheumatologic diseases, other etiologies include extensor terminal tendon injuries, spastic conditions, and fractures to the middle phalanx that heal in hyperextension, and generalized ligamentous laxity. Clinical findings include a hyperextended PIP joint with a flexed DIP joint of the same digit (Fig. 18-85A). The swan-neck deformity can be managed by the application of a small figure-of-eight splint that prevents the PIP joint from fully extending, while still allowing full flexion range.9

Interventions for RA of the Hand and Wrist

b. The type in which joint laxity and tissue laxity become difficult to stabilize after soft-tissue procedures. The patients in this group require careful intervention and control of the ROM and the direction of motion by the use of splints for many months after surgery. The components of the intervention for patients with RA of the hand include the following: 1. Exercises. A combination of active exercises and isometric exercises is recommended to maintain muscle strength and improve range of motion. Range-of-motion exercises that encourage excursion of the long flexors are emphasized. The hand intrinsics are stretched by placing the MCP joints in extension and radial deviation while simultaneously flexing the PIP and DIP joints. Resistive exercises need to be introduced carefully due to the inflammatory nature of RA. Gentle squeezing exercises using a sponge in a tub of warm water are recommended. Bony and soft-tissue surgery will be less than successful in restoring function if there is a residual severe imbalance in the forces acting across the joint. 2. Joint protection/energy conservation.  Joint protection is the process of reducing internal and external stresses on the joints during functional activity and to help prevent poor use and abuse of the hand and wrist. Joint protection techniques include the following: a. Patient education to increase awareness of those activities that are stressful to the joints. In particular, tight and prolonged grasping should be avoided. b. The reduction of forces through the use of adaptive equipment and the avoidance of repetitive activities, positions of deformity, and the lifting of heavy weights. Many excellent self-help devices are available. Unless

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THE EXTREMITIES

there is a reasonable use of the hand, any remaining imbalance will cause failure as shown in the secondary cycle of rheumatoid disease. c. The use of the larger/stronger and more proximal joints and muscles when available. d. The balance of rest and activity by planning ahead and using paced rests. Stress, rest, and sleep can have a significant effect on symptoms. e. The use of energy conservation techniques and labor-saving devices. Energy conservation involves sitting when able, organizing workspace and storage for accessibility, resting during activities when able, and using time savers such as prepared foods. Many different merchants offer adaptive equipment such as zipper pulls, kitchen utensils with enlarged handles, jar openers, and pens with a large grip. f. Elimination of some activities. g. Work simplification. 3. Splinting. Static splinting can be used to immobilize painful joints and prevent further deformity through positioning. For example, trauma to the volar plate may be successfully managed by a dorsal blocking splint to prevent the joint from being fully straightened for the first 3 weeks. Initially, the splint is molded to prevent the PIP joint from extending in the last 20–30 degrees of range, while the patient is encouraged to actively flex toward the palm.9 Each week, the splint is remolded to allow a further 10 degrees of extension. 4. Pain management. The clinician should encourage the patient to investigate alternatives to pain medication, such as relaxation techniques, yoga, adopting a positive outlook, and the use of thermo- or cryotherapy. When surgery is warranted, either an arthrodesis of the wrist can be used, or an arthroplasty. Common indications for arthroplasty include severe pain, deformity and marked limitation of wrist motion, and subluxation or dislocation of the radiocarpal joint.

804

showing cystic or erosive changes in the ulnar head and along the proximal contour of the lunate. Injuries to the central, avascular portion of the disk are not amenable to spontaneous repair, whereas injuries to the vascularized periphery are. The conservative invention for a TFCC injury, depending on the severity of symptoms, typically includes an ulnocarpal support attached to a soft wrist splint for milder cases, and a long-arm cast or splint fitted with the elbow in 90 degrees of flexion, and the forearm and wrist in ulnar deviation and extension for 6 weeks, if the TFCC is unstable. While the wrist is in a cast or splint, the intervention should include patient education to avoid loading the wrist in ulnar deviation, or extension and radial deviation, proximal rangeof-motion and strengthening exercises. Active and active-assisted exercises are initiated to the wrist and forearm after cast removal, with emphasis on flexion and extension initially, followed by pronation/supination, and radial/ulnar deviation. Two weeks after cast removal, assuming the patient is asymptomatic, progressive strengthening is initiated to the hand and wrist, taking care to prevent torsional loads to the wrist.

Osteoarthritis OA is the most common joint disease (see Chapter 2). This condition can be primary or secondary, depending on the presence of a preexisting condition. While primary OA commonly involves the first CMC joint or sometimes the scaphotrapeziotrapezoid joint, it is uncommon in other parts of the joint. Secondary OA of the wrist attributable to an old trauma or infection is very common. In the case of malalignment of the scaphoid, degenerative arthritis will progress according to a very specific pattern that leads to an SLAC (scapholunate advanced collapse) wrist. Degeneration occurs between the radius and the scaphoid and then between the lunate and the capitate. The radiolunate joint is almost never involved. Finally, a scapholunate diastasis develops, and the capitate slides in between the lunate and the scaphoid.

TFCC Lesions

First CMC Joint

Injuries to the TFCC typically occur following a fall on the supinated outstretched wrist or as the result of chronic repetitive rotational loading. Aggravating activities may include tennis or golf or occupational factors.9 Patients with lesions of the TFCC complain of medial wrist pain just distal to the ulna, which is increased with end-range forearm pronation/supination and with forceful gripping. Often there is a painful click during wrist motions. Tenderness is clearly localized to a posterior (dorsal) anatomic depression, which is immediately distal to the ulnar head. There are a number of provocative maneuvers for the TFCC (see Special Tests), but it would appear that the TFCC stress test and the TFCC compression test are the more reliable, especially when used in conjunction with MRI.19 Initial radiographs are usually negative but can provide information as to whether an ulna-plus variance coexists with the triangular fibrocartilage tear (ulnocarpal impingement syndrome). This condition is diagnosed on radiographs

Pain at the base of the thumb is particularly common in postmenopausal women in the fifth the seventh decades of life.9 The pain, which is increased with activities such as opening jars, turning taps and gripping, is located either at the anterior (palmar) surface of the trapeziometacarpal joint, or more posteriorly (dorsally), between the base of the first and second metacarpals.9 The CMC joint ROM is typically restricted in a capsular pattern, the grind test (see Pain Provocation Tests) is positive, and there is usually joint crepitus.36 Careful palpation of the scaphotrapeziotrapezoidal joint and trapezium, just distal to the scaphoid, will assist in determining the source of symptoms.9 Conservative intervention includes splinting, exercises, and patient education.

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Splinting Although a variety of splinting options are available, there is no evidence to support the superiority of one over another.37

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In general, a more flexible neoprene style splint is appropriate for those with mild symptoms, and a rigid thermoplastic style splint is useful for those with more severe pain that limits most activities of daily living.9 Whatever splint is chosen, it should position the CMC joint in anterior (palmar) abduction to maximize the stability and anatomic alignment of the joint, with the IP joint free.

The diagnosis of Dupuytren disease in its early stages may be difficult and is based on a palpable nodule, characteristic skin changes, changes in the fascia, and progressive joint contracture. The skin changes are caused by a retraction of the overlying skin, resulting in dimples or pits. Dupuytren disease can be classified into three biologic stages:

Exercises9

▶▶

Patient Education The patient should be advised to ▶▶

minimize or avoid mechanical stresses including sustained pinching;

avoid sleeping on the hands as this forces the thumb into adduction; and ▶▶ use self-help devices such as jar lid openers and ergonomic scissors. ▶▶

Gout See Chapter 5.

Dupuytren Contracture (Palmar Fasciitis) Population studies have shown that Dupuytren disease nearly always affects Caucasian races, particularly those of northern European descent. The incidence increases with advancing age, and it is exceedingly rare in children. Men are 7–15 times more likely to have a clinical presentation requiring surgery than women, who tend to develop a more benign form of the disease that appears later in life. The etiology of Dupuytren disease is thought to be multifactorial. There is a higher incidence in the alcoholic population, the diabetic population, and the epileptic population. Because of the association between smoking and microvascular changes in the hand, some believe that tobacco may also play a role in this disease.38 Although not usually related to hand trauma, Dupuytren disease occasionally develops after significant hand injuries, including surgery. Dupuytren disease is an active cellular process in the fascia of the hand, which is characterized by the development of nodules in the palmar and digital fascia, which occur in specific locations along longitudinal tension lines. The pathologic changes in the normal fascia result in the formation of tendon-like cords. The characteristic contracture, which behaves similarly to the contracture and maturation of wound healing, is caused by a thickening and shortening of the fascia.38 The contractures form mainly at the MCP and PIP joint, and occasionally at the DIP joint. The most commonly involved digit is the little finger, which is involved in approximately 70% of patients.

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The disease, which is usually bilateral, tends to be more severe in one hand, although there appears to be no association with hand dominance. Up to three rays may be involved in the more severely affected hand. To date, conservative interventions have not yet proven to be clinically useful in the treatment of established contractures. Some surgeons feel that any amount of PIP joint contracture warrants surgery, whereas others feel that 15 degrees or greater is an indication. Surgery is the intervention of choice when the MCP joint contracts to 30 degrees and the deformity becomes a functional problem. Studies have shown that 50% of operative results depend on the postoperative management of effective splinting and exercise. The intervention should be directed toward promoting wound healing, which in turn minimizes scarring and maximizes scar mobility so that hand function can be restored.38 Scar management and splinting are an important part of the postoperative management. The initial splint is positioned to provide slight MCP joint flexion of 10–20 degrees with PIP joint extension to allow maximal elongation of the wound.38 Active, active-assisted, and passive exercises are usually initiated immediately.

The Forearm, Wrist, and Hand

Specific exercises that enhance neuromuscular retraining are important to improve joint stability. These exercises include improving the patient’s awareness and control of the alignment of the thumb while tracing along the line of a tennis ball with the tip of the thumb. Similarly the patient can incorporate the use of chopsticks to improve joint position sense and neuromuscular control, or enhance stability by rotating a credit card in exercise putty.

First stage.  This proliferative stage is characterized by an intense production of myofibroblasts and the formation of nodules. ▶▶ Second stage.  This involutional stage is represented by the alignment of the myofibroblasts along lines of tension. ▶▶ Third stage.  During this residual stage, the tissue becomes mostly acellular and devoid of myofibroblasts, and only thick bands of collagen remain.

Wrist Sprains The most common wrist sprain results from a downward force to the wrist exceeding its normal range of motion. This forced movement of the joint is followed immediately by intense pain that subsides and then returns. Swelling typically occurs within 1–2 hours of the injury, with the degree of joint swelling indicating the severity of the injury. With severe injuries, ecchymosis develops in 6–12 hours. Differential diagnosis includes a carpal fracture, particularly the scaphoid and lunate, traumatic instability, or a ligament tear. Conservative intervention depends on the severity of the sprain but likely includes some form of immobilization of the wrist to avoid exacerbating the injury. Custom splints, which cover the palm and extend to about midforearm, are designed to allow for proper hand and wrist contouring and to allow the fingers to move freely. Cocking the wrist up about 10 degrees places the wrist in a position of rest. Slight sprains typically remain splinted for 3–5 days. The splint is worn at all times except for removal for hygiene

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THE EXTREMITIES

and exercise. More severe sprains take longer to recover, but should still be removed from the splint in 3–5 days to avoid stiffness. Icing for 20–30 minutes, three to four times a day, concurrent with NSAIDs or aspirin can aid in reducing pain and swelling. After splint removal, a rehabilitation program of AROM (wrist curls) should be started. Until the pain and swelling subside, wrist curls can be done in water to reduce muscle effort. The clinician should consider taping the wrist to provide support and help decrease pain. The exercises are progressed to include a strengthening regime based on the hierarchy of strengthening exercises (see Chapter 12).

Perilunate Dislocation A perilunate dislocation results from disruption of the scapholunate ligament, then extension of the injury to the capitolunate articulation and the lunotriquetral ligament. Most carpal dislocations are of the perilunate variety with the lunate dislocating in an anterior (palmar) direction. This is accompanied by damage to both of the interosseous ligaments of the proximal row and possible injury to the median nerve. The usual mechanism of injury is a hyperextension of the wrist during a FOOSH. Patients frequently complain that the pain is aggravated by weight bearing on an extended wrist. Physical examination is often limited, revealing swelling and a deformity, and the injury may be confused with a distal radius fracture. If the median nerve is involved, paresthesias or numbness in the median nerve distribution may be present. The scaphoid shift test is commonly used to test for scapholunate instability (see Special Tests). The dislocation is easily reduced if the intervention occurs soon after the injury. The reduction involves placing the wrist in extension and putting pressure on the lunate, after which the wrist is moved into flexion and immobilized. Once reduced, splinting is used for pain relief and any strong resisted gripping is avoided. Proprioceptive and strengthening exercises are introduced that include isometric training, eccentric training, isokinetic training, and coactivation based on Hagert’s principles of conscious neuromuscular rehabilitation (see Intervention Strategies).6

Intercarpal Instabilities The integrity of the carpal relationship depends on the stability provided by both the interosseous ligaments and the midcarpal ligaments. This relationship ensures that the carpal bones move as a unit. Conversely, disruption of this relationship allows abnormal independent motion of one or two carpal bones. Instability patterns are divided into those that are static and those that are dynamic. Static instability is the more severe of the two and usually involves a complete tear of one of the supporting ligaments or a fracture. Dynamic instability patterns typically occur when the wrist is stressed. Carpal instability patterns that occur within the same row are classified as dissociative while those that occur across different rows are classified as nondissociative. Conservative intervention for carpal instabilities usually involves a trial period of cast immobilization. Surgery is reserved for chronic cases.

UCL Sprain of the Thumb UCL injuries, initially referred to as gamekeeper’s thumb, then breakdancer’s thumb, and more recently as skier’s thumb, involve an injury to the MCP joint of the thumb and are the most common ligament injury of the hand. The injury typically occurs when a radially directed impact forces the thumb into abduction and hyperextension. Symptoms include local swelling, pain, and tenderness to palpation on the ulnar aspect of the MCP joint, instability and weakness during pinch.9 For the purposes of planning the intervention, these injuries can be divided into two categories: ▶▶

Grade I and II sprains, in which the majority of the ligament remains intact. The stability of the joint is tested in full extension and at 30 degrees of flexion, which stress the accessory collateral ligament and the UCL, respectively. An angulation of greater than 35 to 40 degrees greater than the uninvolved side indicates instability and the need for surgical intervention. Grade I and II tears are treated with immobilization in a custom-made thumb splint for 6 weeks (depending on the degree of laxity in pain with stress testing), with additional protective splinting for 2 weeks as necessary. The thumb splint is designed to immobilize the wrist, CMC, and MCP joints of the thumb, thereby permitting the radial wrist extensors and the proximal thumb to rest by preventing any radial force being transmitted to the MCP joint. When applying these splints, it is very important to ensure that the superficial radial nerve and the ulnar digital nerve of the thumb are not compromised. The splint is worn at all times except for removal for hygiene and exercise. AROM of flexion and extension begins at 3 weeks and progresses to strengthening exercises by 8 weeks, taking care not to apply any abduction stress to the MCP joint during the first 2–6 weeks.

▶▶

Grade III tears and displaced bony avulsions are treated with surgery and subsequent immobilization. If the ligament is completely torn, there is a concern for a Stener lesion, in which the proximal end of the torn UCL

Kienböck Disease

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Kienböck disease is an aseptic necrosis or osteonecrosis of the lunate. When the disease becomes advanced, carpal collapse, joint incongruity, and OA develop. The choice of treatment for patients with symptomatic Kienböck disease depends largely on the severity of the disease. Surgical intervention can include excision arthroplasty, limited intercarpal arthrodesis, revascularization, arthrodesis between the radius and the lunate, and vascular bundle implantation.39 Conservative management of Kienböck disease involves immobilization in a short-arm cast. Upon cast removal at 6–10 weeks, AROM exercises are initiated for the wrist, forearm, and thumb. Within 1–2 weeks following cast removal, PROM exercises are initiated. A wrist and thumb static splint is fitted with the wrist in neutral, and the thumb midway between radial and anterior (palmar) abduction, and is worn between exercise sessions and at night.

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protrudes beneath the adductor aponeurosis. Postsurgical rehabilitation involves wearing a thumb spica splint for 3–5 weeks, except during the active flexion and extension exercises. Otherwise, the exercise progression is the same as for the grade I and II sprains. ▶▶ Radial collateral sprains are classified and treated in a similar manner.



TABLE 18-19

Time Frame (Weeks) Intervention Remove the short arm splint and sutures Initiate active and active-assisted wrist extension and flexion Continue interval splint wear during the day between exercises and at night

2–4  

Advance ROM exercises to resistive and gradual strengthening exercises Discontinue the splint at 4 weeks

4–6

Allow normal activities to patient’s tolerance

6

Allow full activity

Ganglia Ganglia are thin-walled cysts containing mucoid hyaluronic acid that develop spontaneously over a joint capsule or tendon sheath. They are the most common soft-tissue tumor in the hand. Common sites for ganglia are the anterior (volar) or posterior (dorsal) surfaces of the wrist and fingers. Ganglia may not cause pain. Frequently, as the ganglion begins to grow, the patient reports aching that is irritated by flexion and extension of the joint. At times, ganglia can occur in other parts of the wrist, causing compression of the ulnar or median nerve. When compression occurs, associated sensory symptoms in the digits or intrinsic muscle weakness may develop. Upon examination, a ganglion is smooth, round, or multilobulated and tender with applied pressure. For symptom relief, immobilization of the wrist through splinting is effective. This may cause the ganglion to shrink temporarily, although it is uncommon for the immobilization to be effective in resolving the ganglion. Needle aspiration can resolve the ganglion. Occasionally, surgical excision is indicated for the patient with significant pain or cosmetic irritation (Table 18-19).

Chondromalacia Chondromalacia of the ulnar head is usually seen in young patients after a fall on the dorsiflexed wrist with the impact predominantly hypothenar, or repeated episodes of stressful pronation and supination (work or leisure activity). The pain is localized to the posterior (dorsal) distal radioulnar area, and manipulation of the ulnar head can elicit crepitation or a painful snap.

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Reproduced with permission from Brotzman SB, Wilk KE, eds. Clinical Orthopaedic Rehabilitation. Philadelphia, PA: Mosby/Elsevier; 2003.

Racquet Player’s Pisiform Racquet player’s pisiform is a condition involving a minor subluxation of the pisiform, with occasional chondromalacia of the articular cartilage of the pisotriquetral joint. The probable mechanism is a torsional stress upon the capsule of the pisotriquetral joint by the powerful and rapid pronation, and supination movements at the wrist seen when wielding a racquet, particularly in badminton, racquetball, and squash players. The typical clinical presentation is one of pain, disability, and swelling on the ulnar aspect of the wrist or proximal palm. The pain is reproduced with passive movement of the pisiform upon the triquetrum with the relaxed wrist flexed and ulnarly deviated. The typical intervention for this condition is surgical excision of the pisiform.

The Forearm, Wrist, and Hand

2    

Ulnar Impaction Syndrome The ulnar impaction syndrome can be defined as excessive impaction of the ulnar head against the TFCC and ulnar carpal bones. This results in a progressive degeneration of those structures. The patient with this syndrome typically presents with ulnar wrist pain and a limitation of motion. Upon physical examination, a combined motion of ulnar deviation and compression reproduces the pain (see “Special Tests”). The differential diagnosis includes ulnar impingement syndrome and arthrosis or incongruity of the DRUJ. It is important to remember that in the absence of obvious structural abnormalities, the ulnar impaction syndrome may result from daily activities that result in excessive intermittent loading of the ulnar carpal bones. Conservative intervention includes the use of an ulnar gutter splint if there is evidence of wrist overloading.

 ehabilitation Protocol After Excision of R Wrist Ganglion

PRACTICE PATTERN 4E: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, RANGE OF MOTION ASSOCIATED WITH LOCALIZED INFLAMMATION Tendinopathy Overuse syndromes are a common cause of tendinopathy, particularly in the “weekend warrior.” As a rule, the tendons of the APL and EPB are involved. There are, however, some uncommon locations and types of tendinopathy. There has been a marked increase in reports of the so-called repetitive strain injury of the upper extremity. One of the difficulties in evaluating this disorder is the establishment of a diagnosis in the absence of objective physical findings or confirmatory diagnostic images or laboratory data. These issues become more complicated when insurers and attorneys ask clinicians to establish a causal relation between the job and the complaints.

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TABLE 18-20

Clinical Findings in Common Forms of Tenosynovitis

THE EXTREMITIES

Tenosynovitis

Findings

Differential Diagnosis

Intersection syndrome

Edema, swelling, and crepitation in the intersection area; pain over the dorsum of the wrist that is exacerbated by wrist flexion and extension, unlike the pain of de Quervain tenosynovitis, which is exacerbated by radial and ulnar deviation; pain extends less radially than it does in de Quervain tenosynovitis

Wartenberg syndrome, de Quervain tenosynovitis

De Quervain

Pain along the radial aspect of the wrist that worsens with radial and ulnar wrist deviation; pain on performing Finkelstein maneuver is pathognomonic

Arthritis of the first carpometacarpal joint, scaphoid fracture and nonunion, radiocarpal arthritis, Wartenberg syndrome, intersection syndrome

Sixth posterior (dorsal) compartment

Pain over the ulnar dorsum of the wrist that is worsened by ulnar deviation and wrist extension; other planes of motion may also be painful; tenderness over the sixth posterior (dorsal) compartment; instability of the extensor carpi ulnaris is shown by having the patient circumduct the wrist while rotating the forearm from pronation to supination

Extensor carpi ulnaris instability, triangular fibrocartilage complex tears, lunotriquetral ligament tears, ulnocarpal abutment syndrome, distal radioulnar joint arthritis, traumatic rupture of the subsheath that normally stabilizes this tendon to the distal ulna

Flexor carpi radialis tunnel syndrome

Pain, swelling, and erythema around the anterior (palmar) radial aspect of the wrist at the flexor carpi radialis tunnel; pain exacerbated by resisted wrist flexion

Retinacular ganglion, scaphotrapezial arthritis, first carpometacarpal arthritis, scaphoid fracture/nonunion, radial carpal arthritis, injury to the anterior (palmar) cutaneous branch of the median nerve, Lindberg syndrome (tendon adhesions between the flexor pollicis longus and the flexor digitorum profundus)

Trigger finger

Pain on digital motion, with or without associated triggering or locking at the interphalangeal joint of the thumb or proximal interphalangeal joint of other fingers; may be crepitus or a nodular mass near the first annular pulley that moves with finger excursion

Connective tissue disease, partial tendon laceration, retained foreign body, retinacular ganglion, infection, extensor tendon subluxation

Data from Brotzman SB, Wilk KE. Clinical Orthopaedic Rehabilitation. Philadelphia, PA: Mosby, 2003; Idler RS. Helping the patient who has wrist or hand tenosynovitis. J Musculoskel Med. 1997; Jan;14(1):21–35.

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Tenosynovitis is frequently seen in inflammatory rheumatic diseases, diabetes mellitus, or hypothyroid conditions (Table 18-20). Conservative intervention includes nonsteroidal medications, splinting, patient education on the neutral rest position for the wrist, activity modification, and the avoidance of exacerbating activities (e.g., forceful gripping and heavy lifting). A stretching and icing regimen is recommended for the wrist flexors or extensors depending on the diagnosis. Occasionally, a series of steroid injections may be warranted. Patients are typically considered for surgery when a tenosynovitis has persisted for a period of 3 months of conservative treatment.

and EPB tendons allow the thumb to flex, extend, and grip objects. Overuse, repetitive tasks which involve overexertion of the thumb, or radial and ulnar deviations of the wrist, and arthritis are the most common predisposing factors, as they cause the greatest stresses on the structures of the first posterior (dorsal) compartment. Such activities include scraping wallpaper, painting, hammering, fly fishing, knitting, and cutting with scissors.40,41 Typically, patients report a gradual and insidious onset of a dull ache over the radial aspect of the wrist made worse by such activities as turning doorknobs or keys. Patients also may note a “creak” in the wrist as the tendon moves. Examination of the wrist may reveal the following9:

De Quervain Disease

▶▶

De Quervain disease is a progressive tenosynovitis or tenovaginitis, which involves the tendon sheaths of the first posterior (dorsal) compartment of the wrist, resulting in a degeneration and thickening of the extensor retinaculum, a stenosing of the fibro-osseous canal, and an eventual entrapment and compression of the tendons.9 In most instances, the first posterior (dorsal) compartment is a single compartment, which contains the APL and the EPB tendons and their associated synovial sheaths. The APL

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A localized swelling and tenderness in the region of the radial styloid process and wrist pain radiating proximally into the forearm and distally into the thumb. ▶▶ Severe pain with wrist ulnar deviation and thumb flexion and adduction. A reproduction of the pain can also be reported with thumb extension and abduction. ▶▶ Crepitus of the tendons moving through the extensor sheath. ▶▶ Palpable thickening of the extensor sheath and of the tendons distal to the extensor tunnel.

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A loss of abduction of the CMC joint of the thumb. ▶▶ A positive Finkelstein test (Fig. 18-50) (see “Special Tests”). ▶▶

Although the diagnosis is mostly clinical, posteroanterior and lateral radiographs of the wrist can be obtained to rule out any bony pathology, such as a scaphoid fracture, radioscaphoid, or triscaphoid (ie, scaphoid, trapezoid, and trapezium) arthritis, and Kienböck disease.

CLINICAL PEARL

splint immobilization of the wrist and thumb with the wrist in 15–20 degrees of extension; ▶▶ electrotherapeutic modalities including iontophoresis/ phonophoresis; ▶▶ manual techniques including deep TFM followed by exercises for stretching and strengthening; and ▶▶ patient education to emphasize the avoidance of any repetitive wrist flexion and extension in combination with a power grip. ▶▶

EPL Tendinopathy The intervention can be conservative or surgical. Conservative intervention usually includes rest, modification of activities, splinting, and antiinflammatory medication. In a study by Lane et al.42 wrist splints and NSAIDs were found to be effective only in patients with minimal symptoms and no restrictions in daily activities. If splinting is appropriate, a thumb spica splint is fabricated with the wrist in 15 degrees of extension, the thumb midway between anterior (palmar) and radial abduction, and the thumb MCP joint in 10 degrees of flexion. As the splint is supposed be worn all day, when fitting the splint it is important that the thumb is able to oppose the index and long finger to aid with hand function. Following the removal of the splint after approximately 3–6 weeks, ROM exercises are prescribed, with a gradual progression to strengthening. Two case reports have been published that describe manual physical therapy treatment for de Quervain disease. In the first report, Backstrom43 reported the complete resolution of symptoms in a patient with a 2-month history of de Quervain tenosynovitis by incorporating Mulligan mobilization with movement (MWM) techniques (radial gliding of the proximal carpal row and ulnar gliding of the trapezium), capitate manipulation, CMC joint mobilizations, and TFM over the first posterior (dorsal) tunnel, into an overall treatment plan. The second case report by Walker10 used an impairment-based treatment approach for eight visits based on the examination findings of isolated radiocarpal, intercarpal, and CMC joint dysfunction. The treatments consisted of manual techniques and self-mobilizations applied to the radiocarpal, intercarpal, and CMC joints. At treatment completion, the patient achieved a pain-free state and nearly full function. These results were maintained at a long-term follow-up performed 10 months after treatment.10 The more invasive intervention begins with cortisone injections. If two to three injections do not give relief, surgical tendon sheath release is an option.

Intersection Syndrome Intersection syndrome is a tenosynovitis of the ECRL and ECRB (radial wrist extensors), where they cross under the APL and EPB. Although similar to de Quervain, differentiation is made with the pain distribution. With the intersection syndrome, the pain is located in the distal forearm, 4–8 cm proximal to Lister’s tubercle, and is exacerbated by wrist flexion and extension, and by resisted wrist extension. The

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This condition is rare except in RA, but it occurs when the EPL muscle extends into a tight third compartment. Overuse (drummer boy palsy), direct trauma, forced wrist extension, and distal radius fractures may cause EPL tendinopathy, which presents with the clinical signs and symptoms of decreased thumb flexion, pain, swelling, and crepitus at Lister’s tubercle.

EIP Syndrome An increase in muscle size of the EI, caused by swelling or hypertrophy from repetitive exercise, may cause stenosis of the fourth posterior (dorsal) compartment and resultant tenosynovitis. A simple test of resistance applied to active index finger extension, while holding the wrist in a flexed position is a reliable provocative test.

The Forearm, Wrist, and Hand

Isolation of the EPB tendon in a separate compartment has been reported to contribute to the pathogenesis of de Quervain disease.21

condition is common in rowers, weightlifters, and canoeists due to repetitive wrist flexion and extension. Intervention, in addition to NSAIDs, involves

ECU Tendinopathy ECU tendinopathy, a tenosynovitis of the sixth posterior (dorsal) compartment, usually presents as chronic dorsoulnar wrist pain, which is aggravated with forearm supination and ulnar deviation, which causes the tendon to sublux palmarly.

FCU Tendinopathy The FCU is the most common wrist flexor tendon to become inflamed and is often associated with repetitive trauma and racquet sports. The clinical signs and symptoms include pain and swelling localized just proximal to the pisiform, which is aggravated by wrist flexion and ulnar deviation.

FCR Tendinopathy FCR tendinopathy usually develops due to stenosis and tenosynovitis in the FCR fibro-osseous tunnel within the transverse metacarpal ligament. FCR tendinopathy usually produces localized pain and swelling and painful deviation of the wrist. FCR tendinopathy frequently coexists with other conditions including fracture or arthritis around the CMC joint of the thumb.

Digital Flexor Tendinopathy and Trigger Digits This condition is typically characterized by painful snapping or triggering of the fingers and thumb due to a disproportion between the flexor tendon and its tendon sheath. The condition invariably occurs at the metacarpal head level and

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THE EXTREMITIES

at the A1 pulley (MCP joint pulley), with the result that the tendon is pulled through too narrow a canal.9 The condition is more common in the fibrous flexor sheath of the thumb, ring, or middle finger.44 The etiology of this condition can be acquired or congenital, although it is more common in patients with diabetes, young children, rheumatic changes of the hand, and menopausal women.44,45 The base of the affected finger is often tender and is usually accompanied by the triggering phenomenon—pain on digital motion, with or without associated triggering or locking. As the condition progresses, it becomes very painful and may result in limited or absent digital motion, especially in the PIP joint. During excursion of the flexor tendon, the clinician may palpate crepitus or a moving nodular mass in the vicinity of, or slightly proximal to, the A1 pulley. The presence of swelling is most consistent with tenosynovitis that occurs secondary to connective tissue disease. Conservative intervention involves the fitting of a handbased MCP flexion block splint in 0 degrees.46 There is no consensus on the optimal orthotic regimen. The purpose of this immobilization is to attempt to alter the mechanical forces on the proximal pulley system while encouraging maximal differential tendon gliding. Patient education plays an important role; the patient should be advised to eliminate any provocative movements such as repetitive grasping or the use of tools that apply pressure over the area. Medical intervention usually involves one or a series of 2–3 corticosteroid injections,47 with open surgical release of the trigger finger reserved for those cases that do not respond to conservative measures.47

Tendon Ruptures One of the main purposes of the hand is to grasp; therefore, the loss of flexor tendons can result in a catastrophic functional loss. The purpose of a flexor tendon repair is to restore maximum active flexor tendon gliding to ensure effective finger joint motion. Laceration or traumatic rupture of the extensor tendons is more common than in flexor tendons due to their superficial location and the fact they are substantially thinner than flexor tendons.48

Flexor Tendons Most flexor tendon ruptures occur silently after prolonged inflammatory tenosynovitis, although the causes can also be traumatic. When all nine flexor tendons to the digits have ruptured, little can be done. Single tendon ruptures are more common, and the FPL tendon is the most vulnerable to attrition rupture where it crosses the scaphotrapezial joint and where local synovitis can create a sharp spike of bone that abrades against this spur and ruptures during use. The FDP tendon to the index finger is also at risk from this bony spur. Flexor tendon injuries of the fingers, palm, wrist, and forearm are classified into five zones according to the level of injury. The zone within which the tendon is repaired dictates to some extent the intervention. ▶▶

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Zone 1.  This zone extends from the insertion of the FDP in the middle phalanx to that of the FDS in the base of

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the distal phalanx. Injuries at this level involve isolated lacerations of the FDS. ▶▶ Zone 2.  This is the region in which both flexor tendons travel within the fibro-osseous tunnel from the A1 pulley to the FDP insertion. Usually, both flexor tendons are injured at this level. ▶▶ Zone 3.  The area in the palm between the distal border of the carpal tunnel and the proximal border of the A1 pulley comprises zone 3. Common digital nerves and vessels, lumbrical muscles, and one or both flexor tendons may be injured in this region. ▶▶ Zone 4.  This zone consists of that segment of the flexor tendons covered by the transverse carpal ligament. Injuries at this level involve median or ulnar nerves and tendons. ▶▶ Zone 5.  The forearm from the musculotendinous junction of the extrinsic flexors to the proximal border of the transverse carpal ligament comprises zone 5. Interference with tendon gliding is less of a problem in this region. Tendon injuries of the thumb are classified using the following three zones: Zone 1.  This is the region from the distal insertion of the FPL on the distal phalanx of the thumb to the neck of the proximal phalanx. ▶▶ Zone 2.  This is the region from the proximal phalanx across the MCP joint to the neck of the first metacarpal. ▶▶ Zone 3.  This is the region from the first metacarpal to the proximal margin of the carpal ligament. ▶▶

There are a number of different procedures and rehabilitation protocols for flexor tendon repairs. In brief, the retracted ends of the tendon are retrieved either by hand and wrist positioning or with a surgical instrument. It is not within the scope of this chapter to discuss suturing techniques, or postsurgical guidelines.

CLINICAL PEARL Surgical repairs and treatment protocols can vary greatly, necessitating a high level of communication between the surgeon and the clinician.

Extensor Tendons Depending on the location and severity of injury to the extensor mechanism, surgery may or may not be indicated. The posterior surface of the fingers and wrist are divided into the following seven zones: Zone 1.  Zone 2.  ▶▶ Zone 3.  ▶▶ Zone 4.  ▶▶ Zone 5.  ▶▶ Zone 6.  ▶▶ Zone 7.  ▶▶ ▶▶

DIP joint region Middle phalanx PIP joint region Proximal phalanx Apex of the MCP joint region Dorsum of the hand Wrist region/dorsal retinaculum

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The thumb tendons are divided into the following five zones: Zone 1.  ▶▶ Zone 2.  ▶▶ Zone 3.  ▶▶ Zone 4.  ▶▶ Zone 5.  ▶▶

IP joint region Proximal phalanx MCP joint region Metacarpal CMC joint region

Rupture of the Terminal Phalangeal Flexor (Jersey Finger) A jersey finger rupture involves a rupture of the FDP tendon from its insertion in the distal phalanx. As there is no characteristic deformity associated with this type of rupture, this condition is often misdiagnosed as a sprained or “jammed” finger. The injury commonly occurs in football when the flexed finger is caught in a jersey while the athlete is attempting to make a tackle, hence the term jersey finger. However, any forceful passive extension that is applied while the FDP muscle is contracting can cause this type of rupture. Although

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In Type I, the tendon retracts into the palm with or without a bony fragment. ▶▶ Type II is the most common. The tendon retracts to the PIP joint, and the long vinculum remains intact. As in type I, type II injuries may have a small bony avulsion. ▶▶ Type III injuries involve a large bony fragment. ▶▶

To test the integrity of the tendon, the clinician isolates the FDP by holding the MCP and PIP joints of the affected finger in full extension and then asks the patient to attempt to flex the DIP. If the patient is able to flex the DIP, it is intact. If not, it is ruptured. The intervention depends on the severity of the injury. If hand function is not seriously affected the condition is just monitored. However, if hand function is impacted, one option is surgical reattachment of the tendon, which requires a 12-week course of rehabilitation.

INTEGRATION OF PRACTICE PATTERNS 4F AND 5F This includes conditions involving impaired joint mobility, motor function, muscle performance, and range of motion, or reflex integrity secondary to referred pain, spinal disorders, peripheral nerve entrapment, myofascial pain syndrome (MPS), and CRPS.

The Forearm, Wrist, and Hand

The mallet finger deformity, one of the most common extensor tendon injuries sustained by the athletic population, is a traumatic disruption of the terminal tendon. This condition is especially common in the baseball catcher and the football receiver and results in a loss of active extension of the DIP joint. The initial injury usually results from the delivery of a longitudinal force to the tip of the finger, which produces a sudden acute flexion force and a subsequent rupture of the extensor tendon just proximal to its insertion into the third phalanx or a fracture at the base of the distal phalanx. The physical examination reveals a flexion deformity of the DIP joint, which can be extended passively but not actively. This lack of active extension at the DIP joint is due to the zero tension being provided by the EDC, in addition to the resulting increased tone in the FDP. The primary goal of treatment is to maximize function and range of motion of the involved DIP joint. This type of injury responds well to a period of conservative splinting and, in the absence of a fracture, the DIP joint is held in constant slight hyperextension for up to 8 weeks. Mallet deformities with an associated large fracture fragment are typically treated with 6 weeks of immobilization in neutral extension following open reduction and internal fixation (ORIF). During the period of immobilization it is essential that the patient continues to exercise the uninvolved PIP joint and to maintain an extension force to the DIP at all times, even if the splint is removed for skincare.9 Once the tendon has healed sufficiently to perform active extension of the DIP, AROM exercises to 20–35 degrees are initiated to the DIP joint. The clinician should continue to monitor for an extensor lag, and it is recommended that the patient continues to wear the splint between exercise sessions, at night, and when competing (as appropriate). Gentle progressive resistive exercises (PREs) using putty or a hand exerciser are initiated at week 8. Usually, the splint is discontinued at 9 weeks if the DIP extension remains at 0–5 degrees and there is no extensor lag. Unrestricted use usually occurs after 12 weeks.

this condition can occur in any finger, the most commonly injured is the ring finger. The following three types are recognized:

Referred Pain A number of structures can refer pain to the wrist and hand, and these include visceral structures, neurologic structures, and the more proximal joints (Chapter 5). The most common joints, which refer pain to the wrist and hand, include the cervical, thoracic, shoulder, and elbow joints.

Tumors See Chapter 5.

Peripheral Nerve Entrapment Peripheral nerve entrapments are common in this region and are typically associated with a history of pain or vague sensory disturbances. Due to the vagueness of the signs and symptoms, nerve injuries are frequently overlooked as a source of acute, or more commonly chronic, symptomatology. An early indicator of peripheral compression neuropathy may be the loss of vibration sensibility. Nerve conduction studies may be performed, focusing on the sites of interest. Diabetes, with its associated neuropathies or cheiroarthropathy, may be an underlying cause of chronic wrist pain.

Radial Nerve The posterior interosseous nerve can be compressed as it enters the posterior (dorsal) wrist capsule by repetitive wrist extension maneuvers, inciting symptomatic inflammation.

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The major disability associated with radial nerve injury is weak wrist and finger extension, with the wrist and fingers adopting a position termed “wrist drop.” The hand grip is weakened as a result of poor stabilization of the wrist and finger joints, and the patient typically demonstrates an inability to extend the thumb, proximal phalanges, wrist, and elbow, depending on the level. Supination of the forearm and adduction of the thumb are also affected. There is also decreased or impaired sensation on the posterior (dorsal) surface of the first interosseous space.

THE EXTREMITIES

Wartenberg Syndrome Wartenberg syndrome is a compression of the superficial sensory radial nerve. Inflammation of the tendons of the first posterior (dorsal) compartment can result in superficial radial neuritis. This results in pain, paresthesias, and numbness of the radial aspects of the hand and wrist. In addition, the tendons of the brachioradialis and ECRL muscles can press on the nerve in a scissor-like fashion when the forearm is pronated, causing a proximal tethering on the distal segment of the nerve at the wrist. Wartenberg sign is described wherein the patient is asked to extend the fingers, and abduction or clawing of the little finger occurs.

Median Nerve Compression at the Wrist Median nerve compression at the wrist, referred to as CTS, is a cause of a cluster of symptoms including chronic wrist pain and functional impairment of the hand. CTS, which results from an ischemic compression of the median nerve at the wrist as it passes through the carpal tunnel, is the most common compression neuropathy. Carpal tunnel pressure appears to be an important factor in the pathophysiology of CTS, as increased pressure on the median nerve can produce short-term sensory and motor nerve conduction deficits and elicit symptoms of median nerve neuropathy. Compression of the nerve in the carpal tunnel is compounded by an increase in synovial fluid pressure and tendon tension, which decreases the available volume. For example, extreme wrist and finger postures can increase the tunnel pressure—the angle of the MCP joints has been found to have a significant effect on carpal tunnel pressure during active wrist flexion and extension and radioulnar maneuvers. Motions performed in 0 degrees MCP flexion exhibit the highest pressures, followed by an MCP angle of 90 degrees. This information should be considered in the design of splints for CTS patients. Other potential causes of increased pressure include fingertip loading; ▶▶ forceful and repetitive contraction of the finger flexors; and ▶▶ acute wrist trauma. ▶▶

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Although it occurs in all age groups, CTS more commonly occurs between the fourth and sixth decades. Personal risk factors include being female, increased basal metabolic rate, while workplace risk factors include high job strain— approximately half of the cases of CTS are related to repetitive and cumulative trauma in the workplace.49,50

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Some authors have found that individuals with CTS usually experience pain symptoms in the neck and the shoulder regions.51,52 Pierre-Jerome and Bekkelund53 found that individuals with CTS, compared to a control group, exhibited higher incidence of narrowing of the cervical foramen.54 A more recent study showed that compared to healthy control participants, individuals with moderate, unilateral CTS exhibited greater forward head posture and decreased cervical range of motion.55 Cervical radiculopathy may be identified by the occurrence of proximal radiation of pain above the shoulder, paresthesias with coughing or sneezing, or a pattern of motor or sensory disturbances outside of the territory of the median nerve.56 The diagnosis of CTS is typically made after a review of the patient’s history and physical examination. The initial characteristic features of CTS include intermittent pain and paresthesias in the median nerve distribution of the hand (although the symptoms may radiate proximally into the forearm and arm), which progressively become more persistent as the condition progresses. If the condition is allowed to progress, muscle weakness and paralysis can occur. The symptoms of CTS are typically worse at night due to the position of wrist flexion typically adopted during sleep and can be associated with morning stiffness. The differential diagnosis for this condition includes cervical dysfunction, thoracic outlet syndrome, pronator syndrome, coronary artery ischemia, tendinopathy, fibrositis, and wrist joint arthritis.55,57 Ulnar neuropathy must also be considered since no more than half of patients with CTS can reliably report the location of their paresthesias.58 Median nerve neuropathies can be due to diabetes, human immunodeficiency virus, nutritional deficiencies, and entrapment/ compression of the nerve.59 Median nerve compression proximal to the carpal tunnel may be divided into two major categories: pronator syndrome and anterior interosseous nerve syndrome (see Chapter 17).59 The physical assessment focuses on an examination of the motor and sensory functions of the hand and upper extremity as compared to the uninvolved extremity. A number of medical tests can be used to help diagnose CTS. These include the median nerve conduction study (NCS) and EMG study. A carpal tunnel view radiograph may be the only view that shows abnormalities within the carpal tunnel. The conservative intervention for mild cases typically includes the use of splints, activity modification, diuretics, and NSAIDs. The rationale for splints is based on observations that CTS symptoms improve with rest and worsen with activity. However, prescription parameters for the type of splint are not standardized, with some advocating neutral positioning,9 and some recommending 0–15 degrees of wrist extension. The length of time for wearing the splint is also undetermined, with some recommending day and night use, while others instruct patients to wear the brace at night and during activities stressful to the wrist. Still others recommend only night use.9 Splints during the day are helpful only if they do not interfere with normal activity. The positioning of the splint may be significant. Ergonomic modifications can help reduce the incidence of CTS and alleviate symptoms in the already symptomatic

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Ulnar Nerve Entrapment of the ulnar nerve can occur at the elbow in the cubital tunnel (Chapter 17). Entrapment of the ulnar nerve at the wrist can occur at Guyon canal. The clinical features of an ulnar nerve entrapment at the wrist are described in Chapter 3. If ulnar neuropathy at the Guyon canal is suspected, it is often helpful to evaluate the pisotriquetral joint and the hook of the hamate. Abnormalities may be present at either site, resulting in secondary ulnar neuropathy. In addition, the clinician must ask the patient whether they have any medical history involving diabetes and peripheral neuropathies. The intervention for ulnar nerve compression can be surgical or conservative depending on the severity. Indications for surgical intervention include preventing deformity and increasing functional use of the hand. Conservative intervention for mild compression involves the application of a protective splint and patient education to avoid positions and postures that could compromise the nerve.

Hand-Arm Vibration Syndrome Vibration is a physical stressor to which many people are exposed at work, in the home, or in their social activities. Humans respond characteristically to certain critical vibration frequencies at which there is maximum energy transfer from a source to a receiver. Hand-arm vibration syndrome (HAVS) is frequently underdiagnosed and misdiagnosed as CTS since the two entities typically coexist. HAVS is associated with occupations involving exposure to sources of vibration including air-compressed drilling, grinding, and electric drills and saws. The pathophysiology of HAVS is poorly understood, but chronic exposure to vibration may produce circulatory, neurologic–sensory–motor, and musculoskeletal disturbances. The diagnosis of HAVS is based on a history of HAV exposure and sensorineural or vascular signs and symptoms, which include the following61: Blanching white fingers (Raynaud phenomenon). This is the most common symptom, and it occurs on exposure to cold. Its extent and frequency of occurrence determines the severity of the vascular grading. ▶▶ Episodic tingling and numbness. The numbness or tingling can be graded. ▶▶ Mild to severe sensory deficits. ▶▶

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Swelling of the digits and forearm tissue. ▶▶ Trophic skin changes. ▶▶

The intervention for HAVS includes maintaining central body temperature, avoiding exposure to cold and vibrating tools, job modification, and splinting at night.61

Myofascial Pain Syndrome The most frequent cause of wrist, hand, and finger pain is a myofascial referral from the forearm flexors and especially from the forearm extensors. Trigger points in these muscles increase tendon tension and, therefore, relative compression of the carpal joints, which causes cracking and crepitus at the wrist due to an abnormal joint glide. The patient often reports a sense of stiffness in the wrist and hand, and pain exacerbated with wrist and finger flexion, which stretches these muscles, and on full wrist extension, which shortens these muscles.

Complex Regional Pain Syndrome The term CRPS refers to a classification of disorders, which can occur even after minor injury to a limb and which is a major cause of disability. CRPS, originally termed causalgia, has since been referred to by a number of names including posttraumatic osteoporosis, Sudeck atrophy, transient osteoporosis, algoneurodystrophy, shoulder–hand syndrome, gardenalic rheumatism, neurotrophic rheumatism, reflex neurovascular dystrophy, and reflex sympathetic dystrophy (RSD). Two types of CRPS are recognized by the International Association for the Study of Pain:

The Forearm, Wrist, and Hand

patient. Patient education is also important to avoid sustained pinching or gripping, repetitive wrist motions, and sustained positions of full wrist flexion. Isolated tendon excursion exercises for the finger flexor tendons and nerve gliding of the median nerve exercises are performed. These include isolated tendon gliding of the FDS and FDP of each digit. The exercises are thought to have a positive effect by facilitating venous return or edema dispersion in the median nerve.60 Evaluation for surgical management is necessary for patients with atrophy of the thenar muscles, decreased sensation, and persistent symptoms that are intolerable despite conservative therapy.

CRPS 1.  This type refers to the pain syndrome, previously termed RSD, which involves a pain syndrome triggered by a noxious event that is not limited to a single peripheral nerve. ▶▶ CRPS 2.  This type refers to the pain syndrome, previously termed causalgia, which involves a pain syndrome that involves direct partial or complete injury to a nerve or one of its major branches. ▶▶

The signs and symptoms for both types include pain, edema, stiffness, skin temperature changes, and sweating.62 More recently, it has been suggested that a third type may exist. This type is characterized by irreversible changes in the skin and bones, marked muscle atrophy, unyielding pain, and severely limited mobility of the affected area.

Type I CRPS The pain of type I CRPS is classified as sympathetically maintained pain or sympathetically independent pain, where sympathetically maintained pain is characterized by an abnormal reaction of the sympathetic nervous system.62 The edema, which can be pitting or nonpitting, is often present throughout all stages of CRPS and may be the result of vasomotor instability coupled with a lack of motion. The stiffness is one of the components of CRPS 1 that increases with time and is due to increased fibrosis in the ligamentous structures and adhesion formation around the tendons.

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A number of psychological components have been proposed, including the following:

THE EXTREMITIES

1. A significant period of stress, anxiety, or depression. 2. Childhood experiences. a. Sexual abuse b. Physical abuse c. Emotional abuse d. Abandonment e. Family history of drug or alcohol abuse 3. Adult experiences. a. Care provider for aging or ill parent(s) or other relative b. Problem children, parents, or siblings c. Unhappy marriage d. Alcoholism e. Grief f. Abuse of any type 4. A low self-esteem. 5. A negative outlook on life. However, there has been no evidence to support such notions. Instead, it is thought that the emotional and behavioral changes noted are a result, rather than a cause, of the prolonged pain and disability.63 The diagnosis of CRPS is made from the physical examination and the patient’s medical history, which may include past events of trauma, persistent pain, hyperalgesia, allodynia (perception of a nonpainful stimulus as painful), edema, and diminished function of the area. The type of pain and its duration are perhaps the most important diagnostic signs. The pain is typically burning in nature and is of a much longer duration than would be expected from the injury.63 A number of other conditions need to be ruled out before establishing a diagnosis of CRPS 1, and these include, but are not limited to, the following: Rheumatoid and septic arthritis Gout ▶▶ Disk herniation ▶▶ Peripheral neuropathy ▶▶ Peripheral nerve entrapment ▶▶ Peripheral vascular disease ▶▶ ▶▶

Classically, CRPS 1 has been subdivided into three clinical phases: ▶▶

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An acute inflammatory phase that can last from 10 days to 2–3 months. This stage is reversible if the patient is treated. The affected limb becomes flushed, warm, and dry because regional blood vessels are relaxed, and stimulation of the sweat glands is reduced.62 The pain is diffuse, severe, and constant with a burning, throbbing, or aching quality. Edema and increased hair and nail growth can also occur. By the end of this stage, the limb turns cold, sweaty, and cyanotic from

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vasoconstriction caused by paradoxical sympathetic stimulation.62 A phase of vasomotor instability. This is the dystrophic stage, which lasts another 3–6 months. Constricted blood vessels can cool limb temperature by nearly 10 degrees.62 The area will be pale, mottled, edematous, and sweaty. Pain remains continuous, burning, or throbbing but is more severe.62 Nails may crack or become brittle and heavily grooved. Limb movement is limited by muscle wasting and joint stiffness. Osteoporosis and contractures can develop.62 ▶▶ A cold end phase. The atrophic stage is characterized by irreversible damage to muscles and joints. Over the next 2–3 months the bones atrophy and the joints become weak, stiff, or even ankylosed.62 The pain lessens and may become spasmodic or breakthrough but is no longer mediated by the sympathetic nervous system.62 The skin is cool and looks glossy and pale or cyanotic. ▶▶

The most effective intervention for CRPS 1 is disputed. However, most agree that the intervention requires a team approach, in which the physical therapist plays a pivotal role and that the earlier the intervention is instituted, the better the prognosis. Immobilization and overprotecting the affected limb may produce or exacerbate demineralization, vasomotor changes, edema, and trophic changes. Physical therapy is the first line of intervention, whether it be the sole intervention or performed immediately following a nerve block.63,64 The most important rule is to minimize pain while employing physical therapy. When excessive pain is created, sympathetically mediated pain may worsen.63 It is vital to not reinjure the region or aggravate the problem with aggressive physical rehabilitation. The patient’s involved limb must be elevated as often as possible to counteract the vascular stasis and actively mobilized several times per day.63 Recovery from muscle dysfunction, swelling, and joint stiffness requires appropriate physical activity and exercise, and pressure and motion are necessary to maintain joint movement and prevent stiffening.63 The progression should occur slowly and gently with strengthening, active-assisted range-of-motion, and AROM exercises. Weight-bearing exercises and active stress loading exercises should also be incorporated. Active stress loading exercises include scrubbing and carrying. Scrubbing is a form of closed kinetic chain exercise for the upper or lower extremity in which the patient in a variety of positions performs a scrubbing action on a firm surface. As its name suggests, carrying exercises for the upper extremity involve having the patient carry small objects in the hand on the affected side and gradually increasing the weight of the object. For the lower extremity, stress loading can be achieved through weight bearing. Sensory threshold techniques can be used. These include fluidotherapy, vibration desensitization, transcutaneous electrical nerve stimulation, contrast baths, and desensitization using light and heavy pressure of various textures over the sensitive area. Topical capsaicin is helpful, as are NSAIDs.

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INTEGRATION OF PRACTICE PATTERNS 4G AND 4I This includes conditions that result in impaired joint mobility, motor function, muscle performance, and range of motion that are associated with fractures and bony or soft tissue surgical procedures.

Distal Radius Fractures

Colles Fracture Colles fracture is a complete fracture of the distal radius with a posterior (dorsal) displacement of the distal fragment. The typical mechanism of injury is a FOOSH. The fracture displacement and angulation are evident on the lateral film—the Colles fracture has the characteristic dorsiflexion or “silver fork” deformity. Radiographs of the AP view show the usual comminuted fracture. Management of this fracture requires a precise reduction of the fracture in order to maintain the normal length of the radius. Although the method of reduction, as well as the position of immobilization, is quite variable, in most cases closed reduction and a cast are chosen. Stable fractures in good alignment may be managed in a short-arm cast. However, the more complicated cases may require open reduction and external fixations. A common sequela of this fracture is a loss of full rotation of the forearm, so once the cast is removed, usually at around 6 weeks post-fracture, exercises should be prescribed to regain these motions.

Smith Fracture A Smith fracture sometimes called a reverse Colles fracture, is defined as a complete fracture of the distal radius with an anterior (palmar) displacement of the distal fragment. The usual mechanism for this type of fracture is a fall on the back of a flexed hand.

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Barton Fracture A Barton fracture involves a posterior (dorsal) or anterior (volar) articular fracture of the distal radius resulting in a subluxation of the wrist. This type of fracture usually results from some form of direct and aggressive injury to the wrist or from a sudden pronation of the distal forearm on a fixed wrist. A technique to reduce these dislocations under anesthesia has been described in the literature.65 The technique involves applying traction to the wrist and then placing the patient’s wrist in full supination, mid-extension, and ulnar deviation, which closes the diastasis by reducing the scaphoid to its correct anatomic plane. An above-elbow cast is then applied for 4 weeks, followed by a forearm cast for a further 3 weeks with the wrist positioned in ulnar deviation. More complicated fractures may require an ORIF with 16 weeks being the average healing time.

Buckle Fracture A buckle fracture is an incomplete, undisplaced fracture of the distal radius, which is commonly seen in children. Immobilization for 3–4 weeks in a short-arm cast or anterior (palmar) splint is adequate. The possibility of abuse should be considered in the child with a fracture. Consultation with an orthopaedist is advisable for fractures in the pediatric population. The fracture is treated with a cast, external fixation, or ORIF. The fracture site is immobilized for 6 weeks if cast, 8 weeks with an external fixator, or 2 weeks if an ORIF with plate and screws is performed. If the fracture is nondisplaced, 2–6 weeks of rehabilitation is recommended, whereas displaced fractures typically require 8–12 weeks. Conservative intervention usually begins while the fracture is immobilized and involves AROM of the shoulder in all planes, AROM of elbow flexion and extension, and finger flexion and extension. The finger exercises must include isolated MCP flexion, composite flexion (full fist), and intrinsic minus fisting (MCP extension with IP flexion). If a fixator or pins are present, pin site care should be performed. Following the period of immobilization, extension and supination are commonly limited and need to be mobilized. AROM exercises of wrist flexion and extension and ulnar and radial deviation are initiated at this time. Wrist extension exercises are performed with the fingers flexed (especially at the MCP joints). The initiation of PROM occurs according to physician preference, either immediately or after 1–2 weeks. Strengthening exercises are introduced as tolerated, using light weights and tubing. Putty can be used to increase grip strength if necessary. Plyometrics and neuromuscular reeducation exercises are next, followed by return to function or sports activities as appropriate.

The Forearm, Wrist, and Hand

Fracture of the distal radius is the most common wrist injury for any age group, but particularly in the elderly. While the older patient usually sustains an extra-articular metaphyseal fracture, the younger patient tends to sustain the more complicated intra-articular fracture. Physical examination reveals swelling of the wrist, possible gross deformity, limited range of motion, and point tenderness over the distal radius. Successful management of a distal radius fracture must take into account the integrity and function of the soft tissues while restoring anatomic alignment of the bones. The clinician should avoid distracting or placing the wrist in a flexed position, so that the mechanical advantage of the extrinsic tendons is maintained, pressure in the carpal canal is not increased, any carpal ligament injury is not exacerbated, and stiffness is not encouraged. The rehabilitation after fracture of the distal radius is nearly uniform among the various fracture types outlined below. It is important that during the period of immobilization the patient exercises the uninvolved digits and is able to move the thumb and fingers, and elbow freely within the cast. The more specific guidelines are listed after each fracture description.

The typical management for a Smith fracture is with closed reduction and long-arm casting in supination for 3 weeks, followed by 2–3 weeks in a short-arm cast.

Fractured Scaphoid The scaphoid is the most commonly fractured carpal bone due to its location and is the only bone fractured in approximately

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THE EXTREMITIES

70% of all carpal fracture cases.9 Most commonly, the injury results from a FOOSH with the wrist pronated. Although a fracture can occur in any part of the scaphoid, the common areas are at the waist and at the proximal pole. Chronic pain, loss of motion, and decreased strength from prolonged immobilization or early arthritis are common following a scaphoid fracture. Patients typically complain of posterior (dorsal) radialsided wrist pain and have tenderness over the anatomic snuffbox. On physical examination, little swelling may be noted, although a loss of the concavity of the anatomic snuffbox is frequently seen.66 It may be good practice to treat all cases of wrist sprain that are accompanied by pain and swelling in the anatomic snuffbox as a scaphoid fracture until proven otherwise. Many investigators feel a reliable test for scaphoid injury is axial compression of the thumb along its longitudinal axis. This test translates force directly across the scaphoid and should elicit pain if there is a fracture. Even with appropriate radiographs, fractures of the scaphoid can be difficult to visualize and are often reported as normal.9 For the patient with pain over the anatomic snuffbox but normal initial radiographs, application of a thumb spica cast for 3 weeks followed by repeat radiographs after 10–14 days is typically indicated. If the radiographs remain normal, but the pain persists, a bone scan or MRI is usually the next step. If the bone scan or MRI is positive, management is continued as for an acute fracture.

CLINICAL PEARL In cases in which there is a high clinical suspicion of a scaphoid fracture, a scaphoid view of the wrist is usually obtained. This is a clenched fist view with the wrist held in ulnar deviation. This view reduces the foreshortening of the scaphoid that occurs on a normal PA view and clearly displays the entire length of the scaphoid.66 Accurate early diagnosis of scaphoid fracture is critical as the morbidity associated with a missed, or delayed diagnosis is significant and can result in long-term pain, loss of mobility, and decreased function.9 This degree of morbidity is related to the scant blood supply to the scaphoid, which results in a high incidence of delayed healing or nonunion, and the fact that scaphoid fractures are inherently unstable. Conservative management of a scaphoid fracture remains controversial. For example, there is no agreement on the optimum position for immobilization or with the type of cast. Current management is immobilization in a long-arm, below elbow, or a scaphoid cast including the thumb CMC and metacarpal joints, with the wrist position and length of immobilization dependent on the location of the fracture: Proximal pole.  Immobilization for 16–20 weeks in a long-arm or short-arm thumb spica, with the wrist positioned in slight extension and radial deviation. ▶▶ Central third.  Immobilization for 6 weeks in a long-arm thumb spica, followed by a further 6 weeks in a short-arm thumb spica. ▶▶ Distal third.  Immobilization for 6–8 weeks in a shortarm thumb spica. ▶▶

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▶▶

Tuberosity.  Immobilization for 5–6 weeks in a long-arm or short-arm thumb spica.

Following the removal of the splint, a capsular pattern of the wrist is usually evident. In addition, there will be a painful weakness of the thumb and/or wrist extension/radial deviation. AROM exercises for wrist flexion and extension and radial and ulnar deviations are initiated as early as possible, with PROM to the same motions beginning after 2 weeks. A wrist and thumb immobilization splint is typically worn between exercises and at night for comfort and protection. At about the same time as the PROM exercises are initiated, gentle strengthening exercises are introduced using 1- to 2-lb weights or putty. Over a period of several weeks, the exercise program is progressed to include weight-bearing activities, plyometrics, open- and closed-chain exercises, and neuromuscular reeducation, before finally progressing to functional and sport-specific exercises and activities as appropriate. Because of the precarious nature of the blood supply and potential for movement at the fracture line, nonunion can occur. SLAC wrist is a late complication of a scaphoid fracture, scapholunate dissociation, Kienböck disease, fracture of the distal radius, Preiser disease, and deposition of crystals of calcium pyrophosphate dehydrate. The SLAC wrist is thought to result from a loss of the stabilizing effect of the scaphoid, with the development of an arthrosis at the radioscaphoid articulation. When the injury has progressed to this state, proximal row carpectomy or wrist fusion is the only option for the hand surgeon.

Carpal Boss A carpal boss is a rounded bony prominence that presents between the base of second and third metacarpal and the trapezoid and capitate, resulting from repeated forced extension of the wrist and subsequent irritation of soft tissues. The ECRL and ECRB are commonly involved. This prominence resembles a ganglion and is not necessarily pathologic, although it can cause pain and irritation of the local soft tissues. Confirmation is through radiographs. Conservative intervention includes a wrist immobilization splint with the wrist positioned in slight extension (10–15 degrees) to reduce tension on the radial wrist extensors.

Metacarpal Fractures Injuries to the metacarpals are the result of either direct or indirect trauma, with nature and direction of the applied force determining the exact type of fracture or dislocation. Most metacarpal fractures occur in the active and working population, particularly adolescents and young adults. Specific injury patterns that occur from commonly seen trauma are as follows: ▶▶

CMC injuries.  Metacarpal base fractures and dislocations of the CMC joint commonly result from an axial load or other stress on the hand with the wrist flexed. CMC joints, especially the central joints, are quite stable. The metacarpal bases are held in position by posterior (dorsal) and anterior (palmar) CMC ligaments, as well as

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Avulsion fracture at the origin of the collateral ligaments.  This type of fracture is caused by forced deviation of the flexed MCP joint. ▶▶ MCP dislocations.  Almost all MCP dislocations occur with the proximal phalanx displaced in a posterior (dorsal) direction on the metacarpal head, as there is no specific posterior (dorsal) restraint to the MCP joint other than the joint capsule and extensor mechanism. ▶▶

Metacarpal fractures may result in considerable functional impairments, including pain, stiffness, and weakness, if not managed well.9 The management of a patient with a metacarpal fracture depends on a variety of factors including the location, the degree of displacement, angulation, and rotation. In addition, the patient’s age, occupation, general health, and concomitant injuries must also be considered. Most metacarpal injuries are managed by closed reduction and immobilization or sometimes controlled mobilization utilizing a posterior (dorsal) block splint. Conservative management is appropriate if the fracture is stable, in good alignment and only minimally displaced.9 Specific indications are further described below. Impaction fractures of the metacarpal bases that are not significantly displaced can be treated with splinting, followed by early mobilization. ▶▶ CMC dislocations and fracture dislocations, especially when multiple, are unstable injuries. In the past, these fractures were managed by closed reduction and external immobilization, which frequently led to grip weakness and residual pain. The current literature supports closed reduction, if joint congruity can be obtained, but with the addition of internal fixation. ▶▶ Displaced fracture dislocations of the fourth and fifth metacarpals, which are accompanied by a fracture of ▶▶

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the posterior (dorsal) hamate, require ORIF. Reverse Bennett fractures frequently need K-wire stabilization to counteract the deforming forces. If little articular incongruity is present, this may be a closed procedure. As the major complication of these fractures is adherence of soft tissues, the primary goals of rehabilitation, once bony healing has occurred, are to restore an optimized soft-tissue balance and glide to allow pain-free motion and strength while simultaneously protecting the healing tissues. Typically, the patient is instructed to begin pain-free AROM exercise immediately, and by 4 weeks, it is likely that a set of buddy straps will replace the splint for ADLs, although continued use of the splint for any sporting or at-risk activities is recommended until the 6-week time period. If there is any residual stiffness or weakness after 6 weeks, specific blocking exercises combined with appropriate splinting and progression of a resistive strengthening program are recommended.9

Finger Fractures Fractures of the finger (phalangeal), which are more common than metacarpal or carpal fractures, represent approximately 45% of fractures of the hand and wrist. Phalangeal fractures can be divided into base, shaft, and neck and head fractures. Conservative intervention for the more stable fractures involves closed reduction in as near normal alignment as possible with an appropriate cast or splint.

The Forearm, Wrist, and Hand

by interosseous ligaments. CMC dislocations may occur with or without fracture. Fracture dislocation of the fifth metacarpal base is a common intra-articular injury and has been dubbed the reverse Bennett fracture. A direct blow to the ulnar border of the hand tends to cause an extra-articular fifth metacarpal base fracture. ▶▶ Metacarpal shaft injuries.  Metacarpal shaft fractures are typically produced by either axial loading, direct trauma, or torsional forces on the digits. Usually, the fractures are classified anatomically as transverse, oblique, or spiral. The fracture pattern often denotes the mechanism of injury, with direct or axial injury leading to transverse or oblique fractures and torsion leading to a spiral fracture. ▶▶ Metacarpal neck fractures.  The most common metacarpal fractures usually result from striking a solid object with a clenched fist and thus are dubbed boxer fractures, although this injury almost never occurs during boxing. Fractures of the fifth metacarpal neck are among the most common fractures in the hand. ▶▶ Metacarpal head injuries.  Metacarpal head fractures, which are rare injuries, result from axial loading or direct trauma. Fractures of the metacarpal head are intraarticular and periarticular. If displaced, metacarpal head fractures usually require ORIF.

Distal Phalanx Fractures Tuft Fracture.  This is the most common fracture of the fingers, frequently resulting from a crush injury. These fractures are often associated with injuries to the nail matrix. Shaft Fracture.  This type of fracture is either longitudinal or more commonly transverse in orientation. If displaced, this type of fracture is usually associated with an injury to the nail matrix. Intra-Articular Fracture. This fracture in adults usually involves either the volar or posterior (dorsal) lip at the end of the bone, whereas in children an epiphyseal separation also may occur. Volar Lip Fracture.  This type of fracture, also referred to as Jersey finger or sweater finger, is also a tendon avulsion injury where the FDP remains attached to the small fracture fragment. Unstable displaced articular fractures require surgical intervention. Generally speaking, following a fracture of the distal phalanx, a protective splint is worn for 2–4 weeks until the fracture site is nontender. AROM begins at 2–4 weeks or earlier if the fracture is stable enough. PROM begins at 5–6 weeks. PREs normally begin at 7–8 weeks. As with metacarpal fractures, blocking exercises can be used to resolve any specific stiffness or weakness. For example, holding the proximal IP joint in extension will facilitate isolated distal IP joint flexion exercise, alternatively holding the MCP joint flex will facilitate active proximal IP joint extension.9

Fractures of the Proximal and Middle Phalanges Shaft Fracture.  The type of shaft fracture depends largely on the mechanism of injury. A direct blow frequently causes

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THE EXTREMITIES

transverse fractures, whereas twisting injuries often cause spiral or oblique fractures. The intervention for this type of fracture depends on the location and the severity. Proximal Phalanx Fractures. Nondisplaced extra-articular fractures are splinted with buddy tape. AROM is initiated immediately, with PROM being initiated at 6–8 weeks. Nondisplaced intra-articular fractures are splinted in the intrinsic plus position for 2–3 weeks. AROM begins at 2–3 weeks, with PROM being initiated at 4–8 weeks. PREs normally begin at clinical union (8–12 weeks). Middle Phalanx Fractures.  If nondisplaced, these fractures are splinted in the intrinsic plus position for approximately 3 weeks. Buddy splinting, the taping of a neighboring finger to the involved finger, may also be an option. AROM is initiated when pain and edema subsides. PROM begins at 4–6 weeks, with PREs normally beginning at 6–8 weeks.

THERAPEUTIC TECHNIQUES Techniques to Increase Joint Mobility The majority of the joint mobility tests described in the Tests and Measures section can also be utilized as mobilization techniques. For each of the techniques, the patient is positioned in sitting with their forearm and wrist in a neutral position, with the clinician positioned to the side of the patient. The amplitude and the velocity of each of the techniques (i.e., grade) are varied according to the stage of healing and the irritability of the joint. The clinician must be cognizant of the joints that are responsible for the individual motions that occur at the wrist and hand and which ones present with convex or concave joint surfaces in order to deliver the most specific technique. Supination–pronation occurs primarily at the ulnomeniscotriquetral joint and the proximal and inferior radioulnar joints. ▶▶ Wrist flexion occurs primarily at the radiocarpal joint (distal radius and the articulating surfaces of the navicular and lunate). ▶▶ Wrist extension occurs primarily at the midcarpal joints (articulating surface of the scaphoid, lunate, and triquetral bones proximally, and the trapezium, trapezoid, capitate, and hamate bones distally). ▶▶

Passive Accessory Mobilizations Distal Radioulnar Joint  Anterior–Posterior Glide.  The clinician glides the radius in an anterior direction to improve forearm pronation and in a posterior direction to improve forearm supination. The intensity of the technique (i.e., grade) is varied according to the irritability of the joint.

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Radiocarpal  Posterior–Anterior Glide (Fig. 18-30).  The posterior glide is used to improve the joint’s ability to flex, whereas the anterior glide is used to improve the ability of the joint to extend.

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Ulnar and Radial Glide (Fig. 18-31). The ulnar (medial) glide is used to improve the joint’s ability to radially deviate, whereas the radial (lateral) glide is used to improve the ability of the joint to ulnarly deviate. Ulnocarpal, Midcarpal, CMC, MCP, and IP Joints  Distraction.  Using a pinch grip of the index finger and thumb of one hand, the clinician palpates and stabilizes the proximal bone of the joint being distracted. With a pinch grip of the index finger and thumb of the other hand, the clinician palpates and mobilizes the distal bone longitudinally (Fig. 18-36). Posterior–Anterior Glide (Flexion/Extension).  Using a pinch grip of the index finger and thumb of one hand, the clinician palpates and stabilizes the proximal bone of the joint being mobilized in a posterior (dorsal)–anterior (palmar) plane. With a pinch grip, the clinician glides the distal bone along the posterior (dorsal)–anterior (palmar) plane of the corresponding joint. The appropriate conjunct rotation of the bone may be added. For example, to restore flexion at the radioscaphoid joint, the clinician rotates the scaphoid toward the center of the palm, while simultaneously gliding the scaphoid in a posterior (dorsal) direction. The clinician can make the technique patient-assisted by flexing/extending the distal bone about the appropriate intraarticular axis to the limit of the physiologic range of motion. From this position, the patient is instructed to perform an isometric contraction against the clinician’s equal resistance. The contraction is held for 3–5 seconds, following which the patient is instructed to completely relax. The new barrier of flexion/extension is localized and the mobilization repeated. First CMC (Trapeziometacarpal) Joint  Posterior Glide.  This technique is used to improve range of motion into trapeziometacarpal joint abduction. Anterior Glide.  This technique is used to improve range of motion into trapeziometacarpal joint adduction. Medial–Lateral Glide (Abduction/Adduction). The medial glide technique is used to improve range of motion into trapeziometacarpal joint flexion. The lateral glide technique is used to improve range of motion into trapeziometacarpal joint extension. The clinician can make the technique patient-assisted by abducting/adducting the distal bone about the appropriate intra-articular axis to the limit of the physiologic range of motion. From this position, the patient is instructed to perform an isometric contraction against the clinician’s equal resistance. The contraction is held for 3–5 seconds, following which the patient is instructed to completely relax. The new barrier of motion is localized and the mobilization repeated.

Intermetacarpal Joints Using a pinch grip of the index finger and thumb of one hand, the clinician palpates and stabilizes one metacarpal. With the thumb and index finger of the other hand, the clinician mobilizes the neighboring metacarpal into an anterior or posterior glide, with the appropriate conjunct rotation.

MCP Joints Posterior–Anterior Glide. A posterior glide is used to improve range of motion into extension for digits two through

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five, whereas an anterior glide is used to improve range of motion into flexion for digits two through five. Ulnar (Medial)–Radial (Lateral) Glide. An ulnar glide is used to improve range of motion into ulnar deviation for digits two through five, whereas a radial glide is used to improve range of motion into radial deviation for digits two through five. First MCP/IP Joint.  A radial glide is used to improve trapeziometacarpal extension, while the ulnar glide is used to improve trapeziometacarpal flexion. The anterior glide can be used to improve the ability of the joint to move into flexion, whereas posterior glide can be used to improve the ability of the joint to move into extension.

Mobilization with Movement

FIGURE 18-86  High-velocity thrust technique to the scaphoid.

MWM techniques67,68 can be used to increase ROM or decrease pain (see Chapter 10). Wrist Joints.  The patient is positioned in sitting with the elbow flexed and the forearm supinated. The clinician stabilizes the distal radius with one hand around the lateral aspect of the forearm and, using the web space of the other hand, applies a pain-free lateral glide to the proximal row of carpals. The patient is then asked to extend or flex his or her wrist to the end of the available range and, with his or her free hand, to apply a passive stretch at the end of the range. On occasion, internal or external rotation of the carpals relative to the radius may need to be combined with the glide. Also, the intercarpal joint may require specific anterior–posterior gliding of one of the proximal row of carpals relative to its distal neighbor.

Techniques to Increase Soft Tissue Extensibility

MCP and IP Joints.  The clinician applies a medial or lateral glide to the involved phalanx in a painless direction after which the patient actively flexes or extends the finger and applies a pain-free, passive end range stretch. On occasion, internal or external rotation of the more distal phalanx may be required in conjunction with the medial or lateral glide to achieve painless end range overpressure.

Tendon Gliding Exercises

A number of techniques can be used to increase the extensibility of the soft tissues of the wrist, hand, and forearm. These include passive or AROM exercises that can be performed by the patient: Wrist flexion and extension Wrist ulnar and radial deviation ▶▶ Finger flexion and extension ▶▶ Finger adduction and abduction ▶▶ Thumb opposition, flexion, extension, abduction, and adduction ▶▶ ▶▶

The Forearm, Wrist, and Hand

IP Joints

Tendon gliding exercises of the flexor tendons are often prescribed to prevent adhesions of the tendons and nerves. Place and Hold Exercises.  These exercises, which are a type of gentle muscle setting exercises that are used before AROM exercises, are initiated to maintain joint mobility and tendon

High-Velocity, Low-Amplitude Thrusting High-velocity thrust techniques can be used with any of the carpals. The following example describes the technique for a posteriorly (dorsally) displaced scaphoid. The patient is positioned in sitting with the forearm of their affected side resting on a table with the anterior (palmar) side facing down. The clinician sits or stands at right angles to the patient’s affected side. The clinician grips the patient’s scaphoid bone between their thumb and index finger (Fig. 18-86). The clinician reinforces this grip by placing the thumb and the index of the other hand on top of them. The patient’s wrist is then passively extended to the end range. At the end of the available range, the scaphoid is thrusted anteriorly (ventrally) while passively extending the wrist slightly.

Transverse Friction Massage Common Sheath of APL and EPB Transverse friction can be applied to the commonly shared sheath of the APL and EPB (Fig. 18-87) or at the point where the tendons pass over the wrist extensors.

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FIGURE 18-87  TFM to common shared sheath of the abductor pollicis longus and extensor pollicis brevis.

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excursion. With the MCP joints maintained in flexion, the IP joints are passively placed in a partially flexed position and the patient holds the position independently for 5 seconds using a minimum contraction of the finger flexors. The exercise can be combined with active wrist extension. IP Flexion or “Hook Fist.”  The hook, this position describes the hand position where the MCP joints are maintained in extension while the DIP and PIP joints are flexed. This results in maximum gliding between the profundus and superficialis tendons, and between the profundus tendon and the bone.

THE EXTREMITIES

Straight and/Fingers, Wrist in Neutral MCP Flexion or “Tabletop.”  With the wrist maintained in neutral flexion/extension, MCP joints are flexed while maintaining the DIP and PIP joints in extension. Straight or “Sublimis” Fist.  The patient moves from the tabletop position to the straight wrist position by flexing the PIP joints while maintaining the DIP joints in extension. Full Fist.  While maintaining the wrist in neutral flexion/ extension, the patient flexes all of the MCP and IP joints simultaneously. Thumb Flexion.  The patient flexes the MCP and IP joints of the thumb throughout the full range to promote maximum gliding of the FPL.

Tendon-Blocking Exercises Blocking exercises attempt to isolate the movement to the involved joint, and usually involve supporting the phalanx or metacarpal below the stiff joint. These exercises are a progression of the flexor tendon gliding exercises and are therefore

not used in the early stages of flexor tendon healing. The patient is positioned in sitting with the forearm supinated and the back of the hand resting on the table. MCP Flexion.  While stabilizing the rest of the fingers in extension against the table with one hand, the patient flexes only the MCP joint of one digit. PIP Flexion.  The patient stabilizes the proximal phalanx of one digit with the opposite hand and, if possible, flexes just the PIP joint of the one digit while keeping the PIP joint extended and the rest of the fingers on the table. DIP Flexion.  While stabilizing the middle phalanx of one digit with the other hand, the patient attempts to flex just the distal phalanx.

Extensor Tendon Gliding Exercises The following progression can be used to rehabilitate extensor tendon injuries. Isolated MCP and IP Joint Flexion.  The patient passively flexes the MCP and IP joints of one finger with the opposite hand while actively maintaining the other fingers in extension. Middle and Ring Finger Flexion.  The patient flexes the middle and ring fingers while maintaining the extension of the index and little fingers to promote isolated control of the EI and EDM tendons. Terminal Range Extension of IP Joints.  Terminal range extension can be achieved by stabilizing the patient’s hand palm side down on a flat surface. The patient is then asked to extend the involved phalanx into hyperextension. A pencil can be placed under the proximal phalanx or middle phalanx so that the PIP or DIP joint can achieve a greater range.

CASE STUDY PAINFUL LEFT THUMB HISTORY History of Current Condition A 23-year-old female patient complained of left thumb pain following a home do-it-yourself project that involved a lot of hammering of nails. The patient described a gradual onset of pain about 2 months ago and described the pain as burning located at the base of the left thumb. The patient also reported some swelling at the wrist. The patient attributed the pain to the hammering of nails as subsequent attempts to use the hammer reproduced the pain. Over time, the pain had worsened to the point where it hurt all of the time, even at night. The NSAIDs prescribed by the physician 2 weeks ago appeared to be helping. Past History of Current Condition No past history of left elbow, wrist, or hand pain. Past Medical/Surgical History Unremarkable except for removal of ganglion cysts from her right wrist/hand about 1 year ago.

Growth and Development Right-hand dominant. Medications None, except for the prescribed NSAIDs. Occupational/Employment/School Office worker. College education. Functional Status/Activity Level The patient reported experiencing pain with vacuuming and lifting heavy pots and pans. The patient’s goals were to decrease pain with activities of daily living. Health Status (Self-Report) In general good health, but pain interferes with gripping tasks at home and at work.

Questions 1. What are some of the more common diagnoses characterized by thumb pain?

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2. What does the history of the gradual onset and of repetitive activity tell the clinician? 3. What findings do you expect to note in the physical examination in terms of palpation, resistive tests, and special tests? 4. What additional questions would you ask to help rule out referral of pain from the cervical spine or shoulder?

5. List the tests you would use to rule out the various diagnoses that you listed in question 1. 6. Does this presentation/history warrant an upper quarter scanning examination? Why or why not?

PAIN, WEAKNESS, AND NUMBNESS OF THE HAND HISTORY History of Current Condition A 49-year-old female complains of insidious onset of right hand numbness and pain, which began about 5 weeks previously. The symptoms are felt mainly in the right index finger, especially when working at her computer at work but also in her right thumb and middle finger after a day at work and at night. The symptoms are also reported to be worse during the night and early morning. The patient has also noted a slight decrease in her grip strength, which prompted her to see a MD, who prescribed PT, ibuprofen, vitamin B6, and a short course of diuretics. The patient denies any neck pain. Past Medical/Surgical History Unremarkable, including no history of previous symptoms or of diabetes mellitus reported by the patient. Medications 800 mg of ibuprofen daily. Other Tests and Measures None. X-rays 1 year ago were unremarkable (per patient). Physician mentioned that further testing may be warranted (nerve conduction velocity, EMG). Social Habits (Past and Present) Smoker (1/2 pack per day). Growth and Development Right-hand dominant.

REFERENCES 1. Standring S, Gray H. Gray’s Anatomy: The Anatomical Basis of Clinical Practice. 41st ed. London, England: Elsevier; 2015. 2. Ward LD, Ambrose CG, Masson MV, Levaro F. The role of the distal radioulnar ligaments, interosseous membrane, and joint capsule, in distal radioulnar joint stability. J Hand Surg Am. 2000;25:341–551. 3. Neumann DA. Wrist. In: Neumann DA, ed. Kinesiology of the Musculoskeletal System: Foundations for Physical Rehabilitation. 3rd ed. St. Louis, MO: Mosby; 2016:218–249.

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Occupational/Employment/School Full-time administrator at local community hospital for last 6 years. Recently promoted which has meant an increase in computer work. Functional Status/Activity Level Symptoms interfering with work and at home with her needle craft. Symptoms also interfering with sleep approximately two times per night.

The Forearm, Wrist, and Hand

CASE STUDY

Questions 1. What are some of the more common diagnoses characterized by symptoms in this distribution? 2. What does the history of the gradual onset and of repetitive activity tell the clinician? 3. What findings do you expect to note in the physical examination in terms of palpation, resistive tests, and special tests? 4. What additional questions would you ask to help rule out referral of pain from the cervical and thoracic spine? 5. What additional questions would you ask to help rule out referral of pain from the shoulder or elbow? 6. List the tests you would use to rule out the various diagnoses that you listed in question 1. 7. Does this presentation/history warrant a scan? Why or why not?

4. Wadsworth C. Wrist and hand. In: Wadsworth C, ed. Current Concepts of Orthopedic Physical Therapy—Home Study Course. La Crosse, WI: Orthopaedic Section, APTA; 2001. 5. Brand PW. Clinical Mechanics of the Hand. St. Louis, MO: CV Mosby; 1985. 6. Hagert E. Proprioception of the wrist joint: a review of current concepts and possible implications on the rehabilitation of the wrist. J Hand Surg. 2010;23:2–17. 7. Hincapie OL, Elkins JS, Vasquez-Welsh L. Proprioception retraining for a patient with chronic wrist pain secondary to ligament injury with no structural instability. J Hand Surg. 2016;29:183–190.

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THE EXTREMITIES 822

8. Freedman DM, Botte MJ, Gelberman RH. Vascularity of the carpus. Clin Orthop. 2001;383:47–59. 9. Wajon A. Wrist/hand. In: Jull G, Moore A, Falla D, Lewis J, McCarthy C, Sterling M, eds. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. London, England: Elsevier; 2015:595–605. 10. Walker MJ. Manual physical therapy examination and intervention of a patient with radial wrist pain: a case report. J Orthop Sports Phys Ther. 2004;34:761–769. 11. Leard JS, Breglio L, Fraga L, et al. Reliability and concurrent validity of the figure-of-eight method of measuring hand size in patients with hand pathology. J Orthop Sports Phys Ther. 2004;34:335–340. 12. Salva-Coll G, Garcia-Elias M, Leon-Lopez MT, Llusa-Perez M, Rodriguez-Baeza A. Effects of forearm muscles on carpal stability. J Hand Surg Eur Vol. 2011;36:553–559. 13. de Carvalho RM, Mazzer N, Barbieri CH. Analysis of the reliability and reproducibility of goniometry compared to hand photogrammetry. Acta Ortop Bras. 2012;20:139–149. 14. Bohannon RW. Muscle strength: clinical and prognostic value of handgrip dynamometry. Curr Opin Clin Nutr Metab Care. 2015;18:465–470. 15. Mentiplay BF, Tan D, Williams G, et al. Assessment of isometric muscle strength and rate of torque development with hand-held dynamometry: test-retest reliability and relationship with gait velocity after stroke. J Biomech. 2018;75:171–175. 16. Schreuders TA, Roebroeck ME, Goumans J, van Nieuwenhuijzen JF, Stijnen TH, Stam HJ. Measurement error in grip and pinch force measurements in patients with hand injuries. Phys Ther. 2003;83:806–815. 17. Tredgett MW, Davis TRC. Rapid repeat testing of grip strength for detection of faked hand weakness. J Hand Surg Br. 2000;25:372–375. 18. Jebsen RH, Taylor N, Triegchmann R, et al. An objective and standardized test for hand function. Arch Phys Med Rehabil. 1969;50:311–319. 19. Prosser R, Harvey L, Lastayo P, Hargreaves I, Scougall P, Herbert RD. Provocative wrist tests and MRI are of limited diagnostic value for suspected wrist ligament injuries: a cross-sectional study. J Physiother. 2011;57:247–253. 20. Waggy C. Disorders of the wrist. In: Wadsworth C, ed. Orthopaedic Physical Therapy Home Study Course—The Elbow, Forearm, and Wrist. La Crosse, WI: Orthopaedic Section, APTA; 1997. 21. Alexander RD, Catalano LW, Barron OA, Glickel SZ. The extensor pollicis brevis entrapment test in the treatment of de Quervain’s disease. J Hand Surg Am. 2002;27:813–816. 22. Park MJ. Radiographic observation of the scaphoid shift test. J Bone Joint Br. 2003;85:358–362. 23. Ahn DS. Hand elevation: a new test for carpal tunnel syndrome. Ann Plast Surg. 2001;46:120–124. 24. Wazir NN, Kareem BA. New clinical sign of cervical myelopathy: Wazir hand myelopathy sign. Singapore Med J. 2011;52:47–49. 25. Oetgen ME, Dodds SD. Non-operative treatment of common finger injuries. Curr Rev Musculoskeletal Med. 2008;1:97–102. 26. Salva-Coll G, Garcia-Elias M, Hagert E. Scapholunate instability: proprioception and neuromuscular control. J Wrist Surg. 2013;2:136–140. 27. Garcia-Elias M, Alomar Serrallach X, Monill Serra J. Dart-throwing motion in patients with scapholunate instability: a dynamic four-dimensional computed tomography study. J Hand Sur Eur Vol. 2014;39:346–352. 28. Feehan L, Fraser T. Early controlled mobilization using dart-throwing motion with a twist for the conservative management of an intra-articular distal radius fracture and scapholunate ligament injury: a case report. J Hand Ther. 2016;29:191–198. 29. Vardakastani V, Bell H, Mee S, Brigstocke G, Kedgley AE. Clinical measurement of the dart throwing motion of the wrist: variability, accuracy and correction. J Hand Sur Eur Vol. 2018;43:723–731. 30. Moritomo H, Apergis EP, Garcia-Elias M, Werner FW, Wolfe SW. International Federation of Societies for Surgery of the Hand 2013 Committee’s report on wrist dart-throwing motion. J Hand Surg Am. 2014;39:1433–1439. 31. Crisco JJ, Coburn JC, Moore DC, Akelman E, Weiss AP, Wolfe SW. In vivo radiocarpal kinematics and the dart thrower’s motion. J Bone Joint Surg Am. 2005;87:2729–2740. 32. Brigstocke GH, Hearnden A, Holt C, Whatling G. In-vivo confirmation of the use of the dart thrower’s motion during activities of daily living. Hand Sur Eur Vol. 2014;39:373–378. 33. Kane PM, Vopat BG, Mansuripur PK, et al. Relative contributions of the midcarpal and radiocarpal joints to Dart-Thrower’s motion at the wrist. J Hand Surg Am. 2018;43:234–240. 34. Balan SA, Garcia-Elias M. Utility of the powerball in the invigoration of the musculature of the forearm. Hand Surg. 2008;13:79–83.

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35. Pratt AL, Burr N, Grobbelaar AO. A prospective review of open central slip laceration repair and rehabilitation. J Hand Surg Br. 2002;27: 530–534. 36. van Vugt RM, Bijlsma JWJ, van Vugt AC. Chronic wrist pain: diagnosis and management. Development and use of a new algorithm. Ann Rheum Dis. 1999;58:665–674. 37. Wajon A, Ada L. No difference between two splint and exercise regimens for people with osteoarthritis of the thumb: a randomised controlled trial. Aust J Physiother. 2005;51:245–249. 38. Saar JD, Grothaus PC. Dupuytren’s disease: an overview. Plast Reconstr Surg. 2000;106:125–136. 39. Takase K, Imakiire A. Lunate excision, capitate osteotomy, and intercarpal arthrodesis for advanced Kienbock disease. Long-term follow-up. J Bone Joint Surg. 2001;83-A:177–183. 40. Chang CY, Kheterpal AB, Vicentini JRT, Huang AJ. Variations of anatomy on MRI of the first extensor compartment of the wrist and association with de Quervain tenosynovitis. Skeletal Radiol. 2017;46: 1047–1056. 41. Willardson HB, Buck S, Neiner J. Linear atrophy and vascular fragility following ultrasoundguided triamcinolone injection for De Quervain tendonitis. Dermatol Online J. 2017;23. 42. Lane LB, Boretz RS, Stuchin SA. Treatment of de Quervain’s disease: role of conservative management. J Hand Surg Br. 2001;26:258–260. 43. Backstrom KM. Mobilization with movement as an adjunct intervention in a patient with complicated de Quervain’s tenosynovitis: a case report. J Orthop Sports Phys Ther. 2002;32:86–94; discussion 94–97. 44. Kumar P, Chakrabarti I. Idiopathic carpal tunnel syndrome and trigger finger: is there an association? Hand Sur Eur Vol. 2009;34:58–59. 45. Makkouk AH, Oetgen ME, Swigart CR, Dodds SD. Trigger finger: etiology, evaluation, and treatment. Curr Rev Musculoskelet Med. 2008;1: 92–96. 46. Shiozawa R, Uchiyama S, Sugimoto Y, Ikegami S, Iwasaki N, Kato H. Comparison of splinting versus nonsplinting in the treatment of pediatric trigger finger. J Hand Surg. 2012;37:1211-1216. 47. Huisstede BM, Hoogvliet P, Coert JH, Friden J, European HG. Multidisciplinary consensus guideline for managing trigger finger: results from the European HANDGUIDE Study. Phys Ther. 2014;94:1421–1433. 48. Owers KL, Grieve PP, Mee S, Chew NS, Ansede G, Lee J. Ultrasound changes in the extensor pollicis longus and flexor pollicis longus tendons following open reduction and internal fixation of displaced intra-articular fractures of the distal radius. J Hand Surg Eur Vol. 2013;38:129–132. 49. Harris-Adamson C, Eisen EA, Dale AM, et al. Personal and workplace psychosocial risk factors for carpal tunnel syndrome: a pooled study cohort. Occup Environ Med. 2013;70:529–537. 50. Burton CL, Chen Y, Chesterton LS, van der Windt DA. Trends in the prevalence, incidence and surgical management of carpal tunnel syndrome between 1993 and 2013: an observational analysis of UK primary care records. BMJ Open. 2018;8:e020166. 51. Chow CS, Hung LK, Chiu CP, et al. Is symptomatology useful in distinguishing between carpal tunnel syndrome and cervical spondylosis? Hand Surg. 2005;10:1–5. 52. Zanette G, Marani S, Tamburin S. Proximal pain in patients with carpal tunnel syndrome: a clinical-neurophysiological study. J Peripher Nerv Syst. 2007;12:91–97. 53. Pierre-Jerome C, Bekkelund SI. Magnetic resonance assessment of the double-crush phenomenon in patients with carpal tunnel syndrome: a bilateral quantitative study. Scand J Plast Reconstr Surg Hand Surg. 2003;37:46–53. 54. De-la-Llave-Rincon AI, Fernandez-de-Las-Penas C, Laguarta-Val S, Ortega-Santiago R, Palacios-Cena D, Martinez-Perez A. Women with carpal tunnel syndrome show restricted cervical range of motion. J Orthop Sports Phys Ther. 2011;41:305–310. 55. De-la-Llave-Rincon AI, Fernandez-de-las-Penas C, Palacios-Cena D, Cleland JA. Increased forward head posture and restricted cervical range of motion in patients with carpal tunnel syndrome. J Orthop Sports Phys Ther. 2009;39:658–664. 56. D’Arcy CA, McGee S. Does this patient have carpal tunnel syndrome? JAMA. 2000;283:3110–3117. 57. Bowles AP, Jr., Asher SW, Pickett JB. Use of Tinel’s sign in carpal tunnel syndrome [letter]. Ann Neurol. 1983;13:689–690. 58. Colorado BS, Osei DA. Prevalence of carpal tunnel syndrome presenting with symptoms in an ulnar nerve distribution: a prospective study. Muscle Nerv. 2019;59:60–63. 59. Lee MJ, LaStayo PC. Pronator syndrome and other nerve compressions that mimic carpal tunnel syndrome. J Orthop Sports Phys Ther. 2004;34:601–609.

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60. Coppieters MW, Alshami AM. Longitudinal excursion and strain in the median nerve during novel nerve gliding exercises for carpal tunnel syndrome. J Orthop Res. 2007;25:972–980. 61. Piligian G, Herbert R, Hearns M, et al. Evaluation and management of chronic work-related musculoskeletal disorders of the distal upper extremity. Am J Ind Med. 2000;37:75–93. 62. Metules TJ. When a simple fall turns into years of pain. RN. 2000;63: 65–66. 63. Dunn D. Chronic regional pain syndrome, type 1: part I. AORN J. 2000;72:422–432, 435–449; quiz 452–458. 64. Kingery WS. A critical review of controlled clinical trials for peripheral neuropathic pain and complex regional pain syndromes. Pain. 1997;73:123–139.

65. King RJ. Scapholunate diastasis associated with a Barton fracture treated by manipulation or Terry-Thomas and the wine waiter. J Royal Soc Med. 1983;76:421–423. 66. Perron AD, Brady WJ, Keats TE, Hersh RE. Orthopedic pitfalls in the ED: scaphoid fracture. Am J Emerg Med. 2001;19:310–316. 67. Mulligan BR. Manual Therapy: “NAGS”, “SNAGS”, “PRP’S” etc. Wellington: Plane View Series; 1992. 68. Mulligan BR. Manual therapy rounds: mobilisations with movement (MWM’s). J Man Manip Ther. 1993;1:154–156.

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Hip Joint Complex

CHAPTER OBJECTIVES At the completion of this chapter, the reader will be able to: 1. Describe the anatomy of the joint, ligaments, muscles, and blood and nerve supply that comprise the hip joint complex. 2. Describe the biomechanics of the hip joint, including the open- and close-packed positions, normal and abnormal joint barriers, force couples, and the static and dynamic stabilizers of the joint. 3. Describe the purpose and components of the examination of the hip joint. 4. Perform a comprehensive examination of the hip joint, including palpation of the articular and soft tissue structures, specific passive mobility, passive articular mobility tests, and stability stress tests. 5. Evaluate the total examination data to establish a diagnosis. 6. Describe the relationship between muscle imbalance and functional performance of the hip. 7. Summarize the various causes of hip dysfunction. 8. Develop self-reliant intervention strategies based on clinical findings and established goals. 9. Develop a working hypothesis. 10. Describe and demonstrate intervention strategies and techniques based on clinical findings and established goals. 11. Evaluate the intervention effectiveness in order to progress or modify an intervention. 12. Plan an effective home program and instruct the patient in same.

C H A P T E R 1 9

center of gravity is located at the second sacral vertebral level, several segments above and medial to the femoral head. Control of the body mass from such a distant fulcrum requires the generation of significant counterbalance forces as well as the ability of the joint to sustain both high compression and tensile strains. Thus, a major function of the hip joint is to provide a pathway for the transmission of forces between the pelvis and the lower extremities.

ANATOMY The hip articulation is a synovial joint formed by the head of the femur inferiorly and the acetabulum of the pelvic bone superiorly (Fig. 19-1). This articulation is classified as an unmodified ovoid (or ball and socket) joint. The hip joint which, although similar in nature to the shoulder joint, differs in the fact that the former has a deeper acetabular socket and acts as a weight-bearing joint with a smaller total arc of motion.

Bony Anatomy Normal hip joint growth and development occur because of a genetically determined balance of growth of the acetabulum and the presence of a strategically located spherical femoral head. The os coxa (hip bone), more commonly referred to as the innominate bone initially begins life as three individual bones: the ilium, the ischium, and the pubis (Fig. 19-1). As life progresses, these three bones fuse together.

Ilium The ilium (see Fig. 19-1) is the largest of these three bones. It is composed of a large fan-like wing (ala) and an inferiorly positioned body. The body of the ilium forms the superior two-fifths of the acetabulum. The wing of the ilium spans superiorly from the posterior superior iliac spine (PSIS) to the anterior superior iliac spine (ASIS). The wing serves as the insertion of the gluteus minimus, medius, and maximus. ▶▶ The anterior surface of the ilium forms a fossa and serves as the proximal attachment of the iliacus muscle. ▶▶

OVERVIEW 824

The structure and design of the hip allow for both mobility and stability, the latter of which is particularly important for weight bearing and ambulation. In the human body, the

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Os coxa Ilium Ischium Pubis Sacroiliac joint

ANATOMY

KEY

Iliac crest

Sacrum Iliac fossa Pelvis Hip joint

Pubic symphysis

Anterior inferior iliac spine

Posterior inferior iliac spine

Acetabulum Superior pubic ramus

Ischial spine

Pubic tubercle

Obturator foramen Femur

Inferior pubic ramus

Ischial tuberosity

Hip Joint Complex

Anterior superior iliac spine

Posterior superior iliac spine

Ischial ramus

B Greater trochanter Head Fovea

Patella

Neck

Knee joint

Lesser trochanter

Tibia

Pectineal line

Fibula

Linea aspera

Popliteal fossa

A

Medial and lateral condyles Medial and lateral epicondyles

C

Anterior

Posterior

FIGURE 19-1  Bones of the lower extremity. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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ANATOMY



TABLE 19-1

 uscles that Attach to the Ischial M Tuberosity

Semimembranosus Semitendinosus Long head of the biceps femoris Adductor magnus Quadratus femoris Gemellus inferior

THE EXTREMITIES

Ischium The ischium (see Fig. 19-1) is composed of a body, which contributes to the acetabulum, and a ramus. The ischium forms the posterior two-fifths of the acetabulum. Together, the ischium and the ramus form the ischial tuberosity. The ischial tuberosity is an important landmark for palpation, as it serves as the attachment for the tendons of several muscles (Table 19-1) and the sacrotuberous ligament. The ischial spine, located on the body of the ischium, serves as the attachment for the sacrospinous ligament.

Pubis The pubis (see Fig. 19-1) is the smallest of the three bones and consists of a body and inferior and superior rami. The pubis forms the anterior fifth of the acetabulum.

Acetabulum The ilium, ischium, and pubis fuse together within the acetabulum and form a deep-seated depression in the lateral pelvis, which allows for the proximal transmission of weight from the axial skeleton to the lower extremity. The orientation of the surface of the acetabulum faces laterally, inferiorly, and anteriorly (see Fig. 19-1). The superior and posterior margins of the acetabulum are reinforced with a compact cortical bone, which extends the peripheral brim of the fossa, enhancing the stability of the joint during weight bearing from both flexed and extended positions. The coverage of the femoral head by the acetabulum is measured by the center edge angle (CEA) of Wiberg (see Clinical Pearl). The absence of a normal femoral head during growth, such as in developmental dysplasia of the hip (DDH), causes the acetabulum to have a flat shape. A deformed head stimulates the formation of a correspondingly deformed acetabulum if the deformation occurs at a young enough age.

CLINICAL PEARL

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The CEA of Wiberg is a common measurement for the depth of the acetabular socket. The CEA is measured from the anterior-posterior radiograph. A line is drawn through the center of the femoral head, and a second line is drawn from the center of the femoral head to the lateral edge of the acetabulum and the CEA is the angle formed between these. Normal coverage is indicated by a CEA

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of approximately 30 degrees, whereas undercoverage, is indicated by a CEA of less than 20 degrees.1 A protrusionacetabulum, or deep socket, is defined by a CEA of 44 degrees or more. This scenario of overcoverage can cause a condition called pincer impingement, described later in the chapter. Another way to calculate femoral head coverage is by determining Lequesne’s acetabular index (AI) from a radiograph. The angle used to calculate the AI is formed by a horizontal line connecting both triradiate cartilages (the joining seam of the three pelvic bones—ischium, ilium, and pubis) and a second line which extends along the acetabular roofs. The normal AI is less than 10 degrees. An increase in the AI is associated with a higher incidence of hip dysplasia. Dysplasia can also be associated with coxa valgus, and femoral neck shaft angles greater than the normal parameters of 125–139 degrees.

Hip dysplasia is considered to be the result of undercoverage of the femoral head. This bony undercoverage can lead to excessive joint stress during normal function. For example, a situation of edge loading of the acetabulum can lead to premature articular cartilage degeneration, hip dysplasia, anteversion, coxa valga, or acetabular labral injury.2 Conversely, excessive bone coverage, or overcoverage, referred to as femoroacetabular impingement (FAI) can predispose an individual to hip injury secondary to alterations in the mechanical loading patterns of the hip joint.2

CLINICAL PEARL FAI refers to morphology variations in the hip joint that results in the abnormal osseous contact between the femur (cam impingement) and/or acetabular rim (pincer impingement) during end-range hip motions.3 While the majority of acetabular development is determined by the age of eight, the depth of the acetabulum increases additionally at puberty, because of the development of three secondary centers of ossification. Around the periphery of the acetabulum is a thickened collar of fibrocartilage known as the acetabular rim, or labrum (see “The Acetabular Labrum” section), that further deepens the concavity and grasps the head of the femur. The transverse acetabular ligament is a fibrous tissue link spanning the inferior acetabular notch that connects the anteroinferior and posteroinferior horns of the semilunar surface of the acetabulum.4 The posterior aspect of the ligament attaches to the bone beneath the lunate surface, and the anterior aspect attaches to the labrum.4 The transverse acetabular ligament contains no cartilage cells.4 The function of this ligament in the hip is currently unknown. The articular surface of the acetabulum is limited to an inverted horseshoe-shaped area covering the anterior, superior, and posterior margins. The articular cartilage is thickest on the superior aspect of the acetabulum, but thins near the center of the joint, and is absent over the acetabular notch

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The femur is the strongest and the longest bone in the body. The proximal end of the femur, the femoral head is angled anteriorly, superiorly, medially to articulate with the acetabulum (see Fig. 19-1). The femoral head is composed of a trabecular bone core encased in a thin cortical bone shell. Approximately two-thirds of the femoral head is covered with a smooth layer of cartilage except for a depression, the fovea capitis, which serves as the attachment of the ligamentum teres. The articular cartilage is thickest on the superior-posterior aspect of the femoral head. The femoral neck is externally rotated with respect to the shaft.

CLINICAL PEARL The trabecular bone in the femoral head and the neighboring femoral neck is specially designed to withstand high loads because of the incorporation of both primary and secondary compressive and tensile patterns. However, within this trabecular system, there is a point of weakness called the Ward triangle, which is a common site of osteoporotic fracture.7

TABLE 19-2

 uscles that Attach to the Greater M Trochanter

Piriformis Gluteus medius Gluteus minimus Obturator internus Gemellus superior Gemellus inferior

Femoral varus (coxa varum) occurs when the angle of inclination is less than 125 degrees, and femoral valgus (coxa valgus) occurs when the angle is greater than 139 degrees (see Biomechanics section).9 The neck of the femur is located between the shaft of the femur and its head. The head-neck offset is measured by the alpha angle. This angle, which determines how spherical the femoral head is, is measured by first drawing a best-fit circle around the femoral head and then drawing a line from this down the femoral neck. The alpha angle is formed between this line and a line drawn from the center of the circle to where the femur deviates from the circle. An alpha angle of greater than 55 degrees is indicative of a condition called cam impingement, described later. On the anterior surface of the femoral neck is the rough intertrochanteric line. The femoral neck serves to extend the weight-bearing forces lateral and inferior to the joint fulcrum. The intertrochanteric crest marks the posterior junction between the neck and the shaft of the femur. The greater trochanter serves as the insertion site for several muscles that act on the hip joint (Table 19-2). The lesser trochanter, located on the posteromedial junction of the neck and the shaft of the femur, is created by the pull of the iliopsoas muscle.

Hip Joint Complex

Femur



ANATOMY

(see Fig. 19-1), the area occupied by the ligamentum teres and obturator artery.5 This relatively small contact area may contribute to the prevalence of degenerative disease of the hip joint in humans. The diameter of the acetabulum is slightly less than that of the femoral head and results in an incongruous fit of the joint surfaces. This incongruity unloads the joint during partial weight-bearing (PWB), by allowing the femoral head to sublux laterally out of the cup, while, in full weight bearing, the femoral head is forced into the acetabulum. In addition, elastic deformation of the acetabulum increases joint congruency of the two-joint surfaces in weight bearing. Finally, a strong vacuum contributes to the joint coaptation.6

Joint Capsule and Ligaments Both the trabecular framework of the head and its pliable hyaline cartilage covering contribute toward the shaping of the femoral head within the acetabulum during full weight bearing. In the transverse plane, the proximal femur is oriented anterior to the distal femoral condyles as a result of a medial portion of the femur.8 The angle that the femoral neck makes with the acetabulum is called the angle of anteversion/ declination (see “Biomechanics” section). The normal range for femoral alignment in the transverse plane in adults is 10–15 degrees of anteversion, depending on the level of the acetabulum. The anteversion of the acetabulum and head of femur reduces the bony stability in the anterior hip joint.9 Increased anteversion is greater than 15 degrees, and relative retroversion occurs at less than 10 degrees. Absolute retroversion occurs at an angle less than 0 degrees. Typically, an infant is born with about 30 degrees of femoral anteversion. This angle usually decreases to 15 degrees by 6 years of age because of bone growth and increased muscle activity.4 In the frontal plane, the femoral neck lies at an angle to the shaft of the femur. This neck-shaft angle, or angle of inclination is normally 125–139 degrees in the adult population.10

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The joint capsule of the hip (Fig. 19-2), a substantial fibrous sleeve, attaches proximally to the pelvis just lateral to the acetabular labrum and extends laterally over the femoral head and neck to attach to the intertrochanteric line anteriorly. Posteriorly, the capsule attaches to the lateral one-third of the femoral neck allowing for the attachment of the obturator externus tendon in the posterior intertrochanteric fossa. The joint capsule is thicker anterosuperiorly, where maximal stress and weight bearing occurs, and thinnest posteroinferiorly. The joint capsule has three thickened regions that constitute the capsular ligaments. These anterior capsular thickenings, which have been studied extensively, include the iliofemoral ligament and the pubofemoral ligament. Despite these studies, the exact functions of each of these ligaments are still debatable. ▶▶

The iliofemoral ligament (Y ligament of Bigelow) (Fig. 19-2) is triangular in shape and consists of two parts: an inferior (medial) portion and a superior (lateral) portion making it resemble an inverted Y. The iliofemoral ligament is the strongest ligament in the body and reinforces the anterior aspect of the hip joint. The ligament, which attaches to the anterior inferior iliac spine

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ANATOMY

L4

Iliac crest

THE EXTREMITIES

Posterior superior iliac spine

Anterior superior iliac spine

Sacroiliac ligament Sacrum

Iliofemoral ligament

Greater sciatic foramen

Pubofemoral ligament

Sacrospinous ligament

Pubis

Ischial spine Sacrotuberous ligament Lesser sciatic foramen

Greater trochanter

Femur

Ischiofemoral ligament

FIGURE 19-2  The hip joint capsule. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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(AIIS) at its apex, is oriented superolaterally and blends with the iliopsoas muscle. The medial portion inserts into the inferior aspect of the trochanteric line while the lateral portion inserts onto the superior aspect of the trochanteric line. By limiting the range of hip extension, this ligament, with the assistance of the pubofemoral ligament, allows maintenance of the upright posture and reduces the need for contraction of the hip extensors in a balanced stance. The ligament exhibits the greater stiffness and prevents anterior translation during extension and external rotation,11 in both flexion and extension.12 Myers et al.13 reported that the iliofemoral ligament significantly limited external rotation and anterior translation of the femoral head and was supported by the labrum acting as a secondary stabilizer.1 Hip adduction tightens the superior portion of the iliofemoral ligament. ▶▶ The pubofemoral ligament (Fig. 19-2) blends with the inferior band of the iliofemoral, and with the pectineus muscle. The orientation of the pubofemoral ligament is more inferior-medial. The ligament attaches medially to the iliopectineal eminence, the superior pubic ramus, and the obturator crest and membrane, and laterally to the anterior surface of the trochanteric line. Its fibers tighten in extension, as with the other hip ligaments, and

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also tighten in external rotation12 and reinforce the joint capsule along the medial surface. ▶▶ The ischiofemoral ligament, which accounts for the posterior thickening of the capsule (Fig. 19-2), winds posteriorly around the femur and attaches anteriorly, strengthening the capsule. This ligament, which tightens with internal rotation of the hip in flexion and extension, as well as adduction of the flexed hip, is more commonly injured than the other hip ligaments. All of these capsular thickenings/ligaments are taut in hip extension, especially the inferior portion of the iliofemoral ligament. Conversely, all the ligaments are relaxed in hip flexion. Because of their inherent strength, the hip ligaments are only usually compromised with severe macrotrauma involving a fracture/dislocation of the hip. The transverse acetabular ligament traverses the acetabular notch, connecting the anterior and posterior labral edges. Collagen fibers from the deepest layer of labral tissues blend into this ligament. The ligament is placed on tensile load during weight bearing when the head of the femur relocates in the acetabulum and widens the acetabular notch. The ligamentum teres, or capitis femoris ligament (Fig. 19-3), an embryonic remnant, is a structure seen only in the hip joint.4

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Joint capsule Iliac crest

Ligament of head of femur Acetabular fossa

Synovial membrane

Ischial spine

ANATOMY

Acetabular labrum

Obturator a.

Sacroiliac joint

Head of femur Neck of femur Zona orbicularis Medial circumflex femoral a.

Hip Joint Complex

Acetabular roof

Greater trochanter Lesser trochanter

FIGURE 19-3  The hip joint. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

This intra-articular ligament spans the hip joint running from the edges of the acetabular notch to the fovea capitis of the femur, attaching the femoral head to the inferior acetabular rim. The ligament is entirely enclosed by a synovial membrane, which forms a sheath around the ligament. Within this sheath, nerves and vessels pass to the femoral head. The ligamentum teres has a rich supply of mechanoreceptors and due to its attachment to the transverse acetabular ligament, becomes taut in weight bearing, suggesting a proprioceptive role, especially in weight-bearing activities.14,15 The blood vessels provide an important source of arterial blood from a tiny posterior branch of the internal iliac artery during femoral head vascular development. Although this arterial supply is a significant source of blood to the femoral head in infants and children,16 it becomes less significant in adulthood, because of collateral circulation from the circumflex arteries (see “Vascular Supply” section) surrounding the femoral neck, although chronic interruption the blood supply to the femoral head has been associated with osteonecrosis and degenerative arthritis.

CLINICAL PEARL Patients with ligamentum teres injuries may complain of deep posterior hip joint pain with hip flexion activities.17 Though traditionally thought to play a minimal role in joint function, more recent findings suggest that the ligamentum teres may play a number of key roles in stabilization.14,18–20 It

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would appear that the ligamentum teres can function analogous to the anterior cruciate ligament as a stabilizer against subluxation of the hip, particularly when the hip is externally rotated in flexion or internally rotated in extension.21 Although not a major stabilizer, a patient with a tear of the ligamentum teres may develop hip microinstability which, when combined with recreational and sports activities, may result in damage to the labrum and cartilage.22 In addition, the ligamentum teres forms a sling-like structure that supports the femoral head inferiorly as the hip goes into flexion and abduction (i.e., squat).1 The ligament tightens during adduction, flexion, and external rotation, and it can become injured during subluxation.23

Acetabular Labrum The acetabular labrum (Fig. 19-3) is a semicircular ring consisting of fibrocartilage and dense connective tissue24 that encases the femoral head and is attached to the acetabular margin. The labrum, which varies greatly in form and thickness, has a triangular cross section: an internal articular surface, an external surface contacting the joint capsule, and a basal surface attached to the acetabular bone and transverse ligaments.4 Most of the labrum is composed of thick, type I collagen fiber bundles principally arranged parallel to the acetabular rim, with some fibers scattered throughout this layer running obliquely to the predominant fiber orientation.25 The normal microvasculature of the acetabular labrum consists of a group of small vessels located in the

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ANATOMY THE EXTREMITIES

substance of the labrum traveling circumferentially around the labrum at its attachment site on the outer surface of the bony acetabular extension.26 In addition, the labrum is surrounded by highly vascularized synovium that is present in the capsular recess.26 The central portion is contiguous with the cartilaginous surface of the acetabulum, and the periphery is continuous with the hip capsule.17 The majority of the acetabular labrum on the articular side is avascular except for the outer third. In addition, cadaver studies have shown it to contain sensory innervations with penetration only into the outer one-third of the substance of the labrum.24 Nerve-endings and sensory end organs in the superficial layers of the labrum participate in nociceptive and proprioceptive mechanisms.27,28 The acetabular labrum of the hip, to a large extent, is analogous to the meniscus of the knee (see Chapter 20) and the labrum of the glenohumeral joint (see Chapter 16) in that it enhances joint stability by deepening the socket by 21%,29 and decreases the forces transmitted to the articular cartilage, by absorbing up to 28% of hip joint forces.29,30 The osseous acetabulum in the hip also provides substantial static stability to the hip joint. Deepening of the socket that is provided by the labrum would, therefore, appear to be less important at the hip. In addition, the labrum functions as a force distributor and shock absorber.17 Another proposed function of the labrum is to improve the mobility of the hip by providing an elastic alternative to the bony rim.

CLINICAL PEARL Injuries to the acetabular labrum can occur through a variety of mechanisms1: ▶▶ The posterior aspect of the labrum undergoes the greatest circumferential strain, with peak force in hip flexion. ▶▶ The anterior aspect of the labrum undergoes the greatest force in combined hip flexion and adduction.

Muscles

830

The hip joint is surrounded by a wide variety of muscles that accelerate, decelerate, and stabilize the hip joint by providing dynamic and passive resistance to external forces that may contribute to excessive motion. Indeed 21 muscles cross the hip, providing both triplanar movement and stability between the femur and the acetabulum.31 Consequently, abnormal performance of the muscles of the hip may alter the distribution of forces across the joint articular surfaces, potentially causing, or at least predisposing, degenerative changes in the articular cartilage, bone, and surrounding connective tissues.31 The origin, insertion, and innervation of these muscles are outlined in Table 19-3. The primary stabilizers of the hip include the quadratus femoris, obturator internus, inferior and superior gemelli, and adductor brevis and pectineus.32 Since the hip joint is able to move through a wide range of motion (ROM), the line of pull of the hip muscles may be altered with changing hip position, which makes describing a muscle’s action difficult. For example, the orientation of the gluteus medius allows it to work as an internal rotator in hip flexion yet as a weak external rotator in hip

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extension.4 Similarly, the tensor fascia latae (TFL) is a hip abductor and flexor, depending upon the hip position, while being a weak internal rotator in all positions.31 The hip muscles and their respective actions are outlined in Tables 19-3 and 19-4. The hip muscles and their respective actions are outlined in Tables 19-3 and 19-4.

CLINICAL PEARL The soft tissue structures around the hip are most resistant to distraction of the hip joint in the lateral and inferior directions,33 which indicate the importance of the capsule and the labrum to joint stability.1

Iliopsoas The iliopsoas muscle, formed by the iliacus and psoas major muscles (see Fig. 19-4), is the most powerful hip flexor while also functioning as a weak adductor and external rotator of the hip. The iliopsoas attaches to the hip joint capsule, thereby giving it some support anteriorly. Since the muscle spans both the axial and appendicular components of the skeleton, it also functions as a trunk flexor, and affords an important element of the vertical stability of the lumbar spine, especially when the hip is in full extension, and passive tension is greatest in the muscle.31,34 Functionally, the hip flexors assist with foot clearance during level ambulation and stair negotiation. Theoretically, a sufficiently strong and isolated bilateral contraction of any hip flexor muscle will either rotate the femur toward the pelvis, the pelvis (and possibly the trunk) toward the femur, or both actions simultaneously.31 Intermuscular cooperation between the iliopsoas group and the rectus abdominis to prevent an anterior tilt and reinforce a neutral pelvis is fundamental to creating a stable proximal platform of the lumbopelvic region for effective therapeutic exercise.31

Iliocapsularis The iliocapsularis muscle is a lesser-known structure that originates from the anterior medial hip capsule and inserts just distal to the lesser trochanter so that it overlies the anterior hip capsule. Its function is to help stabilize and tighten the anterior hip capsule.35 The iliocapsularis muscle has been found to be significantly hypertrophied in dysplastic hips versus normal hips.36

Tensor Fascia Latae The TFL arises from the anterior aspect of the outer lip of the iliac crest and the lateral surface of the ASIS, and part of the lateral border of the notch below it (see Fig. 19-5). As it passes inferiorly, the TFL envelops the muscles of the thigh. The trochanteric bursa is found deep to this muscle, as it passes over the greater trochanter (see later).37 The TFL, which flexes, abducts, and externally rotates the hip, also serves to counteract the backward pull of the gluteus maximus on the iliotibial band (ITB). The attachment of the TFL via the ITB to the anterolateral tibia provides a flexion moment in knee flexion and an extension moment in knee extension. The anteromedial fibers of the TFL have been shown to be increasingly active during jogging, running, and sprinting.1 This is theorized to be because of its role in assisting decelerating hip extension and accelerating hip flexion.

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Origin, Insertion, and Innervation of Muscles Acting Across the Hip Joint Origin

Insertion

Innervation

Adductor brevis

External aspect of the body and inferior ramus of the pubis

The line from the greater trochanter of the linea aspera of the femur

Obturator nerve

Adductor longus

In angle between pubic crest and symphysis

The middle third of the linea aspera of Obturator nerve the femur

Adductor magnus

Inferior ramus of pubis, ramus of ischium, and the inferolateral aspect of the ischial tuberosity

To the linea aspera and adductor tubercle of the femur

Obturator nerve and tibial portion of the sciatic nerve

Biceps femoris

Long head arises from the sacrotuberous ligament and posterior aspect of the ischial tuberosity. Short head does not act across the hip

On the lateral aspect of the head of the fibula, the lateral condyle of the tibial tuberosity, the lateral collateral ligament, and the deep fascia of the leg

Tibial portion of the sciatic nerve, S1

Gemelli (superior and inferior)

Superior-posterior (dorsal) surface of the spine of the ischium and inferior-upper part of the tuberosity of the ischium

Superior- and inferior-medial surface of the greater trochanter

Sacral plexus

Gluteus maximus

Posterior gluteal line of the ilium, iliac crest, aponeurosis of the erector spinae, posterior (dorsal) surface of the lower part of the sacrum, side of the coccyx, sacrotuberous ligament, and intermuscular fascia

Iliotibial tract of the fascia latae and gluteal tuberosity of the femur

Inferior gluteal nerve

Gluteus medius

Outer surface of the ilium between the iliac crest and the posterior gluteal line, anterior gluteal line, and fascia

Lateral surface of the greater trochanter

Superior gluteal nerve

Gluteus minimus

Outer surface of the ilium between the anterior and On the anterior surface of the greater inferior gluteal lines, and the margin trochanter of the greater sciatic notch

Superior gluteal nerve

Gracilis

The body and inferior ramus of the pubis

The superior medial surface of the proximal tibia, just proximal to the tendon of the semitendinosus

Obturator nerve

Iliacus

Superior two-thirds of the iliac fossa and upper surface of the lateral part of the sacrum

Fibers converge with tendon of the psoas major to lesser trochanter

Femoral nerve

Obturator externus

Rami of the pubis, ramus of the ischium, and medial two-thirds of the outer surface of the obturator membrane

Trochanteric fossa of the femur

Obturator nerve

Obturator internus

Internal surface of the anterolateral wall of the pelvis and obturator membrane

Medial surface of the greater trochanter

Sacral plexus

Pectineus

Pectineal line

Along a line extending from the lesser Femoral or obturator trochanter to the linea aspera or accessory obturator nerves

Piriformis

Pelvic surface of the sacrum, gluteal surface of the ilium, capsule of the sacroiliac joint, and sacrotuberous ligament

Upper border of the greater trochanter of femur

Sacral plexus

Psoas major

Transverse processes of all the lumbar vertebrae bodies and intervertebral disks of the lumbar vertebrae

Lesser trochanter of the femur

Lumbar plexus

Quadratus femoris

Ischial body next to the ischial tuberosity

Quadrate tubercle on femur

Nerve to quadratus femoris

Rectus femoris

By two heads, from the anterior inferior iliac spine, and a reflected head from the groove above the acetabulum

Upper border of the patella

Femoral nerve

(Continued)

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Hip Joint Complex

Muscle

ANATOMY

TABLE 19-3

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ANATOMY

TABLE 19-3

Origin, Insertion, and Innervation of Muscles Acting Across the Hip Joint (Continued)

THE EXTREMITIES

Muscle

Origin

Insertion

Innervation

Sartorius

Anterior-superior iliac spine and notch below it

Upper part of the medial surface of the tibia in front of the gracilis

Femoral nerve

Semimembranosus

Ischial tuberosity

The posterior-medial aspect of the medial condyle of the tibia

Tibial nerve

Semitendinosus

Ischial tuberosity

Tibial nerve Upper part of the medial surface of the tibia behind the attachment of the sartonus and below that of the gracilis

Tensor fascia latae

Anterior part of outer lip of the iliac crest and the lateral surface of the anterior-superior iliac spine

Iliotibial tract

TABLE 19-4

Superior gluteal nerve

Hip Actions and Muscles If in Anatomic Position

Hip Action

Prime Movers

Assistant Movers

Flexors

Iliopsoas Sartorius Tensor fascia latae Rectus femoris Pectineus Adductor longus

Adductor brevis Gracilis Gluteus minimus (anterior fibers)

Extensors

Gluteus maximus Semitendinosus Semimembranosus Biceps femoris (long head) Adductor Magnus (posterior head)

Gluteus medius (middle and posterior fibers) Adductor magnus (anterior head)

Abductors

Gluteus medius (all fibers) Gluteus minimus (all fibers) Tensor fascia latae

Sartorius Rectus femoris Piriformis

Adductors

Adductor magnus (anterior and posterior heads) Adductor longus Adductor brevis Gracilis Pectineus

Biceps femoris (long head) Gluteus maximus (posterior fibers) Quadratus lumborum Obturator externus 

External rotators

Gluteus maximus Gemellus inferior Gemellus superior Obturator internus Quadratus femoris Piriformis (at less than 60 degrees hip flexion)

Gluteus medius (posterior fibers) Gluteus minimus (posterior fibers) Biceps femoris (long head) Sartorius Obturator externus Iliopsoas

Internal rotators

Not applicable

Semitendinosus Semimembranosus Gracilis Piriformis (at 90 degrees hip flexion) Gluteus medius (anterior fibers) Adductor longus Adductor brevis Pectineus Adductor Magnus (posterior head) Gluteus minimus (anterior fibers) Tensor fascia latae

Reproduced with permission from Neumann DA. Kinesiology of the hip: a focus on muscular actions. J Orthop Sports Phys Ther. 2010 Feb;40(2):82–94.

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Central tendon of the diaphragm Esophageal hiatus (T10) Muscular portion of the diaphragm

Inferior vena cava

ANATOMY

Caval hiatus (T8)

Esophagus

Aortic hiatus (T12)

Left crus

Right crus

Quadratus lumborum m. Psoas minor and major mm.

L3

Hip Joint Complex

Diaphragm

Abdominal aorta

Iliac crest

L5

Iliacus m.

Inguinal ligament

Iliopsoas m.

Lesser trochanter

FIGURE 19-4  Muscles of the anterior hip. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

CLINICAL PEARL The TFL and conjoined ITB must be closely monitored during therapeutic exercise as uncontrolled hip forces cause compressive bursa/tendinopathies at the greater trochanter and proximal lateral tibia when these two structures become overactive secondary to improper exercise selection and dosage.38

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Gluteus Maximus The gluteus maximus (Fig. 19-5) is the largest and most powerful hip extensor. It is also an important external rotator of the hip when the hip is in an anatomic neutral position.31 The larger, superficial portion of this muscle inserts into the proximal part of the ITB while the deep portion inserts into the gluteal tuberosity of the femur. The inferior gluteal nerve, which innervates the muscle, is located on the deep portion.

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ANATOMY

Iliac crest Anterior superior iliac spine Sacrum

Gluteus medius m. Tensor fasciae latae m.

THE EXTREMITIES

Gluteus maximus m. Adductor magnus m.

Semitendinosus m. Gracilis m.

Greater trochanter

Iliotibial tract Biceps femoris m. (long head)

to flex, and internally rotate the hip. The middle portion, the fibers of which are slightly obliquely oriented, abducts the hip. The posterior portion, the fibers of which are oriented almost parallel to the femoral neck, extends and externally rotates the hip while also stabilizing the femoral head in the acetabulum.1 On the deep surface of this muscle is located the superior gluteal nerve and the superior and inferior gluteal vessels. The gluteus medius (Fig. 19-5) is the primary source of dynamic stabilization of the hip joint in the frontal plane, making it critical for balancing the pelvis during single limb stance, which accounts for approximately 60% of the gait cycle (see Chapter 6).39 During single limb stance, approximately three times the body weight is transmitted to the hip joint with two-thirds of that being generated by the hip-abductor mechanism.39 In addition to its role as a stabilizer, the gluteus medius also functions as a decelerator of hip adduction.

Gluteus Minimus The gluteus minimus (Fig. 19-6), the major internal rotator of the femur, is a relatively thin muscle situated between the gluteus medius muscle and the external surface of the ilium. The gluteus minimus also abducts the thigh, as well as having a primary function as a joint stabilizer, creating compression through its attachment to the capsule.40 The ability to maintain joint centering to facilitate efficient joint mobility and decrease joint injury is an important function of this muscle

Semimembranosus m. Popliteal fossa

Gluteus medius m. (cut) Iliac crest

FIGURE 19-5  Superficial muscles of the posterior hip. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

The gluteus maximus is normally active only when the hip is in flexion, as during walking up an incline, stair climbing or cycling, or when extension of the hip is resisted.31 The superior portion of the gluteus maximus acts as a hip abductor during gait. Fibrous attachments over the sacroiliac joint (SIJ) from the gluteus maximus assist in trunk extension, control of lateral sway, and contribute to bipedal locomotion.38 The hip extensors as a group create the greatest amount of torque across the hip joint.1

Gluteus Medius

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Because of its shape and functional similarities, the gluteus medius is known as the deltoid of the hip and, like the deltoid muscle at the shoulder, the gluteus medius can be divided into three functional parts: an anterior portion, a middle portion, and a posterior portion, each of which are innervated by separate branches of the superior gluteal nerve.1 The anterior portion, the fibers of which are oriented the most vertical, works

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Gluteus maximus m. (cut) Superior and inferior gluteal nn., aa., and vv. Superior gemellus superior m. Obturator internus m. Inferior gemellus superior m. Sacrotuberous ligament Ischial tuberosity

Anterior superior iliac spine Gluteus minimus m. Tensor fasciae latae m. Piriformis m. Gluteus medius m. (cut)

Sciatic n. Quadratus femoris m. Gluteus maximus m. (cut) Adductor magnus m. Iliotibial tract

FIGURE 19-6  Deeper muscles of the posterior hip. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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Piriformis

Rectus Femoris The rectus femoris muscle (Fig. 19-7), one of the four quadriceps muscles (see Chapter 20), is a two-joint muscle that arises from two tendons: one, the anterior or direct, from the AIIS; the other, the posterior or indirect, from a groove above the brim of the acetabulum. The rectus femoris, which is a powerful hip flexor, also contributes to extension of the knee. It functions more effectively as a hip flexor when the knee is flexed, as when a person kicks a ball. During athletic function, the rectus femoris prevents excessive hip extension during gait.41

CLINICAL PEARL

L3

Psoas major m. Iliac crest Iliacus m.

L5

Inguinal ligament

Iliopsoas m.

Tensor fascia lata m. Pectineus m.

Hip Joint Complex

The piriformis (Fig. 19-6) is an external rotator of the hip at less than 60 degrees of hip flexion. At 90 degrees of hip flexion, the piriformis reverses its muscle action, becoming an internal rotator and abductor of the hip. Because of its close association with the sciatic nerve, the piriformis can be a common source of buttock and leg pain (see Chapter 5).

Quadratus lumborum m.

ANATOMY

in relation to pathological conditions related to joint instability, acetabular under coverage, and congenital anomalies.38 It receives support from the TFL, semitendinosus, semimembranosus, and gluteus medius.

Rectus femoris m.

Iliotibial tract

No muscle has the primary function of internally rotating the hip, but a number of muscles, including the anterior fibers of the gluteus medius, gluteus minimus, TFL, adductor longus, adductor brevis, pectineus, and the posterior head of the adductor magnus, have a secondary function of internal rotation.1

Obturator Internus

Vastus lateralis m.

Vastus medialis m.

The obturator internus (Fig. 19-6) is normally an external rotator of the hip and an internal rotator of the ilium but becomes an abductor of the hip at 90 degrees of hip flexion.31 Patella

Obturator Externus The obturator externus (Fig. 19-6), named for its location external to the pelvis, is an adductor and external rotator of the hip.

Patellar ligament

Gemelli The superior and inferior gemelli muscles (Fig. 19-6) are considered extensions of the obturator internus tendon. The superior gemellus is the smaller of the two. Both the gemelli function as minor external rotators of the hip.

Quadratus Femoris The quadratus femoris muscle (Fig. 19-6), another external rotator of the hip, is a flat, quadrilateral muscle, located between the inferior gemellus and the superior aspect of the adductor magnus. The quadratus femoris and the inferior gemellus share the same innervation (L4–L5). The obturator internus and superior gemellus also share the same innervation (L5–S1).

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FIGURE 19-7  Muscles of the anterior hip and thigh. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

CLINICAL PEARL In a manner generally similar to the infraspinatus and teres minor at the glenohumeral joint, the short external rotators of the hip also like to provide an important element of mechanical stability to the hip articulation by producing

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ANATOMY

compression of the hip joint.39 Interestingly, the popular posterior surgical approach to a total hip arthroplasty used by some surgeons necessarily cuts through at least part of the hips posterior capsule, potentially disrupting several of the short external rotators tendons.31 Studies have reported a significant reduction in the incidence of posterior hip dislocation when the surgeon carefully repairs the posterior capsule and external rotator tendons.31,42,43

THE EXTREMITIES

Pectineus The pectineus (see Fig. 19-7) is an adductor, flexor, and internal rotator of the hip. Like the iliopsoas, the pectineus attaches to and supports the joint capsule of the hip.

Ischial tuberosity

Semitendinosus m. Long head of biceps femoris m.

CLINICAL PEARL The hip external and internal rotators’ role in stabilization may become more crucial when the acetabular labrum is torn secondary to the subsequent loss of passive rotational stability.44

Semimembranosus m.

Short head of biceps femoris m.

Sartorius The sartorius muscle (see Fig. 19-7) is the longest muscle in the body. The sartorius is responsible for flexion, abduction, and external rotation of the hip, and some degree of knee flexion.

Hamstrings The hamstrings muscle group consists of the biceps femoris, the semimembranosus, and the semitendinosus.

836

Biceps Femoris.  The biceps femoris (see Fig. 19-8), which arises by way of a long and short head, extends the hip, flexes the knee, and externally rotates the tibia. Only the long head, which originates from the ischial tuberosity and lower part of the sacrotuberous ligament, acts on the hip. The short head arises from the lateral linea aspera, lateral supracondylar line, and intermuscular septum. The tibial portion of the sciatic nerve innervates the long head and the fibularis (peroneal) division innervates the short head The long head is active during conditions that require lower amounts of force, such as decelerating the limb at the end of the swing phase and during forceful hip extension.31 The biceps femoris is the most commonly strained muscle of the hamstring complex (53%).45 The anatomy of the biceps femoris may help to explain its higher rate of injury. Firstly, both the long and the short head have separate nerve supplies. This dual innervation may lead to asynchronous stimulation of the two heads— a mistimed contraction of the different parts of the muscle group may mean a reduced capacity to generate effective tension to control the imposed loads of the muscle.46 There may also be anatomical variations in the attachments of the biceps femoris, which may predispose certain people to injury. Due to the origin of the long head of the biceps femoris, it could be argued that the biceps femoris has a triarticular function and is, therefore, more predisposed to injury than the other hamstring muscles.46 The insertion of the biceps femoris into the head of the fibula may also be a predisposing factor to injury—previous knee or ankle injury resulting in alteration in the movement of the superior tibiofibular joint may

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Tibia

Head of fibula

FIGURE 19-8  The hamstrings. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

affect the biomechanics of the biceps femoris although this notion is speculative.46 However, incomplete knee excursion caused by meniscal damage may lead to excessive loading of the biceps femoris. In addition to the anatomical reasons, the biceps femoris is susceptible to high rates of injury as it is subjected to the greatest amount of eccentric load during high-speed activities such as sprinting.47 Given the rotational demands of many sports, this function may also predispose the biceps femoris to injury. Semimembranosus.  The semimembranosus (see Fig. 19-8) gains its name from its membranous origin at the ischial tuberosity beneath the semitendinosus and inserts onto the medial tibial condyle, posterior oblique ligament, arcuate ligament, and posterior joint capsule. The semimembranosus is innervated by the tibial division of the sciatic nerve. Semitendinosus.  The semitendinosus (see Fig. 19-8) arises from the ischial tuberosity by a conjoint tendon with the biceps femoris and inserts as part of the pes anserinus on the superior and medial aspect of the tibia, and deep fascia of the leg at Gerdy’s tubercle. The semitendinosus is innervated by the tibial division of the sciatic nerve.

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Increased anterior pelvic tilt has been linked to hamstring strains in runners, which is likely due to the increased tension on the muscle group, because of the lengthened position. A common cause for an increased anterior pelvic tilt is decreased mobility of the anterior capsule or decreased extensibility of the hip flexors.48 All three muscles of the hamstring complex (except for the short head of the biceps) work with the posterior adductor magnus and the gluteus maximus to extend the hip.49 The hamstrings also flex the knee and weakly adduct the hip. The long head of the biceps femoris helps with external rotation of the thigh and leg; the more medial semimembranosus and semitendinosus muscles assist with internal rotation of the thigh and leg.49 When the hamstrings contract, their forces are exerted on both the hip and knee joints simultaneously; functionally, however, they can actively mobilize only one of the two joints at any one time.49 During gait, prior to heel contact, the hamstrings decelerate the knee extensors and hip flexors to prepare for foot contact with the ground (see Chapter 6) and are active for the initial 10% of the stance phase to provide hip extension and stability to the knee through coactivation for dynamic stabilization.49 Compared to walking and

Hip Joint Complex

1. They decelerate knee extension at the end of the forward swing phase. Consequently, hamstring injuries are most likely to occur during the terminal swing phase of running, while contracting eccentrically and while the muscle is in the more lengthened position.50 Through an eccentric contraction, the hamstrings decelerate the forward momentum (i.e., leg swing) at approximately 30 degrees short of full knee extension. The length-tension relationship and changing moment arm of the hamstrings decreases torque production near full knee extension when the hip joint is in 90-degree flexion as in the seated position.51 2. At foot strike, the hamstrings elongate to facilitate hip extension through an eccentric contraction, thus further stabilizing the leg for weight bearing. 3. The hamstrings assist the gastrocnemius in paradoxically extending the knee during the takeoff phase of the running cycle.

ANATOMY

jogging, running is a stressful activity for the hamstrings and increases the high demands on their tendon attachments, especially during eccentric contractions. While running, the hamstrings have three main functions49:

CLINICAL PEARL

Hip Adductors The adductors of the hip (Fig. 19-9) are found on the medial aspect of the joint.

Iliopsoas m.

Obturator externus m.

Pubis

Pubis

Pectineus m.

Adductor brevis m. Adductor longus m.

Linea aspera

Adductor magnus m. (adductor division) Gracilis m.

Adductor hiatus

Adductor magnus m. (hamstring division)

Adductor tubercle

Tibia

A

B

FIGURE 19-9  The hip adductors. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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ANATOMY

Adductor Magnus.  The adductor magnus is the most powerful adductor, and it is active to varying degrees in all hip motions except abduction. In addition, the adductor magnus has the greatest moment arm for hip extension. The posterior portion of the adductor magnus is sometimes considered functionally as a hamstring because of its anatomic alignment. Because of its size, the adductor magnus is less likely to be injured than the other hip adductors.

THE EXTREMITIES

Adductor Longus. The pectineus and adductor longus muscles serve as primary adductors of the hip while contributing to hip flexion. The adductor longus is the most prominent muscle of the adductors during resisted adduction and forms the medial border of the femoral triangle. The adductor longus also assists with external rotation, in extension, and internal rotation in other positions. The adductor longus is the most commonly strained adductor muscle due to its limited mechanical advantage.52 This mechanical disadvantage is due to the large distance from the axis of rotation to the center of mass of the lower extremity, resulting in the requirement of a greater force production to achieve the intended movement.38 Gracilis.  The gracilis (see Fig. 19-9), the longest of the hip adductors, is also the most superficial and medial of the hip adductor muscles. The gracilis functions to adduct and flex the thigh and flex and internally rotate the leg. The other adductors of the hip include the adductor brevis, obturator externus, and the pectineus muscles. The main action of this muscle group is to adduct the thigh in the open kinetic chain and stabilize the lower extremity to perturbation in the closed kinetic chain. Each individual muscle can also provide assistance in femoral flexion and rotation.31

Bursa There are more than a dozen bursae in this region.53 The more clinically significant ones are described below.

Iliopsoas Bursa

838

Many names have been used to describe the iliopsoas bursa (IPB), including the iliopsoas, iliopectineal, iliac, iliofemoral, and subpsoas bursa. The IPB is the largest and most constant bursa about the hip, present in 98% of normal adult individuals, usually bilaterally.4 The IPB is situated deep to the iliopsoas tendon and serves to cushion the tendon from the structures on the anterior aspect of the hip joint capsule. Its dimensions may be up to 7 cm in length and 4 cm in width.4 Anatomic boundaries of the bursa include the iliopsoas muscle anteriorly, the pectineal eminence and the hip joint capsule posteriorly, the iliofemoral ligament laterally, and the acetabular labrum medially. As with other bursae, the IPB can become inflamed and distended. Inflammation and distension of this bursa are most commonly associated with rheumatoid arthritis, but it is also seen in association with athletic activity, overuse and impingement syndromes, osteoarthrosis, pigmented villonodular synovitis (PVNS), synovial chondromatosis, infection, pseudogout, metastatic bone disease, and, in rare cases, after total hip arthroplasty (THA) (see “Interventions” section).54

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Trochanteric Bursa Three bursae are consistently present at the greater trochanter, two major bursae, and one minor bursa. The two clinically significant trochanteric bursae are the subgluteus medius bursa, and the more superficial subgluteus maximus bursa: Subgluteus medius bursa: located at the superoposterior tip of the greater trochanter and functions to prevent friction between the gluteus medius muscle and the greater trochanter and also between the gluteus medius and gluteus minimus muscles. ▶▶ Subgluteus maximus bursa: located between the greater trochanter and the fibers of the gluteus maximus and TFL muscles as they blend into the ITB. ▶▶

Ischiogluteal Bursa The ischiogluteal bursa is located between the ischium and the gluteus maximus muscle. It can be painfully squeezed between the ischial tuberosity and the hard surface of a chair while sitting, producing ischial bursitis. This condition is often referred to as weaver’s bottom.

Femoral Triangle For topographic reasons, it is important to have an understanding of the anatomy of the femoral triangle. The femoral triangle is defined superiorly by the inguinal ligament, medially by the adductor longus, and laterally by the sartorius (Fig. 19-10). The floor of the triangle is formed by portions of the iliopsoas on the lateral side and by the pectineus on the medial side (Fig. 19-10). A number of neurovascular structures pass through this triangle. These include (from medial to lateral) the femoral vein, artery, and nerve (Fig. 19-10). Thus, the clinician should use caution when palpating in this area or applying soft tissue techniques.

Iliacus m. Anterior superior iliac spine

Psoas m.

Inguinal ligament

Femoral sheath and canal

Lateral cutaneous nerve of thigh Iliopsoas m. Sartorius m. (cut )

Femoral: Nerve Artery Vein Lymphatics Pubis Pectineus m. (cut) Femoral triangle Adductor longus m.

FIGURE 19-10  The femoral triangle. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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Vascular Supply The internal iliac artery becomes the femoral artery (Figs. 19-12B and 19-13), as it passes underneath the inguinal ligament. The femoral artery forms two branches. The anterior portion of the femoral neck and the anterior portion of the capsule of the hip joint are supplied by the lateral femoral circumflex artery. The medial femoral circumflex artery (MFCA) perforates and supplies the posterior hip joint capsule and the synovium.4 The deep branch of the MFCA gives rise to two to four superior retinacular vessels and, occasionally, to inferior retinacular vessels.4 Most of the femoral head, comprising its upper one-half or upper two-thirds, is supplied by the obturator artery and a terminal branch of the MFCA (Fig. 19-3).4 The inferior epiphyseal artery, a branch of the lateral circumflex artery, contributes to the vascularization of the lower area of the femoral head. The supply to the femoral head from the ligamentum teres artery is extremely variable.56 The blood supply to the weight-bearing portion of the head of the femur is derived from the MFCA.57 Two other branches are formed from the internal iliac artery: the inferior and superior gluteal arteries. These arteries supply the superior portion of the capsule and the gluteus maximus muscle.

BIOMECHANICS The hip joint has three degrees of freedom, which permit motion in three planes: sagittal (flexion and extension around a transverse axis), frontal (abduction and adduction around

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Hip Joint Complex

The hip joint is innervated primarily by L3 but also has contributions from L1–S1.1 In addition, many nerves have contributions to the hip including the iliohypogastric, ilioinguinal, genitofemoral, lateral cutaneous nerve of the thigh, obturator, and femoral nerves.1 The posterior gluteal region receives cutaneous innervation by way of the subcostal nerve; the iliohypogastric nerve; the posterior (dorsal) rami of L1, L2, and L3; and the posterior (dorsal) primary rami (cluneal nerves) of S1, S2, and S3 (Figs. 19-11, and 19-12A). The anterior region of the hip has its cutaneous supply divided by the inguinal ligament. The area superior to the ligament is supplied by the iliohypogastric nerve. The area inferior to the ligament is supplied by the subcostal nerve, the femoral branch of the genitofemoral nerve, and the ilioinguinal nerve (see Chapter 3). The nerves of the muscles that cross the hip joint (femoral, obturator, superior gluteal, and the nerve to the quadratus femoris) also supply the joint capsule and the joint. Therefore, pain referred from the hip joint may be felt anywhere in the thigh, leg, or foot. Arthrogenic inhibition, defined as the reflex inhibition of the musculature surrounding the joint following effusion or injury, and which also occurs at the knee joint, is evident in the hip joint.55

an anteroposterior axis), and transverse (internal and external rotation around a vertical axis) (Fig. 19-14). All three of these axes pass through the center of the femoral head. The normal motion of the hip joint is primarily rotational, and there is very little translation.58 Control of the hip during movement involves complex interactions between the nervous, muscular, and skeletal systems. Motion at the hip joint can occur through movement of the femur on the pelvis or from the motion of the pelvis on the femur (i.e., anterior or posterior pelvic tilt). The 27 muscles that cross the hip joint act as primary movers and dynamic stabilizers of the hip and lower extremity.59 These muscles provide a myriad of possibilities for compensation and pathology.1 For example, abnormal hip mechanics can result in gluteus medius tendinosis, hip flexor tendinopathy, TFL strain, hamstring tendinopathy, and ITB syndrome. Musculoskeletal disorders of the lower limbs are often associated with poor hip muscle performance and altered kinematics during dynamic weight-bearing tasks, such as running. For example, patellofemoral pain and Achilles pathology have both been linked to hip dysfunction.60 Active range of motion (AROM) of the hip is variable. Hip flexion averages 110–120 degrees, extension 10–15 degrees, abduction 30–50 degrees, and adduction 25–30 degrees. Hip external rotation averages 40–60 degrees and internal rotation averages 30–40 degrees (Table 19-5). Motions about the hip joint can occur independently; however, the extremes of motion require motion at the pelvis.

BIOMECHANICS

Neurology

CLINICAL PEARL End-range hip flexion is associated with a posterior rotation of the innominate bone. The end-range of hip extension is associated with an anterior rotation of the innominate. Hip abduction/adduction is associated with an upward/ downward tilting of the pelvis (see Table 19-6). The hip joint is a marvel of physics, transmitting truly impressive loads, both tensile and compressive making it the fulcrum for all of the forces. Quantitative and qualitative analysis of the generation of compressive forces at the hip and the muscular mechanisms during weight bearing have been thoroughly documented. Depending on the length of the moment arm created by the abductor muscles, the added force of the hip abductors acting on the hip joint can increase the pressures translated across the joint. During ambulation, these compressive joint forces are further multiplied by ground reaction forces and inertial forces related to acceleration and deceleration of the lower limb. Because of muscle tension, compression on the hip is approximately the same as body weight during the swing phase. However, during the support phase, peak joint forces can range from 300% to 400% of body weight at normal walking speed, to 550% of body weight during fast walking and jogging, and as high as 870% of body weight during stumbling.31 Stair climbing and descending increase the loads on the hip by approximately 10% and 20%, respectively.31 When body weight is evenly distributed across both legs during upright standing, the forces acting on the hip joint are

839

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BIOMECHANICS

T12 L1

Subcostal n.

L2 Iliohypogastric n. Ilioinguinal n. L3

THE EXTREMITIES

L4 Lumbosacral trunk L5

Genitofemoral n.

Lumbar plexus

Lateral femoral cutaneous n. Femoral n. Obturator n.

S1 S2

Superior gluteal n.

S3

Inferior gluteal n.

S4

Common fibular n.

S5 Co1

Tibial n. Sciatic n.

Sacral plexus

Posterior femoral cutaneous n. Pudendal n.

A

Coccygeal n.

Tensor fascia lata m. Gluteus maximus m. (cut)

Gluteus minimus m. Superior gluteal n., a., and v.

Pudendal n.

Inferior gluteal n. Nerve to obturator internus and superior gemellus mm.

Gluteus medius m. (cut) Piriformis m.

Perforating cutaneous n. (piercing the sacrotuberous ligament) Inferior rectal n.

Sciatic n.

Posterior femoral cutaneous n.

Common fibular n.

Tibial n. Gluteus maximus m. (cut)

B FIGURE 19-11  Neurology and vasculature of the posterior hip. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

840

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BIOMECHANICS

T12 L1 Subcostal n.

Iliohypogastric n. Ilioinguinal n. Genitofemoral n.

Sartorius m. (cut)

Femoral n. Lateral cutaneous n. of thigh

Gracilis m.

Sciatic n.

Anterior obturator n.

Femoral n.

Anterior and medial cutaneous nn. of thigh Muscular branches Saphenous n.

Anterior compartment of thigh

Posterior obturator n. Anterior branch

Obturator n.

Posterior branch

Vastus lateralis m. Vastus intermedius m. Vastus medialis m.

Medial compartment of thigh

A

Hip Joint Complex

L5

Obturator n.

Femoral: Nerve Artery Vein Lymphatics

Rectus femoris m. (cut)

Adductor canal with femoral a. and v. and saphenous n. Adductor hiatus Saphenous n.

B

FIGURE 19-12  Neurology and vasculature of the anterior hip. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

equivalent to half the partial weight made up of the trunk, head, and upper extremities. Were this partial body weight to represent 60% of total body mass, then each hip would be compressed by a force equal to 30% of the total body weight. In a single-limb support, however, shifts in the center of gravity away from the supporting limb dramatically change the equilibrium forces necessary to maintain balance and create a state of disequilibrium. This state of disequilibrium requires the generation of compensatory forces by the hip musculature, in order to maintain balance. When pain accompanies degeneration of the hip joint articulation, the body compensates by attempting to reduce the forces generated on the articular surfaces. Since the contribution of body mass cannot be changed, the patient

Dutton_Ch19_p0824-p0921.indd 841

attempts to reduce joint pressures by shifting the upper trunk over the supporting limb during the stance phase. While this maneuver decreases the joint compression forces, the energy expended by laterally bending the trunk during stance significantly increases the energy cost of gait. For a patient with a painful hip, the use of a cane or crutch in the hand contralateral to the involved hip can be used to substantially reduce the excessive trunk motion and to decrease pressure on the hip joint. The relationship between the proximal femur, the greater trochanter, and the overall femoral neck width is affected by muscle pull and the forces transmitted across the hip joint. In addition, normal joint nutrition, circulation, and muscle tone during development play an important role.

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BIOMECHANICS

Internal iliac a. Lateral femoral circumflex artery branches: Ascending

THE EXTREMITIES

Transverse Descending

Femoral a. Medial femoral circumflex a. Deep femoral a.

Adductor longus m.

Perforating branches

Femoral a.

Adductor magnus m.

Superior lateral genicular a.

Adductor hiatus

Popliteal a.

Superior medial genicular a.

Inferior lateral genicular a.

Inferior medial genicular a.

FIGURE 19-13 Vasculature of the hip and thigh. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

842

In the anatomic position, the orientation of the femoral head causes the contact force between the femur and the acetabulum to be high in the anterosuperior region of the joint. Since the anterior aspect of the femoral head is somewhat exposed in this position; the joint has more flexibility in flexion than extension. The femoral neck is subjected to shearing and torsional strains because of its oblique orientation to the shaft of the femur. Downward forces act to displace the femoral head inferiorly and to bend the femoral neck downward. To counter these forces, the femoral neck has developed a unique system of obliquely oriented trabeculae that traverse the head and the neck. The angle between the femoral shaft and the

Dutton_Ch19_p0824-p0921.indd 842

neck is called the angle of inclination (Fig. 19-15) and is normally approximately 125 degrees (Fig. 19-15) although it can vary with body types. In a tall person, the angle of inclination is larger. The opposite is true with a shorter individual. The angle of inclination has an important influence on the hips. An increase in this angle causes the femoral head to be directed more superiorly in the acetabulum and is often referred to as coxa valga (Fig. 19-15). Coxa valga has the following effects at the hip joint: It alters the orientation of the joint reaction force (JRF) from the normal vertical direction to one that is almost parallel to the femoral shaft. This lateral shift of the JRF reduces the available weight-bearing surface, resulting in an increase in stress applied across joint surfaces not specialized to sustain such loads. ▶▶ The moment arm of the hip abductors is shortened, placing these muscles in a position of mechanical disadvantage. This causes the abductors to contract more vigorously to stabilize the pelvis, producing an increase in the JRF. ▶▶ It increases the overall length of the lower extremity, impacting other components in the kinetic chain. For example, coxa valga decreases the normal physiologic angle at the knee, which places an increased mechanical stress on the medial aspect of the knee joint and more tensile stress on the lateral aspect of the joint. ▶▶

If the angle of inclination is reduced, resulting in a more horizontal orientation of the femoral neck, it is referred to as coxa vara (Fig. 19-15). This position increases the downward shear forces on the femoral head and the tensile stretching forces through the superior trabecular bone along the lateral portion of the neck. In coxa vara, the joint compression forces are significantly reduced as the greater trochanter is displaced lateral and superior, which increases the effective angle of pull and the lever arm of the hip abductors. While the reduced compressive forces generated across the joint surfaces serve to decrease the incidence of articular cartilage damage, the increase in shearing and torsional forces at the femoral head/ neck junction significantly increases the incidence of damage to the epiphyseal plate. Femoral alignment in the transverse plane also influences the mechanics of the hip joint. The torsion angle of the femur describes the relative rotation that exists between the shaft and the neck of the femur. An anterior orientation of the femoral neck to the transverse axis of the femoral condyles is known as anteversion (Fig. 19-16), or a reverse orientation known as retroversion. Excessive anteversion directs the femoral head toward the anterior aspect of the acetabulum when the femoral condyles are aligned in their normal orientation. Subjects with excessive anteversion usually have more hip internal rotation ROM than external rotation, resulting in an in-toeing gait pattern, and a gravitation toward the typical “frog-sitting” posture as a position of comfort. Some studies have supported the hypothesis that a persistent increase in femoral anteversion predisposes to osteoarthritis (OA) of the hip, and knee. Nyland et al.61 demonstrated that those with increased femoral anteversion had significantly decreased

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BIOMECHANICS

Hip adduction

Hip extension

Hip flexion

Medial hip rotation Lateral hip rotation

FIGURE 19-14  Movements of the hip. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

peak electromyographic (EMG) amplitude of the vastus medialis and gluteus medius which they postulated might lead to an increased risk of knee injury due to a decrease in frontal and transverse plane stability.61 A cadaveric study by Sobczak et al.62 found that anteversion decreased the moment arm of the medial musculature including the gracilis and the semitendinosus, whereas retroversion increased the moment arm of the same muscles. Excessive retroversion of the femur will result in the opposite limitation: increased femoral external rotation ROM and decreased femoral internal rotation ROM.22 Retroversion is associated with an out-toeing gait pattern. In contrast with most other joints in the body, the closepacked position for the hip is not the position of maximal articular congruency. The position of maximum articular congruence corresponds to a quadruped position: 90 degrees flexed, slightly abducted, and externally rotated. The most stable functional position of the hip is the normal standing

TABLE 19-5 Motion Flexion

Normal Ranges and End-Feels at the Hip Range of Motion (Degrees) End-Feel 110–120

Tissue approximation or tissue stretch

Extension

10–15

Tissue stretch

Abduction

30–50

Tissue stretch

Adduction

25–30

Tissue approximation or tissue stretch

External rotation

40–60

Tissue stretch

Internal rotation

30–40

Tissue stretch

Data from Malone TR, McPoil T, Nitz A. Orthopaedic and Sports Physical Therapy, 3rd ed. St. Louis, MO: CV Mosby; 1996.

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Hip Joint Complex

Hip abduction

position: hip extension, slight abduction, and slight internal rotation, which closely resembles the close-packed position of full extension, internal rotation, and abduction. The commonly cited open-packed (resting) positions of the hip are between 10 and 30 degrees of flexion, 10–30 degrees of abduction, and 0–5 degrees of external rotation.

CLINICAL PEARL Rapid flexion of the hip is generally associated with abdominal muscle activation that slightly precedes the activation of the hip flexor muscles.31 This anticipatory activation may reflect a feedforward mechanism intended to stabilize the lumbopelvic region by increasing intra-abdominal pressure and increasing the tension in the thoracolumbar fascia.31,63,64 Without sufficient stabilization of the pelvis by the abdominal muscles, a strong contraction of the hip flexor muscles may inadvertently tilt the pelvis anteriorly, thereby accentuated lumbar lordosis which may contribute to low back pain in some individuals.31 Bending forward at the waist requires a coordinated sequence of movements between the lumbar spine, pelvis, and hips referred to as the lumbopelvic rhythm. As the head and the upper trunk initiate flexion, the pelvis shifts posteriorly to



TABLE 19-6

 ip Motion and Associated Innominate H Motions

Flexion (posterior rotation) Extension (anterior rotation) Abduction (upward) Adduction (downward) Internal rotation External rotation

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BIOMECHANICS 125°

THE EXTREMITIES

A

115°

B

Normal

140°

C

Coxa vara

Coxa valga

FIGURE 19-15  Angle of inclination and coxa vara/valga.

15°

A

Retroversion

maintain the center of gravity over the base of support. The trunk continues to forward bend, being eccentrically controlled by the extensor muscles of the spine, until approximately 45 degrees at which point the posterior ligaments of the spine become taut, and the facets of the zygapophyseal joints approximate. Once all of the vertebral segments are at the end of the range and stabilized by the posterior ligaments and facets, the pelvis begins to rotate forward (anterior pelvic tilt), being controlled eccentrically by the gluteus maximus and hamstring muscles. The pelvis continues to rotate forward until the full length of the muscles is reached. The return to the upright position begins with the hip extensor muscles rotating the pelvis posteriorly through reverse muscle action, then the back extensor muscles extending the spine from the lumbar region upward.

Functional Relationships of the Lower Kinetic Chain Motions and positions at the hip during weight bearing can affect the alignment and function of the distal joints. Hip flexion.  Hip flexion results in knee flexion and ankle dorsiflexion. ▶▶ Hip extension.  Hip extension causes knee extension and ankle dorsiflexion. ▶▶ Hip rotation.  Internal rotation of the hip results in the femur rotating medially on a fixed tibia at the knee, pronation of the foot and eversion of the calcaneus. The reverse occurs with external rotation of the hip. ▶▶

35°

B

Anteversion

5°

C 844

Normal

FIGURE 19-16  Angle of torsion: Anteversion and retroversion.

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Altered pelvic-femoral biomechanics resulting from deficits in hip muscle performance has been linked to numerous lower extremity conditions.65–67 The hip extensor muscles, as a group, produce the greatest torque across the hip of any of the muscle groups. This extensor torque is often used to rapidly accelerate the body upward and forward from a position of hip flexion, such as when pushing off into a sprint, arising from a deep squat, or climbing a very steep hill.31 Furthermore, with the hip markedly flexed, many of the adductor

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CLINICAL PEARL

Rectus abdominis

Taut iliofemoral ligament

Hamstring muscle

FIGURE 19-17  Force couples at the hip.

muscles produce an extensor torque, thereby assisting the primary hip extensors. In a standing position, weakness of the hip extensors causes the pelvis to fall forward.68 With the trunk held relatively stationary, contraction of the hip extensors and abdominal muscles (with the exception of the transversus abdominis) functions as a force couple to posteriorly tilt the pelvis (Fig. 19-17).31 Assuming the trunk remains upright during this action, the lumbar spine must flex slightly, thereby reducing its natural lordotic posture.31 During the stance phase of activities such as walking, running, or hopping, the hip extensors and abductors play a complex role in the control of the lower extremities, pelvis, and trunk.69 This includes deceleration of hip internal rotation and adduction70 and maintenance of the equilibrium of the pelvis and trunk over the stance limb.69 As body weight is dropped onto the forward limb, the extensor muscles contract sharply to preserve upright stance by resisting the forward fall of the pelvis and the trunk.68 The hip’s flexed position, before attaining the passive stability provided by full extension in midstance, creates the demand (see Chapter 6). The most frequent demands placed on the hip abductors occur while walking during the single-limb support phase of walking.31 The external (gravitational) abduction torque about the hip dramatically increases within the frontal plane as soon as the contralateral limb leaves the ground.71 The hip abductors respond by generating an abduction torque about the stance hip that stabilizes the pelvis relative to the femur.71 In addition, the hip abductors can hike the hip when working concentrically, and can lower the pelvis when working eccentrically.

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The biomechanical demands of the hip muscles during running have been principally inferred from analysis of the relative timing and coordination of motion between joint or segments, joint moments, and powers.73 Adaptations in patterns of joint or segmental coordination have the potential to alter joint loading during the stance phase of dynamic activities, and, therefore, may also be associated with the development of lower limb pathologies.69 Determining muscle function during running is fraught with problems as many hip muscles have moment arms about more than one axis,31 and the length of the moment arm typically changes as a function of joint position. For example, the ability of the gluteus maximus to externally rotate the hip decreases with increased hip flexion.

Hip Joint Complex

Gluteus maximus

Increasing running step rate for a given running speed, which conversely reduces step length, has been advocated as a rehabilitation strategy to reduce hip joint loads for those with running-related injuries,72 thereby promoting recovery and reducing reinjury risk73: ▶▶ Increasing the running step rate heightens hamstring and gluteus maximus muscle loading in late swing ▶▶ After foot strike, an increased step rate results in a more erect limb posture,72 which lessens the hip muscle forces and powers needed in the load response phase of stance. This decreased loading is particularly evident in the gluteal muscles and piriformis which are muscles often implicated in running injuries.74,75

BIOMECHANICS

External oblique muscles

CLINICAL PEARL Bartlett et al.76 analyzed the activity and functions of the human gluteal muscle during walking, running, sprinting, and climbing. The study demonstrated that gluteus maximus activity was greatest during sprinting. Running and climbing produced similar levels of intensity to each other, both of which were greater than that of walking. Intriguingly, only the inferior portion of the gluteus maximus muscle had a significant change in the altered trunk pitch angles associated with walking and running, which might suggest that the hip extensors play a limited role in controlling the trunk pitch demands while running. The conclusions from this study would tend to indicate that the large size of the gluteus maximus reflects its multifaceted role during explosive movements as opposed to specifically adapting for submaximal tasks such as endurance running. The functional potential of the entire external rotator muscle group at the hip is most fully recognized while performing pelvic and trunk rotation activities while bearing weight on one limb. For example, with the right femur held relatively fixed, contraction of the external rotators would rotate the pelvis and the attached trunk to the left. This action of planting the limb and cutting to the opposite side is a natural way to abruptly change direction while running.31 The gluteus maximus appears uniquely designed to perform this

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EXAMINATION THE EXTREMITIES

action as, with the right limb securely planted, a strong contraction of the gluteus maximus would, in theory, generate a very effective extension and external rotation torque about the right hip, helping to provide the necessary thrust to the combined-cutting and propulsion action.31 Thus, the abductors and external rotators not only provide stability to the hip joint but are also important in maintaining proper segmental alignment of the extremity during weightbearing tasks.77,78 An inability of the hip abductors and external rotators to produce adequate torque during weightbearing activities can lead to pelvic drop, excessive hip adduction, excessive hip internal rotation, and an increase in the knee valgus angle.78 In sharp contrast to the external rotators, no muscle with any potential to internally rotate the hip lies even close to the horizontal plane in the anatomic position, making it difficult to assign any muscle as a primary internal rotator of the hip.31 Since the overall orientation of the internal rotator muscles is positioned closer to the vertical and horizontal position, these muscles possess a far greater biomechanical potential to generate torque in the sagittal and frontal planes than in the horizontal plane.31 The adductors of the hip are found on the medial aspect of the joint. The primary function of this muscle group is to create an adduction torque bringing the lower extremity toward the midline.9 This adduction torque can also bring the pubis symphysis region of the pelvis closer to the femur.9 From the anatomic position, the adductors are also considered hip flexor muscles. A number of studies have examined the relationship between diminished hip muscle performance and kinematics in individuals with musculoskeletal dysfunction.69 For example, females with patellofemoral pain syndrome have a lower maximum hip abductor and extensor torque and greater peak knee external rotation and hip adduction during the stance phase of running compared to healthy controls.60,79 Similarly, hip OA is associated with lower hip abductor strength, as well as greater pelvic drop and hip internal rotation, during the stance phase of walking.80,81 In addition, in the frontal plane, individuals with weak hip abductors often demonstrate greater trunk motion toward the stance limb, resulting in altered moments at the hip and knee.69

CLINICAL PEARL

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According to Cyriax,82,83 the capsular pattern of the hip is a marked limitation of flexion, abduction, and internal rotation. Kaltenborn84 considers the capsular pattern of the hip to be extension more limited than flexion, internal rotation more limited than external rotation, and abduction more limited than adduction. Klassbo et al.85 performed a theorytesting, observational, cross-sectional, and descriptive study involving 168 patients (mean age 61.7 years, range 36–90 years), of whom 50 had no hip OA, 77 had unilateral hip OA, and 41 had bilateral OA, based on radiological reports. The purpose of the study was to arrange and describe passive range of motion (PROM) patterns and to count the number of hips presenting with Cyriax’s or Kaltenborn’s capsular patterns. One examiner tested PROM

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bilaterally, using a goniometer and a standardized protocol. PROM limitations were calculated by comparing norms from the symptom-free hips (n = 100) in the study, from Kaltenborn, and, in patients with unilateral hip OA (n = 77), from the non-OA hip. The limitations were arranged by size in PROM patterns. The patterns and the numbers of hips with patterns corresponding to Cyriax’s and Kaltenborn’s capsular patterns were counted. Between 68 and 138 PROM patterns were identified by the use of different PROM norms for defining limitations. The results of this study showed that few OA hips showed Cyriax’s capsular pattern and none demonstrated Kaltenborn’s capsular pattern. In addition, it was concluded that it is impossible to anticipate radiological evidence of hip OA from the multitude of PROM patterns. A more useful determination can be made by assessing hip ROM in all planes and, if three planes of motion or more are restricted, OA is likely present.86

EXAMINATION Although injuries of the hip are not as common as injuries to the knee or shoulder, they can create diagnostic and therapeutic challenges, and diseases of the hip can be very disabling. A hip joint injury is often associated with the complex interaction between structural and biomechanical factors. The diagnosis of a hip injury can be challenging due to the similar clinical presentation of intra-articular and extra-articular pathology. The common pathologies and the interventions for the hip joint are detailed after the examination. Table 19-7 outlines the clinical findings, differential diagnosis, and intervention strategies for some hip conditions, and Table 19-8 describes some of the physical findings for some of the more common causes of hip and thigh pain. An understanding of the pathology and the clinical findings is obviously necessary. The goal of the clinical examination is to identify the primary source of hip pain and symptoms. Identifying the primary source of the pain/symptoms is essential if one hopes to provide long-lasting relief. Acute presentations usually have a clear and identifiable cause, whereas in chronic conditions the true etiology may not be as obvious. For example, a protracted hip joint disorder can result in compensations that can develop secondary dysfunctions, which in turn may lead to symptoms such as trochanteric bursitis or chronic gluteal discomfort. As mention of the various pathologies occurs with reference to the examination and vice versa, the reader is encouraged to switch between the two.

CLINICAL PEARL One study demonstrated that the clinical assessment of the hip can be 98% reliable at detecting the presence of a hip joint problem; although the examination may be poor at defining the exact nature of an intra-articular disorder.87 However, as many structures can refer pain to the hip and groin region, the symptoms are often both confusing to the patient and challenging to the clinician. For example, a hip joint disease may coexist with lumbar spine disease.

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TABLE 19-7

History, Clinical Findings, Differential Diagnosis, and Intervention Strategies of Some Hip Conditions Medical Findings

Intervention

Whether to Refer

Legg–Calvé– Perthes disease

Insidious onset (1–3 months) of limp with hip or knee pain

Limited hip abduction, flexion, and internal rotation

Juvenile arthritis and other inflammatory conditions of the hip

Slipped capital femoral epiphysis

Acute (2-cm displacement

Hip pointer

Plain films if suspect fracture

Rest, ice, NSAIDs, local steroid, and anesthetic injection for severe pain; gradual return to activities with protection of site

PT appropriate

Contusion

Plain films negative

Rest, ice, compression, static stretch, and NSAIDs

PT appropriate

Myositis ossificans

Radiograph or ultrasound examination reveals typical calcified, intramuscular hematoma

Ice, stretching of involved structure, NSAIDs; surgical resection after 1 year if conservative treatment fails

PT appropriate; orthopaedic surgery if resection needed

Femoral neck stress Plain films may show cortical defects fracture in femoral neck (superior or inferior surface); bone scan, MRI, and CT may also be used if plain films are negative and diagnosis is suspected

Orthopaedic surgery for ORIF Inferior surface fracture; no weightbearing until evidence of healing (usually 2–4 weeks) with gradual return to activities; superior surface fracture: ORIF

Osteoid osteoma

Plain films; if these are negative and symptoms persist, MRI or CT

Surgical roemoval if unresponsive to medical therapy with aspirin or NSAIDs

Orthopaedic surgery

Iliotibial band syndrome

 

Modification of activity, footwear; stretching program, ice massage, and NSAIDs

PT appropriate

Trochanteric bursitis

Plain films, bone scan, and MRI negative for Ice, NSAIDs, stretching of iliotibial bony involvement band, protection from direct trauma, and steroid injection

PT appropriate

Avascular necrosis of the femoral head

Plain films and MRI

PT trial appropriate; orthopaedic surgery

Piriformis syndrome

EMG studies may be helpful; MRI of lumbar Stretching, NSAIDs, relative rest, and spine, if nerve root compression is correction of offending activity suspected

PT appropriate

Iliopsoas bursitis

Plain films are negative

Iliopsoas stretching and steroid injection

PT appropriate

Meralgia paresthetica

Nerve conduction velocity testing may be helpful

Avoid external compression of nerve — (clothing, equipment, and pannus)

Degenerative arthritis

Plain films help with diagnosis and prognosis

PT trial appropriate; orthopaedic Maximizing support and strength surgery of soft tissues, ice, NSAIDs, modification of activities, cane, and total hip replacement

Protected weight-bearing, exercises to maximize soft tissue function (strength and support), and total hip replacement

CBC, complete blood count; CT, computed tomography; EMG, electromyelography; ESR, erythrocyte sedimentation rate; MRI, magnetic resonance imaging; NSAIDs, nonsteroidal antiinflammatory drugs; ORIF, open reduction with internal fixation; PT, physical therapy; ROM, range of motion.

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Reproduced with permission from Adkins SB, Figler RA. Hip pain in athletes. Am Fam Physician. 2000 Apr 1;61(7):2109–2118.

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TABLE 19-8

 hysical Findings in Some of the More P Common Causes of Hip and Thigh Pain Description of Findings

Osteoarthritis of the hip

Tenderness over the anterior hip capsule Pain reproduced by passive rotation of the hip Restricted range of motion (rotation is usually first affected) Pain reproduced by Stinchfield’s test (see “Special Tests” section) Abductor limp (more severe cases) Functional leg length discrepancy (if abduction contracture has developed)

Type of Pain/ Structure Involved

Potential Causes of Hip Pain

Cause

Articular cartilage

Chondral lesion Osteoarthritis Instability (labral tear)

Childhood disorders 

Congenital dysplasia Legg–Calvé–Perthes disease Slipped capital femoral epiphysis (SCFE)

Inflammation 

Trochanteric bursitis Psoas bursitis Iliotibial band bursitis Tendinopathy (adductor) Toxic synovitis Osteitis pubis

Infection

Septic arthritis Osteomyelitis

Meralgia paresthetica

Altered sensation over the anterolateral thigh Symptoms reproduced by pressure or percussion just medial to the anteriorsuperior iliac spine

Piriformis tendinitis

Tenderness to deep palpation near the hook of the greater trochanter. Pain reproduced by piriformis stretch

Gluteus medius tendinitis

Tenderness just proximal to the greater trochanter Pain reproduced by resisted abduction of the hip

Neoplasm Neurologic

Local nerve entrapment

Trochanteric bursitis

Tenderness over the lateral aspect of the greater trochanter Popping or crepitation felt with flexionextension of the hip (occasionally) Tight iliotibial tract revealed by Ober test (variable)—see “Special Tests” section

Overuse 

Stress fractures of the femur Muscle strains Inguinal hernia Femoral hernia

Referred

Lumbar disk pathology Lumbar spine-degenerative joint disease Athletic pubalgia Radiculopathy Piriformis syndrome Sacroiliac joint pathology Genitourinary tract pathology Abdominal wall pathology Pelvic floor pathologies

Systemic

Rheumatoid arthritis Crohn’s disease Psoriasis Reiter’s syndrome Systemic lupus erythematosus

Trauma

Soft tissue contusion Fractures of the femoral head Dislocation of the femoral head Avulsion injury Myositis ossificans

Vascular 

Avascular necrosis Osteonecrosis

Quadriceps strain or contusion

Tenderness and swelling of the involved area of the quadriceps Weakness of quadriceps contraction Restriction of knee flexion, especially when the hip is extended Palpable divot in the quadriceps (more severe strains) Warmth and firmness in quadriceps (impending myositis ossificans)

Hamstring strain Localized tenderness and swelling at the site of injury Ecchymosis (frequently) Restricted knee extension and straight-leg raising Palpable divot in the injured hamstring (more severe injuries) Abnormal tripod sign Modified with permission from Reider B. The Orthopaedic Physical Examination. Philadelphia, PA: WB Saunders; 1999.

History The importance of history taking cannot be overemphasized as the potential causes of hip pain are numerous (Table 19-9). The history should determine the onset of the symptoms, the mechanism of injury if any, and the patient’s chief complaint. A medical screening questionnaire for the pelvis, hip, and thigh is provided in Table 19-10. It is important for the clinician to determine:

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Hip Joint Complex

Condition

TABLE 19-9

EXAMINATION



Reproduced with permission from Martin RL, Enseki KR, Draovitch P, et al. Acetabular labral tears of the hip: examination and diagnostic challenges. J Orthop Sports Phys Ther. 2006 Jul;36(7):503–515.

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EXAMINATION

TABLE 19-10

Medical Screening Questionnaire for the Pelvis, Hip, and Thigh Region

THE EXTREMITIES

 

Yes

No

Have you recently had a trauma, such as a fall? Have you ever had a medical practitioner tell you that you have osteoporosis? Have you ever had a medical practitioner tell you that you have a problem with the blood circulation in your hips? Are you currently taking steroids or have you been on prolonged steroid therapy? Do you have a history of cancer or has a member of your immediate family (i.e., parents or siblings) ever been diagnosed with cancer? Have you recently lost weight even though you have not been attempting to eat less or exercise more? Have you had a recent change in your bowel functioning such as black stools or blood in your rectum? Have you had diarrhea or constipation that has lasted for more than a few days? Do you have groin, hip, or thigh aching pain that increases with physical activity, such as walking or running?

         

         

       

       

Reproduced with permission from Wilmarth MA. Medical Screening for the Physical Therapist. Orthopaedic Section Independent Study Course 14.1.1. La Crosse, WI: Orthopaedic Section, APTA, Inc.; 2003.

Patient Age

Symptom Fluctuations

The patient’s age may help in the diagnosis. OA of the hip is diagnosed most often in patients over 60 years of age, although it can occur earlier.

The time of day that appears to change the pain for better or worse can provide some clues. Hip joint pathology is usually associated with stiffness of the hip in the morning on arising. Such pathologies include

Pain Location The location of the pain can provide the clinician with some useful information (Table 19-11). Groin pain is a common orthopaedic problem, and the differential diagnosis of groin pain can be extremely challenging given the multitude of structures and conditions that can be potential sources of groin pain. These include referred symptoms due to nerve compression (e.g., obturator or lateral femoral cutaneous nerve of the thigh), or referred symptoms from a sports hernia, the abdominal viscera, and the lumbar spine. For example, lateral and posterior hip (buttock) and thigh pain may be referred from the lumbar spine. In addition, hip joint pathologies (e.g. OA, labral tear, impingement, and osteonecrosis), osteitis pubis, hip flexor and adductor strain, rectus abdominis strain, greater trochanter bursitis, and fractures of the femoral neck and pubic ramus are all capable of producing groin pain. One of the more common causes of groin pain in the older patient is OA of the hip. However, OA of the hip may also cause pain behind the greater trochanter, anterior thigh, and knee because of the various nerves that cross the hip. Additional questioning can provide some guidance. For example, complaints of hip or groin pain, morning stiffness, stiffness after sitting, and hip pain with weight bearing are suggestive of joint involvement, such as OA. However, it is important to identify patients with symptomatic OA correctly and to exclude conditions that may be mistaken for or coexist with OA. Periarticular pain that is not reproduced by passive motion and direct joint palpation suggests an alternate etiology such as bursitis, tendinopathy, or periostitis.

Distribution of Symptoms

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The distribution of painful joints is helpful to distinguish OA from other types of arthritis because MCP, wrist, elbow, ankle, and shoulder arthritis are unlikely locations for OA except after trauma.

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OA of the hip joint; rheumatoid arthritis of the hip joint; prolonged morning stiffness (>1 hour) should raise suspicion for this type of inflammatory arthritis; ▶▶ osteonecrosis of the femoral head. ▶▶ ▶▶

Motion Restrictions The first two motions that are diminished in hip OA are usually hip internal rotation and hip flexion, although as previously discussed, this can vary significantly.88 A significant decrease or loss of motor function will always necessitate imaging studies to rule out an avulsion fracture, and/or nerve injury (see Chapter 7).

Mechanism of Injury Patients who present with acute macrotrauma (e.g., falls and motor vehicle accidents) and who report having difficulty moving the hip or bearing weight require radiographs to rule out a fracture and/or dislocation. Falls on the outside of the hip are a common cause of trochanteric bursitis or contusion of the iliac crest (hip pointer). Such an injury may also involve the abdominal and/or gluteal muscles at their attachment sites. When the abdominal muscles are involved, patients may complain of pain with deep inspiration or have difficulty with trunk rotation. Macrotraumatic forces applied along the femur such as those that occur with dashboard injuries and falls on the knee can result in damage to the articular cartilage, an acetabular labrum tear, a pelvic fracture, or a hip subluxation. An immediate loss of movement following direct trauma to this area usually indicates the presence of a hip or pelvic fracture or a dislocation. Posterior contusions to the gluteus maximus and sciatic nerve can occur from a direct blow to the buttock. In such cases, the patient may complain of pain in the buttocks and of pain, numbness, and/or tingling

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Differential Diagnosis for Pain in the Hip or Buttock Area Potential Cause

Pain Distribution

Potential Cause

Groin area

Stress fractures of the pelvis and femur Crystal-induced synovitis (gout) An inguinal/femoral hernia Muscle calcification Hip adductor strain Iliopectineal bursitis

Groin and inner thigh region          

Transient synovitis Infection Loosened prosthesis Inflamed lymph nodes Lower abdominal muscle strain Referred pain from viscera or spinal nerve Sprain of pubic symphysis Osteitis pubis Abdominal muscle strain Bladder infection Trochanteric bursitis Tendinitis of abductors or external rotators Apophysitis of greater trochanter Referred pain from mid or lower lumbar spine Thrombosis of gluteal arteries Strain of quadriceps Meralgia paresthetica Entrapment of femoral nerve Thrombosis of femoral artery or great saphenous vein Stress fracture of femur Referred pain from hip or mid-lumbar spine Strain of adductor muscles Entrapment of obturator nerve Referred pain from hip or knee Apophysitis or sartorius or rectus femoris Strain of gluteal, oblique abdominals, tensor fascia, latae, and quadratus lumborum Entrapment of iliohypogastric nerve Referred pain from upper lumbar spine

Iliopsoas strain or avulsion fracture of the lesser Trochanter Arthritis of the hip Hip arthrosis Femoral neck fracture Osteonecrosis of the femoral head Pubic symphysis dysfunction: ▶  Osteitis pubis ▶  Osteomyelitis pubis ▶  Pyogenic arthritis ▶  Pubic fracture ▶  Pubic osteolysis ▶  Postpartum symphyseal pain Sacroiliac joint lesion Tumor Ureteral stone Hernia Inflammatory synovitis (e.g., rheumatoid arthritis, ankylosing spondylitis, and systemic lupus erythematosus) Subluxation Dislocation

Pubic area

Lateral buttock area

Anterior and lateral thigh Medial thigh

Anterior superior iliac spine Iliac crest

Hip Joint Complex

Pain Distribution

EXAMINATION

TABLE 19-11

Adapted with permission from Malone TR, McPoil T, Nitz A. Orthopaedic and Sports Physical Therapy. 3rd ed. St. Louis, MO: CV Mosby; 1996.

radiating down the course of the sciatic nerve. Both the athlete and nutritionally compromised individual are at risk of pelvic rami or femoral neck stress fractures. Anterior blows to the thigh can produce quadriceps contusions. These contusions can also result in myositis ossificans. The femoral nerve is fairly well protected and not usually injured. Acute muscle strains in the hip and thigh region, especially of the hamstrings, are usually seen in the athletic individual, most often occurring following a short sprint, jump kick, fall, or collision. Quadriceps strains, usually involving the rectus femoris, occur in sprinters and kickers. The most frequently strained adductors are the longus and magnus while hamstring injuries usually involve the biceps femoris.89–91

CLINICAL PEARL Ironically, in general, a history of a significant traumatic event is a good prognostic indicator of a potentially correctable problem,92 whereas arthritis is an indicator of poor long-term outcomes.93

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If the patient is unable to recall a specific mechanism, the clinician should suspect a systemic (see “Systems Review” section and Chapter 5) or biomechanical cause. The hip is a region that is prone to overuse injuries. Walking or running can aggravate trochanteric bursitis, iliotibial band friction syndrome (ITBFS), hamstring and adductor strains, or a femoral neck stress fracture. Pain with bursitis is frequently referred along the course of the muscle it underlies and nearby neurologic structures. Obturator internus bursitis can refer pain to the back and buttock or along the course of the sciatic nerve. Subtrochanteric bursitis commonly refers pain to the low back (LB), lateral thigh, knee, and hip. Iliopectineal bursitis can refer pain along the course of the femoral nerve and anterior thigh. Ischiogluteal bursitis can refer pain along the posterior femoral cutaneous or sciatic nerve.

The Behavior of the Symptoms Reports of twinges of pain with weight-bearing activities may indicate the presence of a loose body within the joint. Noises in and around the joint can result from many causes so are

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EXAMINATION

not particularly diagnostic. One of the more common causes for clicking is a “snapping” hip, especially if the snapping consistently occurs at approximately 45 degrees of hip flexion. This type of snapping hip is thought to be because of the iliopsoas tendon riding over the greater trochanter or anterior acetabulum. The other types of snapping hip are described in the “Interventions” section. If the pain is associated with the clicking, it requires further investigation.

CLINICAL PEARL THE EXTREMITIES

Mechanical symptoms such as locking, catching, popping, or ones that are sharp stabbing in nature are better prognostic indicators of a correctable problem.94

Aggravating or Relieving Factors Information must be gathered with regard to the activities or positions that appear to aggravate or lessen the symptoms. For example, prolonged sitting on a hard surface may aggravate the ischial bursa whereas buttock pain with prolonged sitting on a soft surface is more likely to be the result of a lumbar disk lesion. Rising from a seated position can be especially painful, and the patient may experience an accompanying catching or sharp stabbing sensation. Entering and exiting an automobile is often difficult because the hip is in a flexed position along with twisting maneuvers. As the hip is a weight-bearing joint and weight-bearing tends to aggravate articular pathologies, it is very important to gather information concerning the role of weight bearing in painful activities, particularly whether the patient has pain at rest as well as during weight bearing, or whether specific weight-bearing activities (e.g., stair climbing and walking) are the cause of increased pain. Questions about the work environment, athletic participation, and other daily and recreational activities help the clinician identify risk factors for the cumulative trauma that might not be apparent to the patient. Activities and positions

TABLE 19-12

852

that aggravate and alleviate symptoms should be identified (Table 19-12). The hip and pelvic areas are also common sites for pain referral (Table 19-11). The differential diagnosis of hip pain is described in Chapter 5. To help determine the symptom distribution, a pain diagram should be completed by the patient (see Chapter 4). Following its completion, the patient should be encouraged to describe the type of symptoms experienced for each of the areas highlighted on the diagram, as well as the motions or positions that increase or decrease the symptoms. Since the lumbar spine can refer symptoms to the hip region, the clinician should always rule out the involvement of the lumbar spine before a hip problem is suspected. The most common source of referred pain from the LB includes both neurogenic (nerve root compression) and spondylogenic (facet or SIJ) causes. Brown et al.95 identified a limp, groin pain, and limited hip internal rotation as signs that significantly predicted a hip problem rather than a lumbar problem. Finally, the clinician should determine the impact that the patients’ condition has on their activities of daily living (ADL).

Systems Review Referred pain to the hip is common and should be considered in the absence of acute trauma or when symptoms do not clearly originate from the hip. Pain may be referred to the hip region from a number of neuromusculoskeletal sources (see Chapter 5). In addition to those already mentioned, these can include pubic symphysis dysfunction; SIJ dysfunction; ▶▶ lumbar and low thoracic disk-degenerative disease; ▶▶ lumbar stenosis with neurogenic claudication; ▶▶ peripheral nerve entrapments (the lateral cutaneous nerve of the thigh); ▶▶ ▶▶

Subjective Reports and Possible Diagnoses

Subjective Report

Possible Diagnosis

Pain that is usually worse with sitting on hard surfaces, cycling, and prolonged standing

Ischiogluteal bursitis

Pain with squatting, lying on the involved side, climbing stairs, and walking

Subtrochanteric bursitis

A clicking or popping sound that occurs during running and dancing activities

Snapping hip syndrome

Pain with prolonged sitting, trunk flexion, and coughing/sneezing

Lumbar disk herniation

Pain with activities that involve lumbar extension

Spinal stenosis, spondylolisthesis, or facet syndrome

Pain at night unrelated to movement

Malignancy

Pain with walking, which is relieved with cessation of the activity

Vascular claudication

Pain that appears to be affected by the weather

Arthritic condition or fibromyalgia syndrome

Progressive loss of or change in motor, bowel, bladder, or sexual function

Myelopathy, conus medullaris syndrome, or cauda equinus syndrome

Data from Feinberg JH. Hip pain: differential diagnosis. J Back Musculoskelet Rehabil. 1994 Jan 1;4(3):154–173.

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Complaints associated with referred pain include thigh pain, knee pain, and leg pain with or without hip pain, which may be indicative of lumbar radiculopathy; ▶▶ pain that is decreased with walking up stairs, which may indicate the presence of lumbar spine stenosis. ▶▶



TABLE 19-13

 ed Flags for the Pelvis, Hip, and Thigh R Region

Condition

Red Flags

Colon cancer

Age over 50 years Bowel disturbances (e.g., rectal bleeding or black stools) Unexplained weight loss History of colon cancer in immediate family Pain unchanged by positions or movement

Pathological fractures of the femoral neck

Older women (>70 years) with hip, groin, or thigh pain History of a fall from a standing position Severe, constant pain that is worse with movement A shortened and externally rotated lower extremity

Osteonecrosis of the femoral head (avascular necrosis)

History of long-term corticosteroid use (e.g., in patients with rheumatoid arthritis, systemic lupus erythematosus, or asthma) History of avascular necrosis of the contralateral hip Trauma

Reproduced with permission from Wilmarth MA. Medical Screening for the Physical Therapist. Orthopaedic Section Independent Study Course 14.1.1. La Crosse, WI: Orthopaedic Section, APTA, Inc.; 2003.

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Hip Joint Complex

Referred pain is often related to posture and positioning. Other conditions that can refer symptoms to the pelvis, hip, and thigh region in an adult include cancer, pathological fractures of the femoral neck, and osteonecrosis of the femoral head (avascular necrosis). In the child, pain and loss of range at the hip joint should always alert the clinician to the possibility of transient synovitis, Legg–Calvé–Perthes disease, or a slipped femoral capital epiphysis (Table 19-13). The Cyriax lower quarter scanning examination can be used to screen for the presence of upper or lower motor neuron lesions or the referral of symptoms from the spine (see Chapter 4). Key muscle testing is used to test for neurologic weakness (see also “Active, Passive, and Resistive Tests” section). Trigger points in patients with myofascial pain syndrome can cause both localized and referred symptoms that often closely resemble the referral patterns of a radiculopathy. The clinician should revise the diagnosis and change the plan of care, or refer the patient to the appropriate clinician, when the patient’s history, reported activity limitations, or

impairments of body function and structure are not consistent with a physical therapy diagnosis/classification, or when the patient’s symptoms are not diminishing with interventions aimed at normalization of the patient’s impairments of body function.96 Evidence of intense inflammation on examination suggests infectious or microcrystalline processes such as gout or pseudogout. Weight loss, fatigue, fever, and loss of appetite should be sought out because these are clues to systemic illness such as polymyalgia rheumatica, rheumatoid arthritis, lupus, or sepsis. Examples of viscerogenic referred pain (see Chapter 5) include renal calculi (pain radiates into the groin), ovarian cysts or an ectopic pregnancy (pain radiating into the back or hip, or along the course of the sciatic nerve when there is direct compression), and diverticulitis or inguinal hernias (pain radiating across the abdomen or back or into the groin). Referred pain to the buttock can be a form of vasculogenic pain (see Chapter 5) and occurs in patients who have vascular claudication from stenosis of the distal aorta or common iliac vessels. If, following the history and systems review, the clinician is concerned with any signs or symptoms of a visceral, vascular, or systemic disorder, the patient should be referred to the appropriate healthcare professional.

EXAMINATION

myofascial pain syndrome; ▶▶ spondyloarthropathy. ▶▶

Tests and Measures The hip can be one of the most challenging joints to examine. Unlike the knee or ankle, the joint is not readily palpable, and one must rely on a number of provocative tests and maneuvers to identify intra-articular or bony abnormalities. Even many of the soft tissue structures are difficult to manually identify but can usually be isolated with proper clinical skills.

Observation The most important aspect of inspection is stance (standing and sitting) and gait. The patient is observed from the front, back, and sides for general alignment of the hip, pelvis, spine, and lower extremities (see Chapter 6). While standing, a slightly flexed position of the involved hip and the ipsilateral knee is a common finding associated with hip pathology. In the seated position, slouching or listing to the uninvolved side avoids extremes of flexion. An antalgic gait may or may not be present depending on the severity of the symptoms. The clinician observes the hip region, noting any scars, anatomical abnormalities, muscle atrophy, bruising, swelling, etc. A localized soft tissue mass or swelling may indicate bursitis, an acute muscle contusion or tear with a hematoma, an avulsion fracture, myositis ossificans, a tumor, infection, or deep vein thrombosis (DVT). ▶▶ Asymmetric muscle atrophy is usually an indication of a radiculopathy or peripheral neuropathy, but can also be seen with a tendon rupture. ▶▶ An ecchymosis may be seen with contusions, muscle tear, fracture, and patients with a bleeding diathesis. ▶▶

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EXAMINATION

Vesicular skin lesions that have a dermatomal distribution may be found in cases of herpes zoster. Café au lait spots greater than 3 cm and greater than six in number are characteristic of neurofibromatosis. ▶▶ Skin rashes may be because of secondary psoriatic arthritis, drug reactions, or one of the collagen vascular diseases. ▶▶ Obvious joint or bony deformity should raise suspicion of a fracture or dislocation. ▶▶

THE EXTREMITIES

Both pain and musculotendinous dysfunction can produce movement and postural dysfunctions at the hip joint.97 According to Kendall,98 the ideal alignment of the pelvis is indicated when the ASIS is on the same vertical plane as the symphysis pubis. The degree of pelvic tilt, which is measured as the angle between the horizontal plane and a line connecting the ASIS with the PSIS, varies from 5 to 12 degrees in normal individuals. Both a low ASIS in women and a structurally flat back in men can cause structural variations in pelvic alignment, which can be misinterpreted as acquired postural impairments.97 According to Sahrmann, all of the following are necessary to indicate the presence of a postural impairment of the hip97: An increase or decrease in the depth of the normal lumbar curve. ▶▶ A marked deviation from the horizontal line between the ASIS and PSIS. ▶▶ An increase or decrease in the hip joint angle in the anterior–posterior plane, with neutral knee joint alignment. ▶▶

The following should be examined97: ▶▶

The glutei should be symmetrical and well rounded, not hanging loosely. The pelvic crossed syndrome (see Chapter 6) demonstrates weakness and inhibition of the glutei muscles. This syndrome can be easily identified by having the patient perform a partial bridge with single leg support. This maneuver results in cramping of the hamstrings within a few seconds if the pelvic crossed syndrome is present. Atrophy of one buttock cheek compared with the other side may also indicate a superior or inferior gluteal nerve palsy. A balling-up of the gluteal muscle typically indicates a grade III tear of the gluteal muscles. Buttock swelling occurs with the “sign of the buttock.”

CLINICAL PEARL The pelvic crossed syndrome is exhibited by adaptively shortened hip flexors and hamstrings and inhibited glutei muscles and lumbar erector spinae. Swelling over the greater trochanter could indicate trochanteric bursitis. ▶▶ Adaptive shortening of the short hip adductors is indicated by a distinct bulk in the muscles of the upper third of the thigh. ▶▶

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▶▶

The bulk of the TFL should not be distinct. A visible groove passing down the lateral aspect of the thigh may indicate that the TFL is overused, and both it and the ITB are adaptively shortened.

The architecture and position of the hip joint and lower extremity is observed. In acute arthritis and gross osteoarthrosis, the hip joint is usually held in flexion and external rotation. This may be compensated for by an anterior tilt of the pelvis, together with an increased lordosis of the lumbar spine. ▶▶ Excessive external rotation of the leg, accompanied with toeing-out, occurs in extreme femoral neck retroversion, or a slipped femoral epiphysis. ▶▶ Increased hip flexion in standing can result from weakness or excessive lengthening of the external oblique or rectus abdominis muscles. Increased hip flexion may also be because of a hip flexion contracture. ▶▶ Increased hip extension in relaxed standing is indicative of a swayback posture. This is characterized by a posterior pelvic tilt and hyperextension of the knees and results in a stretch on the anterior joint capsule of the hip and stress on the iliopsoas muscle and tendon. ▶▶

▶▶

Lateral asymmetry in relaxed standing is characterized by a high iliac crest on one side. The difference in height between the two crests must be greater than one-half inch to have clinical significance. Lateral asymmetry may indicate a positive Trendelenburg sign (see “Special Tests” section), which indicates hip-abductor weakness.

Observation of the lower components of the kinetic chain includes the degree of genu varum/valgus (see Chapter 20); ▶▶ the degree of tibial torsion (see Chapter 20); ▶▶ the amount of calcaneal inversion/eversion (see Chapter 21). ▶▶

Gait.  Analysis of both the stance and swing phases of gait is essential (see Chapter 6). Determinants of the stance-phase of gait involve interaction between the pelvis and hip and distal limb joints (knee and ankle). The clinician should note whether: the patient is using an assistive device. If they are, is it fitted at the correct height and do they use it correctly? ▶▶ there is a lack of hip motion, particularly extension. A lack of hip extension can have an impact on gait (see Chapter 6). ▶▶ there is a lateral horizontal shift of the pelvis and trunk over the stance leg during the swing phase. This may indicate a positive Trendelenburg sign (see “Special Tests” section). Activation of the abductor mechanism on weight bearing is necessary to stabilize the hip and pelvis and prevent excessive lateral tilting of the pelvis to the contralateral side during the swing phase. ▶▶ the ankle alignment is neutral. Increased ankle pronation increases the degree of hip internal rotation which ▶▶

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EXAMINATION

can place greater stress on hip rotators. This can be especially traumatic to those hip rotators that cross bony prominences, increasing the risk of bursitis; conversely, supination causes greater external rotation.

▶▶

High step.  The patient places one foot on a chair and then leans on it (Fig. 19-18). This maneuver flexes the raised hip and extends the other. The test is repeated on the other side. This test gives the clinician an indication as to the range of flexion and extension at the hip.

▶▶

Unilateral standing.  The patient stands on one leg (Fig. 19-19). An inability to maintain the pelvis in a horizontal position during unilateral standing is called a positive Trendelenburg (see “Special Tests” section).

Palpation The palpatory examination is done to identify both anatomic abnormalities and potential sources of symptoms other than from the hip joint itself. Given the location of the hip joint,

Hip Joint Complex

Strong activation of the hip extensors (with the abductors) is necessary at initial contact into the early stance, from 30 degrees initial flexion to approximately 10 degrees of extension at terminal stance. If the hip flexors are short or stiff in relation to the abdominal muscles, there may be an exaggeration in the anterior pelvic tilt and increased lumbar extension during this phase.97 Joint Loading Tests.  Pain on weight bearing is a common complaint in some patients with hip joint pathology, including rheumatoid arthritis and OA. Depending on the capability of the patient, the following weight-bearing tests may produce pain:

FIGURE 19-19  Trendelenburg sign indicating weakness of the left hip abductors.

palpation is usually unrevealing as far as any specific areas of discomfort related to an intra-articular source of hip symptoms. A palpable mass following acute trauma that is not well defined usually indicates a muscle tear, a muscle spasm, or hematoma. A mass that developed 2–3 weeks after the initial injury and is warm and erythematous may be the first indication of myositis ossificans. Bursitis usually presents with some localized swelling, warmth, and erythema, and no history of acute trauma. Trigger points are usually identified as discrete nodules or bands within muscle tissue. There is no associated swelling and no warmth or erythema. Postural or bony malalignment can increase the risk of both acute traumatic and overuse injuries. The anatomic relationships of the joints of the lower extremity should be compared, looking for valgus and varus deformities, pes cavus or planus, spine mobility, hip anteversion, pelvic asymmetry, and leg length discrepancies (see Chapter 29).

CLINICAL PEARL The following are useful landmarks to use when locating the hip joint center of rotation7: ▶▶ The midpoint between the ASIS and pubic symphysis, over the femoral pulse. ▶▶ The superior tip of the greater trochanter in line with the center of rotation.

FIGURE 19-18  High step.

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Anterior Aspect of Hip and Groin Anterior-Superior Iliac Spine. The anterior iliac spine serves as the origin for the sartorius muscle and the TFL.

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EXAMINATION

Both can be located by flexing and abducting the patient’s hip, which produces a groove that resembles an inverted V close to the ASIS. The lateral side of the inverted V is formed by the TFL while the medial side is formed by the tendon of the sartorius.

THE EXTREMITIES

Anterior Inferior Iliac Spine.  The AIIS can be palpated in the space formed by the sartorius and the TFL, during passive flexion of the hip in the space known as the lateral femoral triangle. The lateral cutaneous nerve of the thigh passes through this triangle. Compression of this nerve produces a condition called meralgia paresthetica (see Chapter 5). The AIIS serves as the origin for the rectus femoris tendon. Pubic Tubercle.  The pubic tubercle is located by finding the groin crease and then traveling in an inferomedial direction, or by following the tendon of the adductor longus proximally. In males, the spermatic cord runs directly over the tubercle and can be tender to palpation in normal individuals. Inguinal hernias are usually found superior and medial to the tubercle while femoral hernias are located lateral to the tubercle. Adductor Magnus. The adductor magnus is palpable in a small triangle in the distal thigh, posterior to the gracilis muscle and anterior to the semimembranosus. Rectus Femoris.  The rectus femoris has its origin at the AIIS, which is located just distal to the ASIS, between the TFL and sartorius. Iliopsoas Bursa.  At the iliopectineal eminence, the iliopsoas muscle makes an angle of about 30 degrees in a posterolateral direction. To palpate this bursa, the patient is positioned in supine, with the hip being positioned in approximately 40 degrees of flexion and external rotation, and resting on a pillow. At the proximal end of the femur, the clinician palpates the adductor tubercle and then moves to the ASIS. From there, the clinician proceeds to the inguinal ligament, under the fold of the external oblique, and into the femoral triangle. The psoas bursa is located under the floor of the triangle, close to the pubic ramus. Femoral Triangle. The femoral artery lies superficial and medial to the iliopsoas muscle and is easily located by palpation of the pulse. The femoral nerve is the most lateral structure in the femoral triangle. To examine the femoral triangle, the patient is positioned in supine and, if it is possible for the patient to do this, the heel of the leg is placed on the opposite knee. This places the patient in a position of flexion– abduction and external rotation. Inguinal Ligament.  The inguinal ligament is located in the fold of the groin, running from the ASIS to the pubic tubercle. It can be located by using transverse palpation. Adductor Longus. Together with the gracilis, the adductor longus forms the medial border of the femoral triangle. The gracilis is located medial and posterior to the adductor longus. The adductor longus is best viewed during resisted adduction, when it forms a cord-like structure just distal to the pubic tubercle, before crossing under the sartorius. It is often tender in dancers, cheerleaders, and others who perform strenuous activities requiring abduction at the hip.

Lateral Aspect of the Hip.  The patient is positioned in side lying. Iliac Crest.  The iliac crest is easy to locate. The cluneal nerves are superficial structures and can be located just superior to the crest. Greater Trochanter.  The superior border of the greater trochanter represents the transverse axis of hip, and when the leg is abducted, an obvious depression appears above the greater trochanter. The gluteus medius inserts into the upper portion of the trochanter and can be palpated on the lateral aspect. Palpation of the greater trochanter is also used to assess the angle of anteversion and retroversion using the Craig test (see “Special Tests” section). Lesser Trochanter. The lesser trochanter, covered as it is with the iliopsoas and adductor magnus, is very difficult to palpate directly, but it can be located on the posterior aspect if the hip is placed in extension, and internal rotation, and the palpation is performed deeply lateral to the ischial tuberosity. Piriformis Attachment. The origin of the piriformis can be found on the medial aspect of the superior point of the greater trochanter. Moving inferiorly from this point and the quadratus femoris located on the quadrate tubercle, the following tendon insertions can be palpated: superior gemellus, obturator internus, and inferior gemellus. Psoas.  The insertion for the psoas is located on the inferior aspect of the greater trochanter and can be found by placing the patient’s hip in a position of maximal internal rotation. Once the superior aspect of the greater trochanter is located, the clinician moves in a posterior/medial/inferior direction to locate the inferior aspect of the greater trochanter. Subtrochanteric Bursa.  The subtrochanteric bursa cannot be palpated directly. However, it can be tested by positioning the patient’s leg in hyperadduction. At this point, the patient is asked to abduct the hip isometrically against the clinician’s resistance. The contraction of the hip abductors compresses the bursa and may cause pain if the bursa is inflamed. Posterior Aspect of the Hip.  The patient is positioned in side lying or prone. Quadratus Lumborum.  Palpation of the quadratus lumborum is best accomplished with the patient in side lying, with the arm abducted overhead to open the space between the iliac crest and the 12th rib. Ischial Tuberosity.  A number of structures have their attachments on the ischial tuberosity. These include the ischial bursa, the semimembranosus tendon, the sacrotuberous ligament, the biceps femoris and semitendinosus tendons, and the tendons of the quadratus femoris, adductor magnus, and inferior gemellus. The ischial tuberosity is best palpated in the side-lying position with the hip flexed to 90 degrees (see Chapter 29). This position moves the gluteus maximus upward, permitting direct palpation at the tuberosity. The ischial bursa is located on the inferior and medial aspect of the ischial tuberosity. A diagnosis of ischial bursitis is usually based on a history of pain with sitting on a hard surface and finding tenderness with palpation of the ischial tuberosity.

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Active, Passive, and Resistive Tests

A

Normal lumbar and hip flexion

B

Limited hip flexion and excessive lumbar flexion

C

Hip Joint Complex

The clinical procedures for performing ROM measurements vary and disagreement exists about the accuracy of visual estimates compared to goniometer measurements. A study by Holm et al.99 comprising 25 patients (6 M, 19 F; mean age 68.5 years, range 46–76 years) with osteoarthrosis of the hip, verified both clinically and radiologically, examined the reliability of goniometric measurements and visual estimates of hip ROM. Hip ROM measurements (abduction VIDEO, adduction VIDEO, extension VIDEO, flexion VIDEO, and internal VIDEO/ external rotation VIDEO) were recorded by four different teams on the same day and were repeated 1 week later. Teams 1, 2, and 3 consisted of physiotherapists using standardized goniometric measurements. Team 4 involved an experienced orthopaedic surgeon making the assessments from visual estimates only. With the exception of abduction (p = 0.03), there were no significant differences between the measurements recorded on the first and second occasions for the same teams. The coefficient of variance was 5.5% for flexion (lowest) and 26.1% for extension (highest). Reproducibility was best for flexion.

There was also high reliability when all the arcs of motion were summed up (abduction + adduction + extension + flexion + internal/external rotation). With the exception of internal rotation, there were highly significant differences between the teams when two people performed the measurements compared to the values measured by a single individual. Concordance, expressed as the standardized agreement index, between visual estimates made by one individual (the orthopaedic surgeon) and goniometric measurements made by two experienced physiotherapists, was 0.77–0.83, which indicates good agreement. During the examination of the ROM, the clinician should note which portions of the ROM are pain free and which portion causes the patient to feel pain. The screening of active and passive lumbar motion is indicated for all patients with a potential hip pathology. An assessment of the lumbopelvic rhythm (see Chapter 28) can alert the clinician to the primary area of a particular limitation. Active trunk motion in all planes and manual overpressure at end ranges should be administered to fully clear the lumbar spine. During normal forward bending, the patient should be able to touch their toes without bending the knees and with a flattening of the lordosis (Fig. 19-20). However, if the hamstrings are adaptively shortened, toe touching cannot be accomplished even with a flattening of the lordosis. If the tightness is located in the LB, as the patient bends forward, no flattening of the lordosis occurs, and the patient is unable to touch the toes even with good hamstring flexibility. If lumbar screening reproduces

EXAMINATION

Sciatic Nerve.  One of the most important structures to palpate in this area is the sciatic nerve. It can be located by palpation at a point halfway between the greater trochanter and ischial tuberosity. Tenderness of this nerve can be produced by a piriformis muscle spasm or by direct trauma, referred to as piriformis syndrome (see Chapter 5).

Limited lumbar flexion and excessive hip flexion

FIGURE 19-20  Lumbopelvic rhythm.

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EXAMINATION THE EXTREMITIES

the patient’s hip symptoms, then further spine evaluation is warranted. The SIJ should be evaluated in hip patients with complaints of posterior hip or buttock pain (see Chapter 29). The capsular pattern of the hip appears variable and is an unreliable method for determining the presence of OA when used alone.85 Twinges of pain with active motions may indicate the presence of a loose body within the joint. At the end of available AROM, passive overpressure is applied to determine the end-feel. The normal ranges and end-feels for the various hip motions are outlined in Table 19-5. Abnormal end-feels common in the hip include a firm capsular end-feel before expected end range; empty end-feel from severe pain, as in the sign of the buttock; and a bony block in cases of advanced OA.7 Horizontal abduction and adduction of the femur occur when the hip is in 90 degrees of flexion. Since these actions require the simultaneous, coordinated actions of several muscles, they can be used to assess the overall strength of the hip muscles. Resisted testing of the muscles that cross the hip joint (Table 19-4) is performed to provide the clinician with information about the integrity of the neuromuscular unit, and to highlight the presence of muscle strains (see “Systems Review” section). While there is no evidence of neuromotor dysfunction in people with hip related pain, anatomical studies support a theoretical model for their importance in promoting joint stability in other regions of the body. A number of recent studies have suggested optimal exercises to activate the hip abductors, hip extensors, and hip rotators due to their importance with joint stability.32 If the history indicates that repetitive motions or sustained positions cause the symptoms, the clinician should have the patient reproduce these motions or positions.100

CLINICAL PEARL In the child, pain and loss of range at the hip joint should always alert the clinician to the possibility of transient synovitis, Legg–Calvé–Perthes disease, or a slipped femoral capital epiphysis (see Chapter 30). In addition to reports of pain and overall ROM, the clinician also notes information about weakness, joint end-feel, palpation of the moving joint, and muscle tightness.

FIGURE 19-21  Hip flexion with knee flexed.

▶▶

The action of the sartorius muscle, which flexes, abducts, and externally rotates the hip, is tested by asking the patient to bring the plantar aspect of the foot toward the opposite knee VIDEO. The clinician applies resistance at the medial malleolus and at the lateral aspect of the thigh to resist flexion, abduction, and external rotation.

A painless weakness of hip flexion is rarely a good sign. Although it may indicate a disk protrusion at the L1 or L2 level, these protrusions are not common. A more likely scenario is compression of the nerves by a neurofibroma or a metastatic invasion. Pain with the active motion or resisted tests should prompt the clinician to examine the contractile tissues individually. Passive stretching can also produce pain in a contractile structure. Extension.  The primary hip extensor is the gluteus maximus (Table 19-4). The hamstrings also serve as hip extensors. Hip extension also involves assistance from the adductor magnus, gluteus medius, and minimus, and indirect assistance from the abdominals and the erector spinae. The patient is positioned in prone or over the end of a table. As the clinician monitors motion at the pelvis to ensure the lumbar spine does not extend, the patient is asked to lift the thigh toward the ceiling (Fig. 19-22). With a normal

Flexion.  The six muscles primarily responsible for hip flexion are the iliacus, psoas major, pectineus, rectus femoris, sartorius, and TFL (Table 19-4). The primary hip flexor is the iliopsoas muscle. Hip flexion motion can be tested in sitting or supine, first with the knee flexed (Fig. 19-21) and then with the knee extended. With the hip flexed and the knee extended, normal hip flexion should be 80 degrees with knee extension to 20 degrees.101 With the hip flexed, the ROM should be approximately 110–120 degrees. More hip flexion should be available with the knee flexed. Resisted tests are then performed. ▶▶

858

To test the strength of the iliopsoas, the patient is seated with the thigh raised off the bed and resistance is applied by the clinician VIDEO.

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FIGURE 19-22  Hip extension.

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The normal ROM for hip extension is approximately 10–15 degrees. Reduced hip extension with the knee flexed can be the result of a number of reasons, including adaptive shortening of the iliopsoas, characterized by an increased lumbar lordosis, an externally rotated lower extremity, and a noticeable groove in the ITB in standing102; ▶▶ a hip flexion contracture. ▶▶

As before, the pelvis is monitored, and the patient is asked to raise the thigh off the table. The strength of the gluteus maximus is tested with the knee flexed (Fig. 19-23) VIDEO. The role of the hamstrings at the hip can be tested with the knee extended. By observing the patient’s shoulder during this test, the recruitment pattern can be analyzed. The opposite

CLINICAL PEARL Although hip extensor strength in the elderly has been identified as the primary predictor of walking ability, physical performance, and balance, assessment of hip extensor strength in this population is commonly overlooked, as the presence of pain, contractures, and reduced mobility often limits the ability of the elderly patient with hip or spine impairment to adopt the prone position.68 In these situations, the clinician should modify the testing position to accommodate the patient. Abduction/Adduction.  Hip adduction (Fig. 19-24) and abduction (Fig. 19-25) ROM can be tested in supine or side lying making sure that both ASIS are level, and the legs are perpendicular to a line joining the ASIS. Abduction.  The patient is positioned in supine. The clinician monitors the ipsilateral ASIS, and the patient is asked to abduct the leg. The abduction motion is stopped when the ASIS is felt to move. The prime movers of this movement are the gluteus medius/minimus and the TFL. The quadratus lumborum functions as the stabilizer of the pelvis. The strength of the hip abductors can be tested against gravity in the side-lying position VIDEO, or in standing: ▶▶

FIGURE 19-23  Hip extension with knee flexed.

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Hip Joint Complex

1. An initial activation of the hamstrings and erector spinae with a delayed contraction of the gluteus maximus. The biceps femoris has a tendency to become shortened and overactive, resulting in delayed activation of the gluteus maximus. 2. The erector spinae initiate the movement with a delayed activity of the gluteus maximus. This would lead to little, if any, extension of the hip, as the leg lift would be achieved by an anterior pelvic tilt and a hyperextension of the lumbar spine. This is a very poor movement pattern.

shoulder should be seen to rise from the bed. With the abnormal pattern, the same shoulder rises from the bed. Patients who use this abnormal recruitment pattern will often have well-developed thoracic musculature on the posterior aspect and, as a result, develop problems at the thoracolumbar junction. Resistance is then applied by the clinician. A strong and painful finding with resisted hip extension may indicate a grade I muscle strain of the gluteus maximus or hamstrings. It may also indicate gluteal bursitis or a lumbosacral strain. The strength of the medial and lateral hamstrings is also tested using resisted knee flexion, with the patient positioned in prone (see Chapter 20).

EXAMINATION

recruitment pattern, the order of firing should be gluteus maximus, opposite erector spinae, and then the ipsilateral erector spinae and hamstrings. Poor recruitment patterns are demonstrated as follows:

Standing. The patient is positioned in standing with both lower extremities in 50 degrees of knee flexion and 30 degrees of hip flexion. The clinician places the palm of each hand on the lateral aspects of the patient’s thighs

FIGURE 19-24  Hip adduction ROM using antigravity position.

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EXAMINATION THE EXTREMITIES

FIGURE 19-25  Hip abduction ROM.

FIGURE 19-26  Differentiating hip-adductor muscles—knee flexed.

before asking the patient to push outward against the hands. This weight-bearing method of assessing hip abductor muscle performance has been shown to be a reliable method to assess hip muscle strength.78 ▶▶ Side lying.22 The patient is positioned in side lying on the nontested side, with the trunk in neutral alignment and the pelvis perpendicular to the testing surface. The nontested hip and knee are flexed. The patient’s tested limb is placed in hip abduction, and neutral rotation, and neutral flexion/extension. The clinician then monitors for compensation as the patient holds the test position. If the patient can maintain the test position for three seconds without compensation, resistance may be applied. The clinician places one hand on the iliac crest to prevent the pelvis from rotating or tilting and uses the other hand to place resistance at the distal thigh or ankle (depending on the strength of the clinician/patient) in the direction of femoral adduction.

The primary hip adductor is the adductor longus. Adaptive shortening of the hip adductors can theoretically result in inhibition of the gluteus medius, a decrease in frontal stability, ITB tendinopathy, and anterior knee pain. Pain can be referred from the hip adductors into the anterolateral hip, groin, medial thigh, the anterior knee, and medial tibia. Pain in these regions with passive abduction, or active adduction, may indicate a strain of one of the adductors. The cause of the pain can be differentiated between the two-joint gracilis and the other hip adductors (longus, brevis, and pectineus) in the following manner. The patient is positioned in supine, with the tested leg over the edge of the table, monitored by the clinician. The clinician places the involved hip into the fully abducted position, and the knee is flexed (Fig. 19-26). If no pain is reproduced with this maneuver, the patient is asked to extend the knee (Fig. 19-27), thereby bringing in the gracilis and implicating it if the pain is now reproduced. This can be confirmed with resisted hip adduction and knee flexion. If the other adductors are implicated, this can be confirmed with resisted adduction (longus and brevis) or resisted hip adduction and hip flexion (pectineus). The strength of the hip-adductor muscle group can also be tested in side lying VIDEO, by flexing the uninvolved leg over the tested leg or by supporting the upper leg and then applying resistance. This position also stretches the hip abductors and can be a source of pain in the case of an ITBFS.

The correct sequence of firing for the hip abductors in side lying should be gluteus medius, followed by the quadratus lumborum and TFL after approximately 15 degrees of hip abduction. Altered patterning demonstrates the following:

860

1. External rotation of the leg during the upward movement, indicating an initiation and dominance of the movement by the TFL, accompanied by a weakness of the gluteus medius/minimus. The TFL has a tendency to become shortened and overactive. 2. Full external rotation of the leg occurs during the leg lift, indicating a substitution of hip flexion and iliopsoas activity for the true abduction movement. If the piriformis is shortened and overactive, the external rotation of the leg is reinforced. 3. A lateral pelvic tilt at the initiation of movement, indicating that the quadratus lumborum, which has a tendency to become shortened and overactive, is both stabilizing the pelvis and initiating the movement. This is indicative of a very poor movement pattern. Adduction.  Hip adduction is tested with the patient supine and with the uninvolved leg adducted over the other leg or held in flexion (Fig. 19-24). As before, the ASIS is monitored for motion, indicating the end of the range for adduction.

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FIGURE 19-27  Differentiating hip-adductor muscles—knee extended.

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EXAMINATION

A strong and painful finding with resisted adduction is usually the result of an adductor longus lesion, whereas a painless weakness with resisted abduction is often found in a palsy of the fifth lumbar root because of a disk herniation at the same level.

Patient seated. The patient is positioned sitting with the hip at 90 degrees of flexion. The sitting position assists in stabilizing the pelvis, and the pelvis should be closely monitored to avoid pelvic movement. The hip to be measured is placed at 0 degrees of abduction, and the contralateral hip is placed in about 30 degrees of abduction. The reference knee is flexed to 90 degrees, and the leg is passively moved to produce hip rotation. The tibiofemoral joint must be controlled to prevent motion (rotation or abduction/adduction), which could be construed as hip rotation.103 The motion is stopped when the clinician reaches a firm end-feel or when pelvic movement is necessary for additional movement of the limb. Limited internal rotation ROM when the hip is flexed to 90 degrees has been associated with bony impingement due to FAI.104 ▶▶ Patient prone. The patient is positioned prone with the feet over the edge of the bed. The hip being measured is placed in 0 degrees of abduction, and the contralateral hip is placed in about 30 degrees of abduction. Manual stabilization is applied to the pelvis to prevent pelvic movement and also at the tibiofemoral joint to prevent motion (rotation or abduction/adduction), which could be construed as hip rotation.103 The reference knee is flexed to 90 degrees, and the leg is passively moved to produce hip rotation. The motion is stopped when the clinician reaches a firm end-feel or when pelvic movement is necessary for additional movement of the limb. ▶▶ Patient supine. The patient is positioned in supine, with the leg in 90 degrees of hip flexion and 90 degrees of knee flexion. Hip IR (Fig. 19-28) and ER (Fig. 19-29) are then assessed.

Hip Joint Complex

Internal and External Rotation.  Although a number of muscles contribute to external rotation of the femur (see Table 19-4), six muscles function solely as external rotators. These are the piriformis, gemellus superior, gemellus inferior, obturator internus, obturator externus, and quadratus femoris. Normal ROM for hip external rotation is approximately 40–60 degrees. Excessive external rotation of the hip may indicate hip retroversion. The major internal rotator of the femur is the gluteus minimus, assisted by the gluteus medius, TFL, semitendinosus, and semimembranosus. The internal rotators of the femur are estimated to be only approximately one-third the strength of the external rotators. Normal ROM for hip internal rotation is approximately 30–40 degrees. Excessive internal rotation of the hip may indicate hip anteversion. Internal and external rotation of the hip can be measured with the patient in a variety of positions22: ▶▶

If an asymmetry exists between the two positions such that more ROM is available in the prone position compared with supine, a muscle restriction is likely present. When the asymmetry of internal rotation ROM is much greater than

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FIGURE 19-28  Supine hip IR.

the external rotation range in both the hip flexed and hip extended positions, structural anteversion may be present. If retroversion is present, the range of external rotation is greater than the range of internal rotation in both the flexed and extended positions of the hip.

FIGURE 19-29  Supine hip ER.

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EXAMINATION

It is important to remember that if an athlete is not getting enough rotation at the hip joint, compensation will occur with increased motion through the lumbar spine, the latter of which has a limited capacity for rotation. In addition, a decrease in hip rotation may create an increased shear force through the pubic symphysis, increasing the risk for developing osteitis pubis.105 Once the ROM measurements have been established, the strength of the internal rotators VIDEO and external rotators VIDEO is then assessed.

THE EXTREMITIES

Functional/Outcome Assessment There are over 40 hip outcome reporting measures in use today. Unfortunately, many of these measures are geared toward an older, less mobile, and less active age group. This creates a statistical phenomenon known as the ceiling effect. The ceiling effect occurs when the highest potential score on a rating tool is unable to properly assess a patient’s level of ability. It is, therefore, important to always choose an ageappropriate assessment tool. The most basic outcome measure for the hip is gait analysis, the function of the hip can be assessed through observation during functional activities such as sit to stand, or through

TABLE 19-14

use of a self-report measure, which allow a patient to rate his or her capacity to perform ADL. Table 19-14 outlines a functional assessment tool for the hip. Other tests that can be used include22: The Harris Hip Rating Scale (Table 19-15) is the most commonly used functional outcome assessment for the hip after total hip arthroplasty. The Modified Harris Hip Score (MHHS)92 is a disease specific selfreport questionnaire with questions related to pain and functional ability that excludes the clinician’s judgment of deformity and ROM which allows the patient to complete the questionnaire independently. ▶▶ Copenhagen Hip and Groin Outcome Score (HAGOS).106 The HAGOS was developed to assess patient’s hip and groin disability in a young, physically active patient. The HAGOS includes 37 items, consisting of 6 subscales: symptoms (7 items), pain (10 items), ADL (5 items), sports/recreation (8 items), physical activity (2 items), and quality of life (5 items). The response to each item is on a 5-point Likert scale, with a possible score range of 0–4. The score on each subscale was normalized to 100, with 100 referring to no problem and 0 to extreme problems. ▶▶

Functional Tests of the Hip

Starting Position

Action

Functional Test

Standing

Hip flexion: lift foot onto an 8-inch/20-cm step and return

5–6 repetitions: functional 3–4 repetitions: functionally fair 1–2 repetitions: functionally poor Zero repetitions: nonfunctional

Standing

Hip extension: sit in a chair and return to standing 

5–6 repetitions: functional 3–4 repetitions: functionally fair 1–2 repetitions: functionally poor Zero repetitions: nonfunctional

Standing 

Hip abductors: lift leg to the articular surfaces balance on one leg while keeping pelvis level

Hold 1–1.5 minutes: functional Hold 30–59 seconds: functionally fair Hold 1–29 seconds: functionally poor Cannot hold: nonfunctional

Standing 

Hip adductors: walk sideways 6 minutes

6–8 minutes one way: functional 3–6 minutes one way: functionally fair 1–3 minutes one way: functionally poor 0 minute: nonfunctional

Standing 

Hip internal rotation: test leg off floor (holding onto object for balance if necessary), internally rotate non–weight-bearing hip

10–12 repetitions: functional 5–9 repetitions: functionally fair 1–4 repetitions: functionally poor Zero repetitions: nonfunctional

Standing, facing closed door

Hip external rotation: test leg off floor (holding onto object for balance if necessary), externally rotate non–weight-bearing hip 

10–12 repetitions: functional 5–9 repetitions: functionally fair 1–4 repetitions: functionally poor Zero repetitions: nonfunctional

Data from Palmer ML, Epler M. Clinical Assessment Procedures in Physical Therapy. Philadelphia, PA: JB Lippincott; 1990.

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Harris Hip Rating Scale

Harris Hip Function Scale     44 40 30 20 10 0       11 8 5 0   11 7 5 4 2 0 0   11 8 5 2 0     4 2 1 0   4 2 0   5 3 0   1 0   4 0

Range of motion (5 points maximum) Instructions Record 10 degrees of fixed adduction as “–10 degrees abduction, adduction to 10 degrees” Similarly, 10 degrees of fixed external rotation as “–10 degrees internal rotation, external rotation to 10 degrees” Similarly, 10 degrees of fixed external rotation with 10 degrees further external rotation as “–10 degrees internal rotation, external rotation to 20 degrees” Permanent flexion (1) _____ A.  Flexion to (0–45 degrees) (45–90 degrees) (90–120 degrees) (120–140 degrees) B.  Abduction to (0–15 degrees) (15–30 degrees) (30–60 degrees) C.  Adduction to (0–15 degrees) (15–60 degrees) D. External rotation in extension to (0–30 degrees) (30–60 degrees) E. Internal rotation in extension to (0–60 degrees)

Range   _____ degrees         _____ degrees       _____ degrees     _____ degrees       _____ degrees

Index Factor   1.0 0.6 0.3 0.0   0.8 0.3 0.0   0.2 0.0     0.4 0.0

Index Value*

Hip Joint Complex

(Circle one in each group) Pain (44 points maximum) None/ignores Slight, occasional, no compromise in activity Mild, no effect on ordinary activity, pain after unusual activity, uses aspirin Moderate, tolerable, makes concessions, occasional codeine Marked, serious limitations Totally disabled Function (47 points maximum) Gait (walking maximum distance) (33 points maximum) 1. Limp: None Slight Moderate Unable to walk 2. Support: None Cane, long walks Cane, full time Crutch Two canes Two crutches Unable to walk 3.  Distance walked: Unlimited Six blocks Two to three blocks Indoors only Bed and chair Functional activities (14 points maximum) 1. Stairs: Normally Normally with banister Any method Not able 2.  Socks and tie shoes: With ease With difficulty Unable 3. Sitting: Any chair, 1 hour High chair, ½ hour Unable to sit ½ hour any chair 4.  Enter public transport: Able to use public transportation Not able to use public transportation Absence of deformity (requires all four) (4 points maximum) 1.  Fixed adduction female; unilateral Male > female; blacks > whites

Observation

Short limb, associated with torticollis

Irritable child; motionless hip; prominent greater trochanter; mild illness

Short limb; high greater trochanter; quad atrophy; adductor spasm

Decreased flexion, abduction, and external rotation; thigh atrophy; and muscle spasm

Position

Flexed and abducted

Flexed, abducted, and externally rotated

 

 

Pain

 

Mild pain with palpation and passive motion; often referred to knee

Gradual onset; aching in hip, thigh, and knee

Vague pain in knee, Acute: severe pain in suprapatellar area, knee; moderate: pain thigh, and hip; pain in in thigh and knee; extreme motion tenderness over hip

50% sharp pain and Insidious onset and pain Severe pain in groin area with fall in barometric 50% insidious and pressure intermittent pain in extreme ends of range

History

May be breech birth

Steroid therapy; fever

20–25% familial, low birth weight, and growth delay

Low-grade fever

May be trauma

 

May be prolonged trauma and faulty body mechanics

May be trauma and fall

Range of motion

Limited abduction

Decreased (capsular pattern)

Limited abduction and extension

Decreased flexion, limited extension, and internal rotation

Limited internal rotation, abduction, and flexion; increased external adductor spasm

Decreased range of motion

Decreased motion, external and internal rotation, and extreme flexion

Limited

Special tests

Joint aspiration Galeazzi’s sign, Ortolani’s sign, and Barlow’s sign

 

 

 

 

 

 

Gait

 

Antalgic gait after activity

Refuses to walk and antalgic limp

Coxalgic limp Acute: antalgic; chronic: Trendelenberg external rotation

Limp

 

Radiologic findings

Upward and lateral CT scan: localized abscess; increased displacement separation of and delayed ossification development of acetabulum

In stages: increased density, fragmentation, and flattening of epiphysis center

Normal at first, widened medial joint space

Displacement of upper femoral epiphysis, especially in frog position

Increased bone density, osteophytes, and subarticular cysts; degenerated articular cartilage

Fracture line and possible displacement; short femoral neck

Septic Arthritis Less than 2 years; rare in adults

Refuses to walk

Slipped Femoral Capital Epiphysis

Degenerative Avascular Necrosis Joint Disease

Fracture

Males 10–17 years; females 8–15 years

30–50 years

40 years

Older adults

Male > female

Female > male

Female > male

Short limb, obese, quadriceps atrophy, and adductor spasm

 

Frequently obese, joint crepitus, and atrophy of gluteal muscles

Ecchymosis; may be swelling; short limb

Flexed, abducted, and externally rotated

 

 

External rotation

Reproduced with permission from Richardson JK, Iglarsh ZA. Clinical Orthopaedic Physical Therapy. Philadelphia, PA: WB Saunders, 1994.

Flattening followed by collapse of femoral head

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TABLE 19-21

Differential Diagnosis for Common Causes of Hip Pain

Condition

Patient Age (year)

Mechanism of Injury/Onset

Area of Symptoms

Symptoms Aggravated by

Observation

Trochanteric bursitis 

15–45 

Direct trauma Microtrauma

Lateral aspect of hip/thigh 

Lying on involved side  

Unremarkable  

Groin strain 

20–40 

Sudden overload 

Anteromedial thigh Medial thigh

Running  

Possible bruising around medial thigh 

Hamstring muscle tear

15–45

Sudden overload

Buttock and posterior thigh

Running

Possible bruising around posterior thigh

Piriformis syndrome 

25–55 

Gradual  

Buttock and posterior thigh Back of leg

Prolonged sitting  

Unremarkable  

Hip OA 

50+ 

Gradual  

Anterior thigh Anteromedial thigh

Weight-bearing  

Possible atrophy of thigh muscles Altered gait

Iliotibial band syndrome 

25–55 

Overuse  

Lateral aspect of thigh Lateral aspect of knee

   

Unremarkable  

Psoas bursitis

20–40

Overuse

Anteromedial thigh

 

Unremarkable

Lumbar/thoracic disk pathology 

20–50 

Gradual Sudden overload 

Varies according to spinal nerve root involved but occurs in dermatomal distribution

Lumbar/thoracic flexion (bending/sitting)  Activities that increase intrathecal pressure

May have associated deviation of trunk

(Continued)

Hip Joint Complex

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908

THE EXTREMITIES

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TABLE 19-21

Differential Diagnosis for Common Causes of Hip Pain (Continued)

AROM

PROM

Resisted

Tenderness with Palpation

Painful hip abduction with rotation  

Pain at end-range hip ER Pain with hip ER with abduction

Pain with resisted hip abduction Pain with resisted hip IR

Lateral thigh over greater trochanter  

Hip extension only limited movement 

Pain at end-range hip extension Pain at end-range hip abduction

Pain with resisted hip adduction  

Proximal medial thigh  

Hip ER limited and painful

Pain at end-range hip flexion

 

 

SLR limited and painful 

Pain at end-range hip extension Pain with passive SLR

Pain with resisted hip extension Pain with resisted knee flexion

Posterior thigh  

SLR limited and painful 

Pain at end-range hip ER Pain with passive SLR

Pain with resisted hip ER  

Buttock  

Limited hip IR and extension

Pain at end-range hip IR

Weak hip abduction

Anterior hip

Painful hip IR

All movements feel stiff

General weakness of hip muscles

 

Painful hip extension

 

 

 

Pain on moving from knee extension to flexion 

Pain at end-range hip ER with abduction 

All resistive tests negative  

Lateral epicondyle of femur Lateral aspect of knee

Hip extension with only limited movement

Pain at end-range hip extension

Pain with resisted hip flexion

Anterior hip

Increased symptoms with trunk flexion

Symptoms invariably increased with passive SLR

Fatigable weakness of associated myotome

Possible tenderness over involved spinal segment

Increased symptoms with hip flexion with knee extended (SLR)

 

 

 

AROM, active range of motion; ER, external rotation; IR, internal rotation; OA, osteoarthritis; PROM, passive range of motion; SLR, straight-leg raise.

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Adductor-related ▶▶ Iliopsoas-related ▶▶ Inguinal-related ▶▶ Pubic-related ▶▶ Hip-related ▶▶ FAI-related ▶▶ Other (other orthopaedic, neurological, rheumatological, urological, gastrointestinal, dermatological, oncological, or surgical conditions) ▶▶

Once the diagnosis has been established, the conservative intervention should be causal: A period of relative rest and antiinflammatory medications. ▶▶ TFM can be applied locally. ▶▶ Ultrasound, electrical stimulation, thermotherapy, and cryotherapy as appropriate. ▶▶ Stretching as tolerated to the muscles surrounding the injured area: ■■ The short and long adductors. ■■ Hip flexors (iliopsoas and rectus femoris). ■■ Hip internal rotators. ■■ Abdominals. ■■ Gluteal muscles. ▶▶

▶▶

▶▶

Strengthening of the same muscle groups. The strengthening exercises are performed isometrically initially, and then concentrically and eccentrically, and finally isokinetically as appropriate. Core stability training. A particularly effective form of core strengthening for athletic pubalgia, developed by Alex McKechnie, uses diagonal elastic tubing resistance between

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the upper and lower extremities. These exercises combine a contraction of the pelvic floor and transversus abdominis muscles while performing activities such as squats (Fig. 19-59), lunges (Fig. 19-58), and sport-specific movements. ▶▶ Proprioception training. Effective warm-ups and preparation before the sporting activity can play an important preventative role. In cases of failed conservative intervention, which is common, surgical intervention (pelvic floor repair) or cessation of the offending activity becomes the patient’s only choice.248 Postsurgical rehabilitation uses many of the same exercises and modalities as in the traditional rehabilitation program outlined above.

INTEGRATION OF PRACTICE PATTERNS 4C, 4F, AND 5F: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, ROM ASSOCIATED WITH SPINAL DISORDERS, SIGN OF THE BUTTOCK, MYOFASCIAL PAIN DYSFUNCTION (REFERRED PAIN PATTERNS), AND PERIPHERAL NERVE ENTRAPMENTS

Hip Joint Complex

a thorough knowledge of the differential diagnosis. Once serious pathology has been ruled out, the clinician should screen for potential lumbar spine- and SIJ-related pathology using the subjective history and clinical examination tests that are highly sensitive.249 A lack of peripheralization or centralization (sensitivity, 92%; negative likelihood ratio = 0.12) of the athlete’s symptoms with repeated lumbar spine ROM testing and negative straight leg raise (sensitivity, 97%; negative likelihood ratio = 0.05) and slump testing (sensitivity, 83%; negative likelihood ratio = 0.32) assist with ruling out the potential existence of discogenic/radiculopathy pathology.249 Palpation of the relevant structures should help in locating the cause, as will resistive testing of the various muscles. Acute strains often occur at the musculotendinous junction, specifically of the adductor longus, rectus femoris, and iliopsoas muscles.249–251 Acute adductor longus and rectus femoris injuries may also involve a tendinous rupture/avulsion, primarily at the proximal insertions.249–251 In contrast to strains, groin overuse injuries more often involve bone and tendons and their insertions, and rarely involve the rectus femoris.249 Until recently, there has been little agreement regarding terminology, definitions, and classification of groin pain in athletes.249 Groin pain can be classified according to cause in the following manner252–254:

If the tests and measures of the hip are negative for a hip disorder or a dysfunction of the lower kinetic chain, the clinician should examine the lumbar spine and SIJ, both of which can refer pain to this region. Many internal disorders such as femoral and inguinal hernias, pelvic inflammatory disease, prostatitis, and nephrolithiasis can produce pain in the lower abdomen and groin region (see Chapter 5). These are all out of the scope of practice for the physical therapist, and proper referral to an internist, urologist, or gynecologist should be sought.

Sign of the Buttock The sign of the buttock is a collection of signs that indicate the presence of serious pathology posterior to the axis of flexion and extension in the hip. Among the causes of the syndrome are osteomyelitis, fracture of the sacrum/pelvis, infections, sacroiliitis, gluteal hematoma, septic bursitis, ischiorectal abscess, tumor, and rheumatic bursitis. Typical findings include gross hip weakness with empty end-feel. The involved buttock looks larger. The seven signs of the buttock are a limited straight-leg raise; ▶▶ limited hip flexion; ▶▶ limited trunk flexion; ▶▶ a noncapsular pattern of hip restriction; ▶▶ painful and weak hip extension; ▶▶ gluteal swelling; ▶▶ an empty end-feel on hip flexion. ▶▶

If the sign of the buttock is present, a medical referral is necessary.

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Meralgia Paresthetica

THE EXTREMITIES

Patients with meralgia paresthetica typically describe burning, coldness, lightning-type pain, deep muscle achiness, and tingling or frank anesthesia in the anterolateral thigh (see Chapter 5). There may also be local hair loss in the anterolateral thigh.255 The symptoms may be exacerbated when the hip is extended, as in prone lying, or when standing erect. Sitting may relieve the symptoms in some patients but exacerbate them in others. Eventually, there may be no position that provides relief.255 The initial intervention of meralgia paresthetica is conservative, and patients may benefit from analgesics, NSAIDs, looser clothing, and weight loss.

Piriformis Syndrome Piriformis syndrome is the result of entrapment of the sciatic nerve by the piriformis muscle, as it passes through the sciatic notch (see Chapter 5).

Entrapment of the Obturator Nerve Compression of the anterior division of the obturator nerve in the thigh has been described recently as one possible cause for adductor region pain, and entrapment of this nerve has been documented by nerve conduction studies. The fascia over the nerve is thought to contribute to compression of the nerve, or perhaps allow for the development of a compartment syndrome.

Myofascial Pain Dysfunction Myofascial pain is referred to the hip from the following muscles: quadratus lumborum, piriformis, gluteus minimus, and adductor longus. Quadratus Lumborum.  This muscle is perhaps one of the most overlooked sources of hip pain. The more superficial trigger points of this muscle refer pain to the lateral ilium and greater trochanter and may also refer pain into the groin in the region of the inguinal ligament. The tenderness in the trochanteric region can be misdiagnosed as trochanteric bursitis. Clinical findings can include restriction of hip joint movements by lumbar spasm; trochanteric and buttock tenderness; ▶▶ a contralateral short leg; ▶▶ an ipsilateral flexed innominate. ▶▶ ▶▶

Conservative intervention includes gentle, pain-free static stretching of the muscle, soft tissue techniques, and progressive strengthening.

910

Gluteus Minimus.  Trigger points may be located in the posterior and anterior portions of this muscle. The posterior trigger point refers pain to the medial lower buttock and into the posterior thigh and calf. These trigger points have the potential to increase the tone in the hamstring and calf muscles. Stretching the gluteus minimus before hamstring and calf stretching allows these two muscles to lengthen much more readily. The anterior trigger point refers symptoms to the lower buttock, and down the lateral thigh and leg as far as the lateral malleolus, on occasion. Conservative intervention includes gentle, pain-free static stretching of the muscle, soft tissue techniques, and progressive strengthening.

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Adductor Longus.  Trigger points in this muscle strongly refer to the anterior hip and anterior knee. Clinical findings include pain with resisted strength testing; positive FABER test for pain; ▶▶ marked restriction of hip abduction. ▶▶ ▶▶

Conservative intervention includes gentle, pain-free static stretching of the muscle, soft tissue techniques, and progressive strengthening.

PRACTICE PATTERN 4G: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, AND ROM ASSOCIATED WITH FRACTURES Avulsions Apophyseal avulsions of the pelvis and proximal femur occur most commonly to male athletes 10–20 years old, usually as the direct result of vigorous or uncoordinated activities such as kicking, jumping, hurdling, sprinting, and punting, involving the sartorius or TFL. Anterior Iliac Spine.  The anterior iliac spine is a common site of the injury, especially during the middle-to-late teenage years when the iliac crest unites with the ilium. Clinical findings can include point tenderness; crepitus; ▶▶ hematoma; ▶▶ limited hip motion; ▶▶ pain with resisted hip flexion and passive hip extension that increase pain at the site. ▶▶ ▶▶

Conservative intervention includes ice and hip spica compression, followed by bed rest, progressing to crutch ambulation and activity modification. Return to normal activity follows a period of strength, flexibility, and functional training. Hamstring Tendon.  Complete and partial avulsions of the proximal hamstring tendon from the ischial origin are common during sporting activities that generate forceful hip flexion moments while the knee is extending.256 The patient typically presents with a significant gait abnormality and an inability to fully extend the trunk and bear weight on the involved side.256 These injuries are often treated with open surgical repair. Ischial Apophyseal.  This injury commonly occurs during the teenage years, especially 13–16 years, as the apophysis has the least amount of bony bridging or fusion at a time when the individual is the most active. The most common mechanisms of injury are sprinting and overzealous stretching. Common clinical findings include ischial tenderness and pain, especially when sitting. Ischial apophyseal avulsion fractures that are displaced less than 1 cm can be treated conservatively256 by avoiding hamstring stretching and tension for several weeks to prevent further displacement and allow healing.257

Stress Fractures of the Femoral Neck/Head Stress fractures result from accelerated bone remodeling in response to repeated stress (see Chapter 2). Although stress

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obtained until the athlete is full weight bearing without pain. Water running and water walking are progressed. If these remain pain free, running on land is commenced, with the initial run being no further than one-quarter mile. ▶▶ If there is an overt fracture line on the radiographs with no displacement and provided that only the cortex is involved, an initial period of either bed rest or complete non-weight bearing is necessary. The patient is progressed to partial and then full weight bearing on crutches as symptoms permit. Roentgenograms every 2–3 days during the first week are necessary to detect any widening of the fracture line. If healing does not occur, internal fixation with some form of hip pin is indicated.

Fatigue stress fractures are caused by repetitive and abnormally high forces from muscle action and/or weight-bearing torques and are often found in persons with normal bone densities. This type of stress fracture at the hip is most common in athletes involved in intense training, including military personnel. ▶▶ Insufficiency stress fractures are associated with individuals who have compromised bone densities. Since insufficiency stress fractures are associated with decreased bone mineral density, they tend to be most common in the elderly, especially postmenopausal women. Other predisposing factors for poor bone density include radiation treatments, rheumatoid arthritis due at least in part to the associated disuse and either corticosteroid or methotrexate treatment, renal failure, coxa vara, metabolic disorders, and Paget’s disease.

Hip fracture, defined as a fracture of the proximal third of the femur, is the orthopaedic problem with the highest incidence, cost, and risk. The morbidity rates after the fracture is 32–80%.262 Hip fractures are associated with substantial morbidity and mortality in the elderly. Approximately 90% of hip fractures result from a simple low energy fall.263 The most common risk factors for falls (and thus hip fractures) are age, gender, race, institutionalization/hospitalization, medical comorbidities (cardiac disease, stroke, dementia, poor hip fracture, osteoporosis), hip geometry, medication, bone density, diet, smoking, alcohol consumption, fluorinated water, urban versus rural residents, and climate. A number of hip fractures exist:

▶▶

The physical examination is often negative, although there may be a noncapsular pattern of the hip,261 an empty end-feel, or pain at the extremes of hip internal or external rotation or pain with resisted hip external rotation. In addition, the auscultatory patellar-pubic percussion test may be positive (see “Special Tests” section). Differential diagnosis includes OA of the hip, referred symptoms from the spine, trochanteric bursitis, or septic arthritis. Radiographs taken soon after the symptoms begin have been reported to be positive in only 20% of cases. Diagnosis is best confirmed with bone scintigraphy (scan), although these have been shown to be prone to false negatives. The intervention varies according to the bone scintigraphy findings. ▶▶

If there is a positive scan only, or sclerosis and no fracture line on the radiographs, the intervention ranges from modified bed rest to non-weight bearing with crutches until symptoms subside. Once pain free, weight bearing is progressed. When significant PWB is pain free, cycling and swimming may be permitted. Weekly radiographs are

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An overt fracture with radiographic evidence of opening or displacement is significant and requires surgical intervention, usually in the form of a hip screw and plate. Displaced fractures must be treated as an orthopaedic emergency.

Hip Joint Complex

fractures are a relatively uncommon etiology of hip pain, if not diagnosed in a timely fashion, progression to serious complications can occur.258 It is estimated that 1.0–7.2% of all stress fractures involve the femoral neck, with another 5% involving the femoral head.259 The fracture typically occurs on the superior side (tension-side fractures—high risk) or the inferior side (compression-side fractures— low risk) of the femoral neck.260 The tension-side fracture may develop into a complete and displaced fracture if left untreated. The most frequent symptom is the onset of sudden hip pain, usually associated with a recent change in training (particularly an increase in distance or intensity) or a change in training surface. The earliest and most frequent symptom is a pain in the deep thigh, inguinal, or anterior groin area. Pain can also occur in the lateral aspect or anteromedial aspect of the thigh. The pain usually occurs with weight bearing or at the extremes of hip motion and can radiate to the knee. Less severe cases may only have pain following a long run. Night pain may occur if the fracture progresses. Stress fractures are generally classified as fatigue or insufficiency fractures261:

Hip Fracture

Intertrochanteric and Subtrochanteric: Occur on the proximal, upper part of the femur or thigh bone between the greater trochanter, where the gluteus medius and minimus muscles attach, and the lesser trochanter, where the iliopsoas muscle attaches. ▶▶ Femoral neck: Fractures of the femoral neck are proximal to intertrochanteric fractures, whereas subtrochanteric fractures are distal or below to the trochanters. ▶▶

Intertrochanteric.  The intertrochanteric area of the femur, the area of the lesser and the greater trochanters and where the femur changes from an essentially vertical bone to a bone angling at a 45-degree angle from the near-vertical to the acetabulum or pelvis, is proximal to the femoral shaft and distal to the femoral neck. The etiology of intertrochanteric fractures is typically a combination of increased bone fragility of the intertrochanteric area of the femur associated with decreased muscle tone of the muscles in the area secondary to the aging process. The current approach for intertrochanteric fractures is surgical intervention. With few exceptions, open reduction and internal fixation (ORIF) is used to treat essentially all intertrochanteric fractures. Following the procedure, a preventive protocol of antiembolism stockings and anticoagulants

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is followed. Physical therapy involves functional and gait training according to the weight-bearing status, and a progressive exercise program of ROM and strengthening.

and independence in ADL are considered when determining the optimal method of surgical repair.

CLINICAL PEARL CLINICAL PEARL Hip fractures are associated with a high risk of DVT (see Chapter 1). Routine thromboprophylaxis remains critical and is the standard of care.

THE EXTREMITIES

Subtrochanteric.  The subtrochanteric region of the femur is exposed to high stresses during ADLs; during normal ADLs, up to six times the body weight is transmitted across the subtrochanteric region of the femur. These fractures are most frequently seen in two patient populations; older osteopenic patients after a low-energy fall and younger patients involved in high-energy trauma. This region of the femur consists primarily of cortical bone, so healing in this region is predominantly through a primary cortical healing, which makes fracture consolidation quite slow to occur. Surgical treatment can be divided into three main techniques: External fixation: Rarely used but is indicated in severe open fractures. External fixation is usually temporary, and the conversion to internal fixation can be made if and when the soft tissues have healed sufficiently. ▶▶ Open reduction with plates and screws: Following ORIF and plate fixation, minimally protected weight bearing can begin immediately but is advanced slowly beginning approximately 4 weeks after surgery, with full weight bearing anticipated at 8–12 weeks. ▶▶ Intramedullary fixation: Following intramedullary nailing, if the bone quality and cortical contact is adequate, 50% PWB can be allowed immediately. With less stability, patients can perform touchdown weight bearing. ▶▶

As most elderly patients may have difficulty complying with the weight-bearing restrictions, they are often permitted to progress to full postoperative weight-bearing status.

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Femoral Neck Fracture.  Femoral neck fractures are often associated with multiple injuries and high rates of avascular necrosis and nonunion. Hip fractures are common in the geriatric population and can have devastating consequences. A number of factors predispose the elderly population to fractures, including decreased physical activity, osteoporosis, impaired vision, neurologic disease, and poor balance. The decision for operative or nonoperative treatment and the type of surgical intervention are based on many factors. Tensiontype fractures are less stable than compression fractures, the latter of which can be treated nonoperatively. Tension fractures may require operative stabilization with multiple screws or pins as they are potentially unstable. Nondisplaced fractures are often treated conservatively with bed rest and/or the use of crutches until x-ray films show evidence of callus formation and passive hip movement is pain free. In the elderly population, premorbid cognitive function, walking ability,

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Femoral neck fractures are frequently treated using a prosthesis or replacement device (i.e., total hip arthroplasty or hemiarthroplasty). The prognosis for femoral neck fractures depends on the extent of injury (i.e., whether circulation has been disturbed, amount of comminution, and the amount of displacement), the adequacy of the reduction, and the adequacy of fixation. Maintaining aerobic conditioning throughout the rehabilitation process is important. The weight-bearing status following the surgical procedure depends on the stability of reduction, bone, and method of fixation. The exercises performed initially include quadriceps sets, gluteal sets, heel slides, active-assisted hip abduction and adduction, and supine internal and external hip rotation. Once PWB ambulation is allowed, aquatic training such as swimming or deep-water running may be used if available. Once full weight bearing is achieved, exercises begin to address functional strengthening of the gluteus medius, the iliopsoas, gluteus maximus, adductors (magnus, longus, and brevis), quadriceps, and hamstrings. If protected or non–weight-bearing ambulation is necessary, then upper body exercise, such as an upper body ergometer, can be used.

THERAPEUTIC TECHNIQUES More recently, the minimally invasive anterior approach, using one or two small incisions, has become more popular. The rationale for minimally invasive procedures is that the use of small incisions potentially lessens soft tissue trauma during surgery and, therefore, should improve and accelerate a patient’s postoperative recovery. Other benefits include reduced blood loss, reduce postoperative pain, shorter length of hospital stay and lower cost of hospitalization, a more rapid recovery of functional mobility, and a better cosmetic appearance of the surgical scar. A review of the literature reveals inconsistent practice patterns in the physical therapy management of THA patients. Most surgeons have designed their own postsurgical protocols, which should be strictly adhered to. Standard precautions are observed with patients who underwent a lateral or posterolateral approach to prevent posterior hip dislocation. These include the following: Avoidance of hip adduction. Typically an abduction wedge or pillow is prescribed. A pillow is placed between the legs if the patient wants to lie on the side. ▶▶ Avoidance of hip internal rotation. Combinations of hip flexion, internal rotation, and adduction must be avoided for up to 4 months after surgery or until physician clearance. ▶▶

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▶▶

Avoidance of hip flexion greater than 90 degrees (bending forward at the hip, reaching for objects or tying shoes). Elevated chairs or toilet seats can be used to increase compliance, as can an assistive device or reacher.

Precautions for a patient who underwent an anterior/anterior lateral or direct lateral approach, with or without trochanteric osteotomy include:

If a trochanteric osteotomy was performed, or the gluteus medius was incised and repaired, the patient should not perform active, antigravity hip abduction for at least 6–8 weeks or until approved by the surgeon.

Techniques to Increase Joint Mobility Passive Articular Mobilization Techniques In a single-blind randomized study153 investigating interventions for hip OA, 109 subjects were randomly assigned to receive mobilization and manipulation to the hip joint or active exercises designed to improve strength and ROM for nine visits over a period of 5 weeks. Success rates after 5 weeks were 81% in the manual therapy group and 50% in the exercise group. Furthermore, patients in the manual therapy group had significantly better outcomes on pain, stiffness, hip function, and ROM. The effects of manual therapy on the improvement of pain, hip function, and ROM remained after 29 weeks. Mobilizations of this joint are typically performed using a sustained stretch to decrease a hip joint capsular restriction, with the stretch being governed by the direction of the restriction, rather than by the concave–convex rule. For example, if hip joint extension is restricted, the distal femur is moved into the direction of hip extension. The joint is initially positioned in its neutral position and is progressively moved closer to the end of the range. A belt can also be used for this technique. Rotations can be combined with any sustained stretch performed in a cardinal plane. Distraction or compression techniques can be used alone or combined with rotations. Distraction.  Joint distraction mobilizations are indicated for pain and any hypomobility at the hip joint, as in the case when the pain is reported by the patient before tissue resistance is felt by the clinician. The lateral distraction technique (see Fig. 19-30) can be used to increase hip joint ROM into adduction and internal rotation. Leg Traction (Inferior Glide). An inferior distraction (Fig. 19-31) can be used for temporary relief of joint pain, to increase ROM into hip joint abduction and for stretching capsular adhesion that is pronounced in the inferior portion of the joint capsule. Quadrant (Scouring) Mobilizations. Quadrant mobilizations involve flexion and adduction of the hip, combined

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Mobilizations with Movement To Restore Internal Rotation of the Hip.264,265  This technique is employed when the patient presents with early signs of hip joint degeneration, as indicated by minor capsular signs and slight degenerative changes on radiographs. A belt that can be altered in length is required for the technique. The patient is positioned in supine with the involved hip and knee flexed and the foot just off the edge of the bed, with the clinician standing on the involved side, facing the patient’s head. A belt is placed around the back of the clinician, just below the hip joints, and around the patient’s thigh as proximal as possible, so that the belt is approximately horizontal. Using the hand closest to the patient’s head, the clinician grasps the lateral iliac crest of the involved side, with the elbow in the crease of the clinician’s groin to stabilize the pelvis during the maneuver. The clinician wraps the other hand around the patient’s midthigh. From this position, the clinician slowly extends their own hips to apply a distraction force to the patient’s hip joint, while maintaining the fixation of the ilium. If the maneuver produces any pain, it should be discontinued. This should be differentiated from discomfort, which might be caused by inappropriate placement of the belt.

Hip Joint Complex

Avoidance of hip flexion greater than 90 degrees. ▶▶ Avoidance of hip extension, adduction, and external rotation past neutral. ▶▶ Avoidance of the combined motions of flexion, abduction, and external rotation. ▶▶

with simultaneous joint compression through the femur. The flexed and adducted thigh is swept through a 90–140-degree arc of flexion while maintaining joint compression. This arc of motion should feel smooth and should be pain free. In an abnormal joint, pain or an obstruction to the arc occurs during the movement. In selected nonacute cases, the procedure may be used as an effective mobilizing procedure, where grade II to III mobilizations are applied perpendicular to the arc throughout. Posterior Glide.  The posterior glide mobilization (Fig. 19-32) is used to increase flexion and to increase internal rotation of the hip. Anterior Glide.  The anterior glide (Fig. 19-33) is used to increase extension and to increase external rotation of the hip. Inferior Glide.  The inferior glide is used to increase abduction of the hip.

To Restore Flexion of the Hip.  The technique to restore flexion of the hip is identical to the one described above, except that during the distraction, the clinician passively flexes the patient’s hip into flexion by side bending at the waist.266

Techniques to Increase Soft Tissue Extensibility Manual techniques can be used for improving hip ROM. Iliotibial Band.  Stretching of the IT band is commonly prescribed in standing where the patient crosses one leg in front of the other so that the back leg is positioned in internal rotation. The patient then either places both hands on the hips or uses one hand for balance before swaying laterally toward the side of the back leg to impart a stretch on the lateral hip structures on that side. However, this particular maneuver applies more of the stretch to the gluteus medius and lateral capsule than the ITB. However, if the patient performs this sway with both arms held extended overhead, more of the stretch is

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THE EXTREMITIES

imparted on the ITB.267 An alternative maneuver can be used where the patient is positioned in the half kneeling position so that one hip is flexed to 90 degrees and the other knee is on the floor. The patient is asked to maximally drop the pelvis on the side of the flexed hip to adduct that hip. The patient also is asked to extend the hip by means of a posterior pelvic tilt. Iliopsoas.  The patient is positioned in side lying (Fig. 19-91). The patient is instructed to flex the uninvolved hip and maintain its position by using their arms to help stabilize the lumbopelvic region. While monitoring the lumbopelvic motion with one hand, the clinician passively extends the thigh with the other arm/hand. The advantage of this technique is that varying degrees of hip adduction/abduction and knee flexion/extension can be controlled. The disadvantage is that the technique is more physically demanding for the clinician. Iliopsoas and Rectus Femoris. Although a number of exercises have been advocated to stretch these muscle groups, because of their potential to increase the anterior shear of the lumbar vertebrae either directly or indirectly, the standing/ kneeling position is preferred. A pillow is placed on the floor, and the patient kneels down on the pillow with the other leg placed out in front in the typical lunge position (Fig. 19-92). The patient is asked to perform a posterior pelvic tilt and to maintain an erect position with respect to the trunk. From this starting position, the patient glides the trunk anteriorly, maintaining the trunk in a near vertical position. A stretch on the upper aspect of the anterior thigh of the kneeling leg should be felt. The rectus

FIGURE 19-91  Side-lying hip flexor stretch.

FIGURE 19-92  Iliopsoas and rectus femoris stretch.

femoris can be stretched further from this position by grasping the ankle of the kneeling leg and raising the foot toward the buttock (Fig. 19-92). Tensor Fascia Latae.  The patient is positioned supine with the legs straight. The foot of the leg to be stretched is placed on the table on the outside of the uninvolved straight leg. The patient reaches and grasps the knee of the involved leg and pulls the knee across and over the straight leg (Fig. 19-93). Both shoulders should be kept flat on the table. At the point the stretch is felt, the position is maintained for approximately 30 seconds. The stretch is repeated 10 times.

FIGURE 19-93  Tensor fascia latae stretch.

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CASE STUDY RIGHT GROIN PAIN HISTORY General Demographics A 62-year-old male.

Past History of Current Condition A long history of OA of the spine and occasional twinges of pain in the right groin. The patient also has a history of right-sided sciatica. Past Medical/Surgical History The patient had a total joint replacement of the right knee approximately 4 months ago. Medications Celecoxib. Other Tests and Measures Radiographs of right hip are negative for loose bodies, tumors, and fracture. Advanced OA of right hip was noted. Social Habits (Past and Present) Nonsmoker. Drinks occasionally. Active life style. Social History Married. Two children, both live close by. Family History No relevant history of hip problems in family.

Living Environment Lives in an apartment. One flight of stairs to negotiate. Occupational/Employment/School Retired railroad laborer. High school education. Functional Status/Activity Level The patient demonstrates difficulty rising from a chair and transferring from bed to chair. Health Status (Self-report) In general good health, but pain interferes with tasks at home and with helping his sick wife.

Hip Joint Complex

History of Current Condition A patient presents with complaints of aching pain in the right groin that varies in severity and extends down the anterior thigh to the knee. The pain began gradually about 3 months before. Initially, the patient felt stiffness whenever he sat for prolonged periods of time or after a night’s sleep. The patient reports that he can no longer walk as far as he once did and that negotiating stairs was especially painful.

Growth and Development Normal development; left-handed.

Systems Seview Unremarkable.

Questions 1. List the possible structure(s) that can produce groin pain. 2. What might the history of pain with early morning stiffness and pain with stair negotiation tell the clinician? 3. What other activities might increase the patient’s symptoms? Why? 4. To help rule out the various causes of groin pain, what other questions can you ask? 5. What is your working hypothesis at this stage? List the various diagnoses that could present with these signs and symptoms and the tests you would use to rule out each one. 6. Does this presentation/history warrant a Cyriax lower quarter scanning examination? Why or why not?

CASE STUDY THIGH PAIN HISTORY History of Current Condition A 22-year-old male sustained a kick to the right thigh approximately 2 weeks ago while playing college soccer. He complains of a dull ache on the anterior aspect of his thigh. The pain is worse with activities that involve attempting to squat or kick. The patient also reports feeling a lump on the front of his thigh. The patient saw his physician who diagnosed the condition as a deep quadriceps contusion and prescribed 8 weeks of physical therapy.

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Past History of Current Condition No previous history of thigh pain. Past Medical/Surgical History No history of previous knee or hip injury. ▶▶ No back pain/surgery reported. ▶▶ No knee surgeries reported. ▶▶ History of chronic ankle sprains. ▶▶

Medications None.

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Other Tests and Measures Radiograph results pending. Occupational/Employment/School Full-time student at local college for the past 2 years. Functional Status/Activity Level Very active. In addition to soccer, the patient also plays tennis and racquetball. Health Status (Self-report) In general, good health.

THE EXTREMITIES

Questions 1. Given the specific mechanism of injury, list all of the structures you suspect could be injured and will require a specific examination.

REFERENCES

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2. What condition could be present with the history of pain in a muscle belly following a contusion? 3. What other activities do you suspect would increase the patient’s symptoms? Why? 4. In a patient with an insidious onset of pain, what questions would you ask to help rule out the various causes of anterior thigh pain? 5. What is your working hypothesis at this stage? 6. Does this presentation/history warrant a lower quarter scan? Why or why not?

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253. Griffin DR, Dickenson EJ, O’Donnell J, et al. Infographic. The Warwick Agreement on femoroacetabular impingement syndrome. Br J Sports Med. 2016;50:1179. 254. Weir A, Brukner P, Delahunt E, et al. Doha agreement meeting on terminology and definitions in groin pain in athletes. Br J Sports Med. 2015;49:768–774. 255. Ivins GK. Meralgia paresthetica, the elusive diagnosis: clinical experience with 14 adult patients. Ann Surg. 2000;232:281–286. 256. Sherry M. Examination and treatment of hamstring related injuries. Sports Health. 2012;4:107–114. 257. Gidwani S, Bircher MD. Avulsion injuries of the hamstring origin—a series of 12 patients and management algorithm. Ann R Coll Surg Engl. 2007;89:394–399. 258. Boden BP, Osbahr DC. High-risk stress fractures: evaluation and treatment. J Am Acad Orthop Surg. 2000;8:344–353. 259. Clough TM. Femoral neck stress fracture: the importance of clinical suspicion and early review. Br J Sports Med. 2002;36:308–309. 260. Fullerton LR, Jr., Snowdy HA. Femoral neck stress fractures. Am J Sports Med. 1988;16:365–367. 261. Gurney B, Boissonnault WG, Andrews R. Differential diagnosis of a femoral neck/head stress fracture. J Orthop Sports Phys Ther. 2006;36: 80–88. 262. Braithwaite RS, Col NF, Wong JB. Estimating hip fracture morbidity, mortality and costs. J Am Geriatr Soc. 2003;51:364–370. 263. Liporace FA, Egol KA, Tejwani N, Zuckerman JD, Koval KJ. What’s new in hip fractures? Current concepts. Am J Orthop. 2005;34:66–74. 264. Mulligan BR. Manual Therapy: “NAGS”, “SNAGS”, “PRP’S” etc. Wellington: Plane View Series; 1992. 265. Mulligan BR. Manual therapy rounds: mobilisations with movement (MWM’s). J Man Manip Ther. 1993;1:154–156. 266. Mulligan BR. Mobilisations with Movement (MWMS) for the hip joint to restore internal rotation and flexion. J Man & Manip Ther. 1996;4: 35–36. 267. Fredericson M, White JJ, Macmahon JM, Andriacchi TP. Quantitative analysis of the relative effectiveness of 3 iliotibial band stretches. Arch Phys Med Rehabil. 2002;83:589–592.

Hip Joint Complex

241. Woodley SJ, Nicholson HD, Livingstone V, et al. Lateral hip pain: findings from magnetic resonance imaging and clinical examination. J Orthop Sports Phys Ther. 2008;38:313–328. 242. Reiman MP, Goode AP, Hegedus EJ, Cook CE, Wright AA. Diagnostic accuracy of clinical tests of the hip: a systematic review with meta-analysis. Br J Sports Med. 2013;47:893–902. 243. Del Buono A, Papalia R, Khanduja V, Denaro V, Maffulli N. Management of the greater trochanteric pain syndrome: a systematic review. Br Med Bull. 2012;102:115–131. 244. Chowdhury R, Naaseri S, Lee J, Rajeswaran G. Imaging and management of greater trochanteric pain syndrome. Postgrad Med J. 2014; 90:576–581. 245. Reid D. The management of greater trochanteric pain syndrome: a systematic literature review. J Orthop. 2016;13:15–28. 246. Speers CJ, Bhogal GS. Greater trochanteric pain syndrome: a review of diagnosis and management in general practice. Br J Gen Pract. 2017;67: 479–480. 247. Labrosse JM, Cardinal E, Leduc BE, et al. Effectiveness of ultrasoundguided corticosteroid injection for the treatment of gluteus medius tendinopathy. AJR Am J Roentgenol. 2010;194:202–206. 248. Meyers WC, Foley DP, Garrett WE, et al. Management of severe lower abdominal or inguinal pain in high-performance athletes. Am J Sports Med. 2000;28:2–8. 249. Thorborg K, Reiman MP, Weir A, et al. Clinical examination, diagnostic imaging, and testing of athletes with groin pain: an evidencebased approach to effective management. J Orthop Sports Phys Ther. 2018;48:239–249. 250. Serner A, Weir A, Tol JL, et al. Characteristics of acute groin injuries in the adductor muscles: a detailed MRI study in athletes. Scand J Med Sci Sports. 2018;28:667–676. 251. Serner A, Weir A, Tol JL, et al. Characteristics of acute groin injuries in the hip flexor muscles—a detailed MRI study in athletes. Scand J Med Sci Sports. 2018;28:677–685. 252. Griffin DR, Dickenson EJ, O’Donnell J, et al. The Warwick Agreement on femoroacetabular impingement syndrome (FAI syndrome): an international consensus statement. Br J Sports Med. 2016;50:1169–1176.

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The Knee Joint Complex

CHAPTER OBJECTIVES At the completion of this chapter, the reader will be able to: 1. Describe the anatomy of the joint, ligaments, muscles, and blood and nerve supply that comprise the knee joint complex. 2. Describe the biomechanics of the tibiofemoral and patellofemoral joints, including the forces involved with closed-chain and open-chain activities, the open- and close-packed positions, normal and abnormal joint barriers, force couples, and joint stabilizers. 3. Describe the purpose and components of an examination for the knee joint complex. 4. Perform a detailed examination of the knee joint complex, including palpation of the articular and softtissue structures, specific passive and active mobility tests, stability tests, and special tests. 5. Understand the purpose of muscle function testing and extrapolate information from the findings. 6. Describe the significance of muscle imbalance in terms of functional muscle performance. 7. Outline the significance of the key findings from the history, the tests and measures of the knee joint complex, and establish a diagnosis. 8. Describe the common pathologies of the knee joint complex and their relationship to impairment. 9. Develop self-reliant intervention strategies based on clinical findings and established goals. 10. Apply active and passive techniques to the knee joint complex and its surrounding structures, using the correct intensity and duration. 11. Evaluate intervention effectiveness to progress or modify the intervention. 12. Plan an effective home program, and instruct the patient in this program. 922

13. Help the patient to develop self-reliant intervention strategies.

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C H A P T E R 2 0

OVERVIEW The knee joint complex is extremely elaborate and includes three articulating surfaces, which form two distinct joints contained within a single-joint capsule: the patellofemoral joint (PFJ) and tibiofemoral joint. Anatomically and biomechanically the tibiofemoral joint and the PFJ can be considered as separate entities, in much the same way as the craniovertebral joints are when compared with the rest of the cervical spine. In 15–20% of the population, an accessory sesamoid bone occurring in the gastrocnemius, the fabella, is present as part of the knee joint complex.1 The fabella, when present, articulates with the lateral femoral condyle and is hence an articular sesamoid. The knee is one of the most commonly injured joints in the body. The types of knee injuries seen clinically can be generalized into the following categories: Unspecified sprains or strains, and other minor injuries, including overuse injuries ▶▶ Contusions ▶▶ Meniscal or ligamentous injuries ▶▶

It is important that the clinician be familiar with the diagnostic and therapeutic procedures appropriate for all of the categories of injury. It is also important that the clinician have a good understanding of differential diagnosis as pain in the thigh, knee, and calf can result from a broad spectrum of conditions.

ANATOMY TIBIOFEMORAL JOINT The tibiofemoral joint consists of the distal end of the femur and the proximal end of the tibia (Fig. 20-1). The tibiofemoral joint has great demands placed on it in terms of both stability and mobility. The femur is the largest bone in the body and represents approximately 25% of a person’s height.2 Its distal aspect (Fig. 20-1) is composed of two femoral condyles that are separated by an intercondylar notch or fossa. The intercondylar notch serves to accept the anterior cruciate ligament (ACL) and the posterior cruciate ligament (PCL).

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ANATOMY

Femur

Patellar surface of femur

Posterior cruciate ligament

Lateral collateral ligament

Medial meniscus

Lateral meniscus

Medial collateral ligament

Anterior cruciate ligament Lateral collateral ligament Lateral meniscus

Head of fibula Patellar ligament

Head of fibula

Patella

The Knee Joint Complex

Anterior cruciate ligament

Lateral condyle of femur

Interosseus membrane Tibia

A

B

FIGURE 20-1  Anterior and posterior views of the bones of the tibiofemoral joint. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

CLINICAL PEARL A narrow intercondylar notch has been associated with an increase in injuries to the ACL.3 The femoral condyles (see Fig. 20-1) project posteriorly from the femoral shaft. The smaller lateral femoral condyle is ball-shaped and faces outward, whereas the elliptical-shaped medial femoral condyle faces inward. The lateral condyle serves as the origin of the popliteus, whereas the lateral epicondyle serves as the origin of the lateral head of the gastrocnemius and the lateral collateral ligament (LCL). The medial epicondyle (see Fig. 20-1) serves as the insertion site for the adductor magnus, the medial head of the gastrocnemius, and the medial collateral ligament (MCL). The anteroposterior length of the adult medial femoral condyle is on average 1.7 cm greater than that of its lateral counterpart, resulting in an increased length of the articular surface on the medial femoral condyle as compared with that of the lateral femoral condyle.1 Thus, the articulating surfaces are asymmetric, yet work in unison.4 The distal and the posterior portion of the femoral condyles articulate with the tibia. The proximal tibia (see Fig. 20-2) is composed of two plateaus separated by the intercondylar eminence, including the medial and lateral tibial spines. The tibial plateaus are concave in a mediolateral direction. In the anteroposterior direction, the medial tibial plateau is also concave, whereas the

Dutton_Ch20_p0922-p1023.indd 923

lateral is convex, producing more asymmetry and an increase in lateral mobility. The medial plateau has a surface area that is approximately 50% greater than that of the lateral plateau, and its articular surface is three times thicker.1 The concavity of the tibial plateaus is accentuated by the presence of the menisci (see later).

PATELLOFEMORAL JOINT The PFJ is a complex articulation, dependent on both dynamic and static restraints for its function and stability. The patella (Fig. 20-1), a ubiquitous sesamoid bone found in birds and mammals, plays an important role in the biomechanics of the knee. Its articular anatomy is uncomplicated: it is a very hard, triangular-shaped bone, situated in the intercondylar notch and embedded in the tendon of the quadriceps femoris muscle above and the patellar tendon below. The groove has a complex architecture with increasing height of the groove’s lateral facet at the proximal aspect, providing a deeper “patella track” in knee extension.5 In healthy individuals, aspects of the femoral trochlea including its depth, as well as the shape and height of the lateral trochlea, can affect patellar tracking.6,7 From 20 to 30 degrees of knee flexion, the patella is confined within the trochlea and hence, the bony joint components provide inherent stability but, once beyond

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ANATOMY

Patellar ligament

Anterior cruciate ligament

Tibial tuberosity

Head of fibula

Medial collateral ligament

THE EXTREMITIES

Lateral collateral ligament

Medial meniscus

Posterior cruciate ligament

Lateral meniscus

FIGURE 20-2  Articulating surfaces of the tibia. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

this range, there is little intrinsic bony support and stability must be provided by other soft-tissue structures, both passively and actively.6 The thickness of the patella varies considerably, attaining a maximum height of 2–2.5 cm (0.77–1 in) at its central portion.1 The posterior surface of the patella can include up to seven facets. The geometry of these facets varies between individuals and may affect patellar tracking.6 A smaller facet, known as the odd facet, exists medially and is delineated by a second vertical ridge. These concave medial and lateral facets are separated by a vertical ridge and are covered with aneural hyaline cartilage, the thickest cartilage in the body (up to 7 mm thick).1 The articular cartilage of the patella is unique because it lacks conformity with the underlying bone.8 The hyaline cartilage, here as elsewhere, functions to minimize the friction that occurs at the functional contact areas of the joint surfaces. Radiographic and cadaver studies have classified the patella into three Wiberg classifications (type A–C) based on the size and shape of these lateral and medial facets. The patellar surface of the femur is divided into medial and lateral facets that closely correspond to those on the posterior surface of the patella. The PFJ functions to provide the articulation with low friction; ▶▶ protect the distal aspect of the femur from trauma and the quadriceps from attritional wear; ▶▶ improve the cosmetic appearance of the knee; ▶▶ improve the moment arm (distance from the center of gravity and the center of rotation) of the quadriceps. This is achieved by elevating the quadriceps femoris muscle from the center of knee rotation. This increases the efficiency of the quadriceps muscle and provides it with leverage for extending the leg. The patellar contribution to the knee extensor moment arm increases with increasing amounts of knee extension; and ▶▶ decrease the amount of anteroposterior tibiofemoral shear stress placed on the joint.

JOINT CAPSULE AND SYNOVIUM The capsule of the knee joint complex is composed of a thin, strong fibrous membrane, and it is the largest synovial capsule in the body. The capsule ascends anteriorly approximately 2 finger breadths above the patella to form the suprapatellar pouch. Posteriorly, it ascends to the origins of the gastrocnemius. Inferiorly, the capsule attaches to the edges of the articulating surfaces of the tibial plateaus, with the exception of the intercondylar eminence, and a small portion of the anterior intercondylar region.1 A synovial membrane lines the inner portion of the knee joint capsule. By lining the joint capsule, the synovial membrane excludes the cruciate ligaments from the interior portion of the knee joint, making them extrasynovial yet intra-articular. The articularis genu, located superior to the patella, is thought to function to retract the knee capsule during knee extension. Thus, it serves a similar function as the anconeus at the elbow.

PROXIMAL TIBIOFIBULAR JOINT

▶▶

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The proximal, or superior, tibiofibular joint (see Fig. 20-1) is an almost plane joint with a slight convexity on the oval tibial facet and a slight concavity on the fibular head. The joint is located below the tibial plateau on the lateral condyle of the tibia. The tibial articulating facet faces laterally, posteriorly, and inferiorly. Although the joint is often described as a simple, synovial, modified ovoid, it functions as a modified sellar when combined with the distal, or inferior, tibiofibular joint (see Chapter 21). The joint capsule of the proximal tibiofibular joint complex is thicker anteriorly than posteriorly and, in 10% of the population, the synovium is continuous with that of the knee joint.1 The joint receives support from anterior and posterior ligaments and an interosseous membrane. The interosseous

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The static stability of the knee joint complex depends on four major knee ligaments, which provide a primary restraint to abnormal knee motion: Anterior cruciate (Fig. 20-1). It provides the primary restraint to anterior translation and medial rotation of the tibia on the femur and is a secondary restraint to valgus and varus rotation of the tibia. ▶▶ Posterior cruciate (see Fig. 20-1). It provides the primary restraint to posterior translation and medial rotation of the tibia on the femur and is a secondary restraint to valgus and varus rotation of the tibia. ▶▶ Medial (tibial) collateral (see Fig. 20-1). It provides the primary restraint to valgus and lateral rotation of the tibia and is a secondary restraint to the anterior and posterior translation of the tibia on the femur. ▶▶ Lateral (fibular) collateral (see Fig. 20-1). It provides the primary restraint to varus and lateral rotation of the tibia and is a secondary restraint to the anterior and posterior translation of the tibia on the femur. ▶▶

Cruciate Ligaments The two central intra-articular cruciate ligaments derive their name from the Latin word crucere (cross) because they cross each other (Fig. 20-1). Both the ACL and the PCL lie in the

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CLINICAL PEARL When an anterior force is applied to the tibia of a knee with intact ligaments, internal rotation occurs, whereas a posterior force produces external rotation of the tibia. These movements, rotations with coupled anterior and posterior translation, are greater in flexion than near extension.9 The blood supply to the cruciate ligaments is largely provided from the middle and inferior geniculate branches of the popliteal artery. The cruciate ligaments are innervated by the posterior articular nerve, a branch of the posterior tibial nerve.1 The function of this nerve supply is questionable although it may serve as proprioceptive in nature. In addition, the cruciate ligaments contain mechanoreceptors, suggesting that disruption of the ligament structure can produce partial deafferentation of the joint.10 Evidence of a proprioceptive function of the ACL comes from extensive histologic observations demonstrating that the ACL appears to contain proprioceptive nerve endings.1 Although these cruciate ligaments function together, they are described separately.

The Knee Joint Complex

LIGAMENTS

center of the joint, and each is named according to their attachment sites on the tibia.1 The cruciate ligaments, which differ from those of other joints in that they restrict normal, rather than abnormal, motion, are the main stabilizing ligaments of the knee and restrain against anterior (ACL) and posterior (PCL) translations of the tibia on the femur. They also restrain against excessive internal and external rotation and varus/valgus movements of the tibia.

ANATOMY

membrane attaches between the medial border of the fibula and the lateral border of the tibia, providing attachment to the deep anterior and posterior muscles of the leg. The majority of its fibers pass obliquely in an inferior and lateral direction. The proximal tibiofibular joint has more motion than its distal partner. The motion occurring at the proximal joint, consists of two glides, one in a superoinferior direction and the other in an anteroposterior direction.1 These motions are possible because of the orientation of the joint line, which also facilitates an osteokinematic spin of the fibula. The motion at this joint can be decreased by articular fibrosis or by softtissue restraints; the biceps femoris can pull or hold it posteriorly, whereas the tibialis anterior can pull or hold it anteriorly. Although the capsular pattern of restriction for this joint is unclear, it is probably indicated by pain during an isometric contraction of the biceps femoris with the knee at 90 degrees of flexion. The close-packed position for this joint, equally debatable, is probably weight-bearing (WB) ankle dorsiflexion. Both the tibia and the fibula are vulnerable to fracture at the lower third of their shaft. Anterior joint subluxations occur at this joint as a result of medial knee joint strain or an inversion sprain of the ankle. Posterior joint subluxation can occur as a result of a lateral knee joint strain, but this is often missed because of the more serious ligament damage to the knee. The nerve supply to this joint is provided by the common fibular (peroneal) and recurrent articular nerves. The joint receives its blood supply from a perforating branch of the fibular (peroneal) artery and the anterior tibial artery.

Anterior Cruciate Ligament The ACL is a unique structure and one of the most important ligaments to knee stability. In addition to serving as a primary restraint to anterior translation of the tibia relative to the femur, the ACL provides significant mechanical stabilization to the knee joint by preventing excessive hyperextension, as well as tibial rotation and anterior tibial translation while in flexion.11–13 The ACL (see Fig. 20-1) is composed of a vast array of individual fascicles. These, in turn, are composed of numerous interlacing networks of collagen fibrils. The fascicles originate on the inner aspect of the lateral femoral condyle in the intercondylar notch (resident’s ridge), which serves as the anterior limit of the ACL in the anatomical position, and travel obliquely and distally through the knee joint. They enter the anterior intercondylar surface of the tibial plateau, where they partially blend with the lateral meniscus. As the fascicles of the ACL course through the knee joint and attach to their insertion sites, they fan out and give a slight spiral appearance to the ligament, a phenomenon that is more pronounced during knee flexion. The synovial tissue that enfolds the ACL consists of an intimal layer, facing the joint cavity, and a subsynovial layer. The subsynovial layer is in direct contact with the ACL and contains neurovascular structures. The ACL is considered intra-articular yet extrasynovial because of the posterior invagination of the synovial membrane.

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ANATOMY THE EXTREMITIES

Although the posterior articular nerve is the major nerve for the ACL, afferent fibers have also been demonstrated in the medial and lateral articular nerves.1 Like all ligaments, the ACL behaves as a viscoelastic structure, allowing it to dissipate energy and to adjust its length and internal load distribution as a function of load history.14 This means that the normal ACL is capable of microscopic adjustments to internal stresses over time, thus influencing the laxity, stresses, and kinematics of the joint in subtle but potentially important ways. One anatomic factor that contributes to selective fiber recruitment during tensile loading is the specific location of the insertions of the ACL on the femur and the tibia. These differing insertion sites allow different fibers of the ACL to be recruited with every subtle three-dimensional (3D) change in the position of the joint.14 The ACL consists of two functional bundles—the anteromedial (A-M) and posterolateral (P-L) bundles—named for their position on the tibia. The femoral footprints of the A-M and P-L bundles are vertically aligned when the knee is in full extension, and the femoral origin of the A-M bundle is located superior to the P-L insertion.15 In this configuration, the two bundles are parallel to each other, whereas with the knee in 90 degrees of flexion, the two bundles cross each other, and the femoral insertions are nearly horizontally aligned.15,16 The tensile strength of the ACL is equal to that of the knee collaterals, but it is half that of the PCL.14 Since its fibers are unyielding, forcing the ACL more than 5% beyond its resting length may result in rupture.14 Several factors can influence the amount of tension on the ACL16,17: When the knee is in full extension, the A-M and P-L bundles are under tension. ▶▶ When the knee is at 60–90 degrees of flexion, the P-L bundle is lax and allows rotation of the tibia on the femur. ▶▶ The P-L bundle limits anterior translation of the tibia at low angles of knee flexion (0–30 degrees). ▶▶ The A-M bundle primarily resists anterior translation of the tibia and undergoes less change in length than the P-L bundle throughout the range of knee motion. ▶▶ The P-L bundle is maximally lengthened when the knee is in full extension, and the A-M bundle is under maximum tension when the knee is flexed between 45 and 60 degrees. ▶▶ Compressive loading of the tibiofemoral joint, such as that occurs during WB, has been shown to reduce anteroposterior laxity and stiffen the joint when compared with the non–weight-bearing (NWB) position. These changes appear to reflect the increased strain borne by the ACL during the transition from NWB to WB. Thus, the popular belief in the beneficial effects of early WB and closed-kinetic chain exercises (CKCEs) following anterior cruciate reconstruction may be open to question (Table 20-1). ▶▶

Posterior Cruciate Ligament

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The PCL attaches posteriorly to the insertion of the posterior horns of the lateral and medial menisci on the posterior part of the posterior intercondylar fossa of the tibia.1 From here, the PCL extends obliquely medially, anteriorly, and superiorly

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to attach to the lateral surface of the medial femoral condyle (see Fig. 20-1). Overall, the ligament is wider at its femoral origin and narrowest near the tibial insertion.1 The PCL is covered by synovial lining and is therefore considered to be extrasynovial yet intra-articular. Information regarding the biomechanical function of the PCL is scant compared with that of the ACL. It is known that the PCL is 50% thicker and has twice the tensile strength of the ACL.1 The PCL is more vertical in extension and horizontal in flexion. Like the ACL, the PCL consists of two bundles: anterior lateral and posterior medial. Overall, the ligament is most taut with further flexion of the knee.14 Specifically, the anterior lateral bundle is taut in flexion, while the posterior medial bundle is taut in extension. The PCL provides the vast majority of the total restraint to posterior translation of the tibia on the femur, with the remainder being provided by the collateral ligaments, posterior portion of the medial and lateral capsules, and the popliteus tendon. The contribution percentage resisting posterior translation decreases as the knee extends. The PCL also restrains internal rotation of the tibia on the femur and helps prevent posteromedial instability at the knee.14 Other functions of the PCL include acting as a secondary restraint to external rotation of the tibia on the femur at 90 degrees of flexion, assisting with a rolling/gliding mechanism of the tibiofemoral joint, and resisting varus/valgus forces at the knee after the collateral ligaments have failed.14 A significant force is needed to tear the PCL. Thus, tears of the PCL are usually the result of severe contact injuries that often occur in traumatic situations, such as a dashboard injury during a motor vehicle accident. In concert with the PCL are the anterior and posterior meniscofemoral ligaments. Although these ligaments arise from the common PCL origin, they are distinct structures having different insertion sites.18 Both are named with respect to the orientation to the PCL (see “Lateral Meniscus” section). Since the insertion site of the meniscofemoral ligaments is different from that of the PCL, if a midsubstance tear of the PCL occurs, it is possible that one or both of the meniscofemoral ligaments may remain intact.

Medial Collateral Ligament Both the MCL and the LCL are considered to be extraarticular ligaments. The MCL, or tibial collateral ligament (see Fig. 20-1), develops as a thickening of the medial joint capsule.1 It can be subdivided into a superficial band and a deep band. ▶▶

The superficial band is a thick, flat band, and has a fan-like attachment proximally on the medial femoral condyle, just distal to the adductor tubercle, from which it extends to the medial surface of the tibia approximately 6 cm below the joint line, covering the medial inferior genicular artery and nerve.1 The superficial band blends with the posteromedial corner of the capsule and, when combined, is referred to as the posterior oblique ligament. The superficial band is separated from the deep layer of the ligament by a bursa. Since the superficial band is farther from the center of the knee, it is the first ligament injured when a valgus stress is applied.19

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Rank Comparison of Peak ACL Strain Values During Commonly Prescribed Rehabilitation Activities No. of Subjects

Isometric quadriceps contraction at 15 degrees (30 Newton meters [Nm] of extension torque)

4.4 (0.6)%

 8

Squatting with sport cord

4.0 (1.7)%

 8

Active flexion–extension of the knee with 45-N weight boot

3.8 (0.5)%

 9

Lachman test (150 N of anterior shear load: 30 degrees of flexion)

3.7 (0.8)%

10

Squatting

3.6 (1.3)%

 8

Active flexion–extension (no weight boot) of the knee

2.8 (0.8)%

18

Simultaneous quadriceps and hamstring contraction at 15 degrees

2.8 (0.9)%

 8

Isometric quadriceps contraction at 30 degrees (30 Nm of extension torque)

2.7 (0.5)%

18

Stair climbing

2.7 (2.9)%

 5

Anterior drawer (150 N of anterior shear load: 90 degrees of flexion)

1.8 (0.9)%

10

Stationary bicycling

1.7 (1.9)%

 8

Isometric hamstring contraction at 15 degrees (10 Nm of flexion torque)

0.6 (0.9)%

 8

Simultaneous quadriceps and hamstring contraction at 30 degrees

0.4 (0.5)%

 8

Passive flexion–extension of the knee

0.1 (0.9)%

10

Isometric quadriceps contraction at 60 degrees (30 Nm of extension torque)

  0.0%

 8

Isometric quadriceps contraction at 90 degrees (30 Nm of extension torque)

  0.0%

18

Simultaneous quadriceps and hamstring contraction at 60 degrees

  0.0%

 8

Simultaneous quadriceps and hamstring contraction at 90 degrees

  0.0%

 8

Isometric hamstring contraction at 30, 60, and 90 degrees to −10 Nm of flexion torque

  0.0%

 8

The Knee Joint Complex

Peak Strain (Mean ± ISD)

Rehabilitation Activity

ANATOMY

TABLE 20-1

ACL, anterior cruciate ligament; ISD, implied standard deviation. Reproduced with permission from Beynnon BD, Fleming BC. Anterior cruciate ligament strain in-vivo: a review of previous work. J Biomech. 1998 Jun; 31(6):519–525.

▶▶

The deep band (medial capsular ligament) is a continuation of the capsule. It blends with the medial meniscus and consists of an upper meniscofemoral portion and a lower meniscotibial portion.

The anterior fibers of the MCL are taut in flexion and can be palpated easily in this position. The posterior fibers, which are taut in extension, blend intimately with the capsule and with the medial border of the medial meniscus, making them difficult to palpate. Information regarding the biomechanical function of the collateral ligaments is quite scarce compared with that of the ACL. It would appear that the MCL is the primary stabilizer of the medial side of the knee against valgus forces, and external rotation of the tibia, especially when the knee is flexed.20

CLINICAL PEARL The MCL complex acts as the primary restraint to valgus rotation of the tibia, providing as much as 80% of the restraining force to valgus loads.21

Dutton_Ch20_p0922-p1023.indd 927

The LCL provides the primary restraint to varus rotation of the knee, acts as a secondary restraint to external rotation and posterior displacement of the tibia21 and, during normal gait, is the primary passive structure resisting the knee adduction (varus) moment.21

Lateral Collateral Ligament The LCL, or fibular collateral ligament (see Fig. 20-1), arises from the lateral femoral condyle and runs distally and posteriorly to insert into the head of the fibula. The LCL forms part of the socalled arcuate–ligamentous complex. This complex also comprises the biceps femoris tendon, iliotibial tract, and the popliteus. The cord-like LCL develops independently and remains completely free from the joint capsule and the lateral meniscus. It is separated from these structures by the popliteus tendon and straddled by the split tendon of the biceps femoris. The LCL can be divided into three parts: 1. Anterior. This part consists of the joint capsule. 2. Middle. This part is considered to be part of the iliotibial band (ITB) and covers the capsular ligament.

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ANATOMY

3. Posterior. This Y-shaped portion of the ligament is part of the arcuate–ligamentous complex, which supports the posterior capsule. The main function of the LCL is to resist varus forces. It offers the majority of the varus restraint at 25 degrees of knee flexion and in full extension.14 Abnormal varus laxity arising subsequent to injuries of the LCL and other P-L structures has been shown to increase stress on cruciate ligament grafts and has been implicated as one of the causes of crucial ligament reconstruction failure.21

THE EXTREMITIES

SECONDARY RESTRAINTS Some structures in the knee, known as secondary restraints, augment the functions of the ACL and the PCL. These secondary restraints include the structures in the P-L and posteromedial corners of the knee, which serve to control anterior tibial translation relative to the femur.14 Dynamic stability synergistic to the PCL is provided by unopposed contraction of the quadriceps complex, which increases anterior tibial translation. Conversely, an isolated contraction of the hamstrings results in a posterior translation of the tibia, which is synergistic to the ACL. Cocontraction of the hamstrings and the quadriceps has been theorized to minimize tibial translation in either direction. The popliteus muscle–tendon complex (PMTC) contributes to both static and dynamic P-L knee joint stabilization. During concentric activation, the popliteus internally rotates the tibia on the femur. During eccentric activation, it serves as a secondary restraint to tibial external rotation on the femur (see “Popliteus” section).22 The knee joint is also strengthened externally by the patellar ligament, oblique popliteal ligaments, and the fabella. The patellar ligament, or patellar tendon, lies in the thickened portion of the quadriceps femoris tendon between the top of the patella and the tibia (Fig. 20-1). The patellar ligament strengthens the anterior portion of the knee joint and prevents the lower leg from being flexed excessively. ▶▶ The oblique popliteal ligament, located on the posterior surface of the knee joint, is a dense thickening in the posterior capsule made up of a continuation of the popliteal tendon and part of the insertion of the semimembranosus.1 It arises posterior to the medial condyle of the tibia and extends superomedially to attach to the posterior fibrous capsule. The oblique popliteal ligament provides reinforcement to the lateral capsule, limits A-M rotation of the tibia, and prevents hyperextension of the knee. ▶▶ The fabella is located in the P-L corner of the knee and may be osseous or cartilaginous in makeup. When the fabella is present, there is a fabellofibular ligament, which courses superiorly and obliquely from the lateral head of the gastrocnemius to the fibular styloid. The fabellofibular ligament helps prevent ▶▶

928

Dutton_Ch20_p0922-p1023.indd 928

excessive internal rotation of the tibia and adds further ligamentous support on the lateral and P-L aspects of the knee.1

CLINICAL PEARL Purists classify the patellar tendon as a ligament because it serves as the connection between two bones (tibia and patella). However, because this structure attaches the quadriceps unit to the tibia, it functions as a tendon.

MENISCI The word meniscus comes from the Greek word mēniskos, meaning “crescent,” diminutive of mēnē, meaning “moon.”23 The lateral and medial menisci (Fig. 20-2), attached on the top of the tibial plateaus, lie between the articular cartilage of the femur and the tibia. Both menisci are recognized as being vital for the normal function and long-term health of the knee joint. The characteristic crescent shape of the medial and lateral menisci is achieved between the 8th and 10th week of gestation.1 The unique and complex structure of the menisci makes treatment and repair challenging and, if left untreated, may lead to degenerative joint changes.24 The blood supply of the meniscus, which is key to successful meniscal recovery or repair, comes from the perimeniscal capsular arteries, which are branches of the lateral, medial, and middle genicular arteries, which in turn are branches of the popliteal artery.1 Although the developing menisci are highly vascular throughout, by adulthood this vascularity has significantly reduced such that only the outer 10–25% of the lateral meniscus (with the exception of the P-L corner of the lateral meniscus adjacent to the popliteus tendon) and the outer 10–30% of the medial menisci are vascularized (referred to as the red zone), which allows these areas to have the potential for healing.1 The remaining inner portions of the menisci (65–75%) are considered avascular and have less potential to heal. These inner portions receive nourishment from the synovial fluid by diffusion or mechanical pumping (i.e., joint motion).23 However, despite the lack of vascularity to the inner portions, tears involving the avascular zone may heal. This healing capacity may be improved with the addition of a fibrin clot or with such techniques as trephination (making a burr hole).

Medial Meniscus The crescent-shaped, or U-shaped, medial meniscus (see Fig. 20-2), with the wider separation of its anterior and posterior horns, is larger and thicker than its lateral counterpart and sits in the concave medial tibial plateau.25 The medial meniscus is significantly wider posteriorly than anteriorly. It is attached to the anterior and posterior tibial plateau by coronary ligaments. These ligaments connect the outer meniscal borders with the tibial edge and restrict movement of the meniscus. The medial meniscus also has an attachment to the deeper portion of the MCL and the knee joint capsule. The horns of the lateral meniscus are closer together than

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The lateral meniscus, which forms a C-shaped incomplete circle,25 sits atop the convex lateral tibial plateau (see Fig. 20-2). It occupies a larger portion (approximately 80%) of the articular surface than the medial meniscus (approximately 60%) and is more mobile than its medial counterpart.23 Both horns of the lateral meniscus are attached to the tibia.23 The periphery of the lateral meniscus attaches to the tibia, the capsule, and the coronary ligament, but not to the LCL. The posterior horn of the lateral meniscus attaches to the inner aspect of the medial femoral condyle via the anterior and posterior meniscofemoral ligaments of Humphrey and Wrisberg, respectively23: The ligament of Humphrey, also known as the anterior meniscofemoral ligament, runs anteriorly to the PCL and inserts on the posterior aspect of the lateral meniscus.18 ▶▶ The ligament of Wrisberg, also known as the posterior meniscofemoral ligament, runs posteriorly to the PCL to insert either into the superior/lateral aspect of the tibia, the posterior aspect of the lateral meniscus, or the posterior capsule.1 ▶▶

The meniscofemoral ligaments become taut with internal rotation of the tibia and help with stabilization of the meniscus.1

CLINICAL PEARL The lateral meniscus often is associated with the appearance of synovial-filled cysts, which may occur following a minor injury to the meniscus and produce a small internal tear. As fluid begins to congregate within this tear, it is pushed deeper and deeper into the meniscus. The swelling eventually produces a small bulge on the lateral aspect of the meniscus. The lateral meniscus has an interesting relationship with the popliteus tendon, which supports it during knee extension and separates it from the joint (see later discussion).1

Menisci Function The menisci assist in a number of functions, including load transmission, shock absorption, joint lubrication and nutrition, secondary mechanical stability (particularly the posterior horn of the medial meniscus that blocks anterior

Dutton_Ch20_p0922-p1023.indd 929

Load Transmission The meniscus is viscoelastic, with greater stiffness at higher deformation rates. Many studies have confirmed the role of the menisci in load transmission by showing decreased contact area and increased peak articular stresses following partial or total meniscectomy. WB produces axial forces across the knee, which compress the menisci, resulting in “hoop” (circumferential) stresses. By converting joint loading forces to radial-directed hoop stresses on their circumferential collagen fibers, and taking advantage of their viscoelastic nature, the menisci transmit approximately 50% of the joint load when the knee is in extension, and approximately 90% when the knee is in flexion.14 The lateral meniscus carries 70% of the compressive load in the lateral compartment, compared with just 40% of the medial meniscus in its respective compartment.25

Shock Absorption Because of their viscoelastic nature, the menisci are able to assist in shock absorption. During the normal gait pattern, the articular surface of the knee bears up to six times the body weight, with over 70% of that load borne by the medial tibial plateau.25 The medial tibial plateau bears most of this load during stance when the knee is extended, with the lateral tibial plateau bearing more of the much smaller loads imposed during the swing phase. This is compensated for by the fact that the medial tibial plateau has a surface area roughly 50% larger than the lateral plateau, and articular cartilage that is approximately three times thicker than the lateral articular cartilage.1

The Knee Joint Complex

Lateral Meniscus

translation of the tibia on the femur),25 and the guiding of movements.

ANATOMY

those of the medial, which makes the former almost circular and the latter nearly semilunar (see Fig. 20-2). The anterior horn is attached to the tibial plateau near the intercondylar fossa anterior to the ACL.1 There is significant variability in the attachment location of the anterior horn of the medial meniscus.23 The posterior horn of the medial meniscus, which is attached to the posterior intercondylar fossa of the tibia between the lateral meniscus and the PCL, receives a piece of the semimembranosus tendon.23 The transverse genicular ligament serves as a link between the lateral and medial menisci.

Joint Lubrication The menisci assist in joint lubrication by helping to compress synovial fluid into the articular cartilage, which reduces frictional forces during WB. A meniscectomy increases the coefficient of friction within the knee, thereby increasing the stresses on the articular surfaces.

Joint Stability The menisci deepen the articulating surfaces of tibial plateaus. This increases the stability of the knee, especially during axial rotation and valgus–varus stresses.14 If the ACL is intact, the menisci do not significantly contribute to anteroposterior stability. However, in an ACLdeficient knee, the posterior horn of the medial meniscus functions as a secondary restraint to an anteroposterior translation by wedging between the femur and the tibia. In contrast, the increased mobility of the lateral meniscus prevents it from contributing to anteroposterior stability.26 This difference helps to explain the higher incidence of medial meniscus tears seen in ACL-deficient knees.26

Proprioception Mechanoreceptors have been identified in the anterior and posterior horns of the menisci.27 The presence of these

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ANATOMY

mechanoreceptors would seem to suggest that the menisci are capable of detecting proprioceptive information in the knee joint, thus playing an important afferent role in the sensory feedback mechanism of the knee.23

Factors guiding “screw-home” rotation

Guiding Movement

THE EXTREMITIES

During flexion and extension of the knee, the menisci move posteriorly and anteriorly, respectively. The lateral meniscus has greater mobility because it does not attach to the LCL, and, as mentioned previously, its capsular attachment is interrupted by the passage of the popliteus tendon. The posterior medial corner of the medial meniscus has the least amount of motion because it is constrained by its attachment to the tibial plateau by the meniscotibial portion of the posterior oblique ligament, which has been reported to be more prone to injury.23 During knee motion, the menisci move on the tibial plateau with the femoral condyles to maintain joint congruence. The femur, accompanied by the menisci, rolls anteriorly on the tibia during extension and posteriorly during flexion (Fig. 20-3). ▶▶

Femur Tension in articular cruciate ligament

Lateral pull of quadriceps

During flexion of the knee, the menisci move posteriorly. The medial meniscus is moved about 5 mm by the pull of the semimembranosus tendon, and the lateral meniscus is pulled about 11 mm by the popliteus, resulting in an external rotation of the tibia.

During extension, the menisci move anteriorly. During external rotation of the tibia, the menisci will follow the displacement of the femoral condyles, which means that the medial meniscus is pushed posteriorly, and the lateral meniscus is pulled anteriorly. During internal rotation, the opposite occurs. These rotations are conjunct, integral with flexion and extension, but can also be adjunct and independent, best demonstrated with the knee semiflexed. Conjunct external rotation of the tibia on the femur during the last stages of knee extension is part of a locking mechanism called the “screw home” mechanism, described later. ▶▶ The medial coronary ligament is stretched during external rotation of the tibia, whereas the lateral coronary ligament is stretched during internal rotation of the tibia.

Shape of medial femoral condyle

Tibia External rotation

Fibula

▶▶ ▶▶

A

Extension Path of the tibia on the femoral condyles Intercondylar groove

Lateral epicondyle

Full extension

Medial epicondyle

Screw-home rotation 30° flexion

60° flexion

BURSAE There are a number of bursae situated in the soft tissues around the knee joint. The bursae serve to reduce friction and to cushion the movement of one body part over another.

90° flexion

B FIGURE 20-3  Tibiofemoral motions.

Superficial and Deep Infrapatellar Bursae The superficial infrapatellar bursa is located between the patellar tendon and the skin, whereas the deep infrapatellar bursa is located between the patellar tendon and the tibia.

Prepatellar Bursa 930

The prepatellar bursa is located between the skin and the anterior aspect of the patella.

Dutton_Ch20_p0922-p1023.indd 930

Tibiofemoral Bursa The tibiofemoral bursae consist of a bursa between the head of the gastrocnemius muscle and the joint capsule on both sides, a bursa between the LCL and both the biceps femoris and popliteus, and a bursa between the MCL and the femoral condyle. There are also a number of bursae between the

10/07/19 2:37 PM

CLINICAL PEARL A “Baker cyst” may occur with fluid accumulation when there is a natural connection between the semimembranosus bursa and the knee joint.

Synovial fluid secretion Joint stability ▶▶ Neurovascular supply ▶▶ Occupiers of dead space ▶▶ ▶▶

PLICA Synovial plica represents a remnant of the three separate cavities in the synovial mesenchyme of the developing knee. These cavities are supposed to coalesce into one cavity at the 12-week stage of fetal growth.1 The size and extent of this remnant depend on the degree of reabsorption. The three joints involved in the developing knee from which the remnants evolve are113 1. the joint between the fibular and the femur; 2. the joint between the tibia and the femur; and 3. the joint between the patella and the femur. The most common plica in the knee is called the anterior or inferior plica, or mucous ligament.1 This plica is represented by a tape-like fold running from the fat pad to the intercondylar notch of the femur and overlying the ACL. The plicae to the medial and lateral sides of the patella, which run in a horizontal plane from the fat pad to the side of the patellar retinaculum, are referred to as the superomedial or superolateral plicae or the suprapatellar membrane, or the medial or lateral synovial shelf.1 It has been suggested that symptomatic synovial plicae are one of the causes of anterior pain in the knee in children and adolescents.

RETINACULA The wing-like retinacula of the knee are formed from structures in the first and second layers of the knee joint. The retinacula can be subdivided into the medial and the lateral retinacula for clinical examination and intervention purposes.1 The retinacula serve to connect the patella to a number of structures, including the femur, menisci, and tibia, both medially and laterally.

Dutton_Ch20_p0922-p1023.indd 931

The superficial retinaculum consists of fibers from the vastus lateralis (VL) and the ITB. ▶▶ The deep retinaculum consists of the lateral patellofemoral ligament, the deep fibers of the ITB, and the lateral patellotibial ligament. These structures connect the patella to the ITB and help prevent medial patellar excursion. ▶▶

Although partially located deep to the ITB, the lateral retinaculum is blended with the biceps femoris to form a socalled conjoint tendon.1 This relationship may explain why adaptively shortened hamstrings can lead to patellofemoral symptoms. It is also well established that adaptive shortening of the lateral retinaculum is a common finding in patellofemoral dysfunction. Given the fact that the medial retinaculum is thinner than the lateral retinaculum, it is not thought to be as significant to patellar positioning and tracking as its lateral counterpart.

The Knee Joint Complex

There are three fat pads located at the anterior knee: the quadriceps fat pad, the prefemoral fat pad, and the infrapatellar (Hoffa) fat pad. The fat pads of the knee house neurovascular projections. The functions of the fat pads include the following:

The lateral retinaculum is the stronger and thicker of the two. It consists of two distinct layers of fibrous connective tissue: the superficial and deep retinacula. These structures are oriented longitudinally with the knee extended.1

ANATOMY

various tendons of the pes anserinus and between the MCL and the superficial pes anserinus. The bursae around the knee can have contact with each other and with the knee joint capsule.

MUSCLES The major muscles that act on the knee joint complex are the quadriceps, the hamstrings (semimembranosus, semitendinosus, and biceps femoris), the gastrocnemius, the popliteus, and the hip adductors (Table 20-2).

Quadriceps The four muscles that make up the quadriceps are the rectus femoris, the vastus intermedius, the VL, and the vastus medialis (Fig. 19-7). The quadriceps tendon represents the convergence of all four muscles tendon units, and it inserts into the anterior aspect of the superior pole of the patella. The quadriceps muscle group is innervated by the femoral nerve. The quadriceps muscles can act to extend the knee when the foot is off the ground, although more commonly, they work as decelerators, preventing the knee from buckling when the foot strikes the ground.14

Rectus Femoris The rectus femoris (see Fig. 19-7), which originates at the anterior inferior iliac spine (AIIS), is the only quadriceps muscle that crosses the hip joint. The other quadriceps muscles originate on the femoral shaft. This gives the hip joint substantial significance with respect to the knee extensor mechanism in the examination and intervention.14,28 The line of pull of the rectus femoris, with respect to the patella, is at an angle of about 5 degrees with the femoral shaft (see Fig. 20-12).

Vastus Intermedius The vastus intermedius (see Fig. 19-7) has its origin in the proximal part of the femur, and its line of action is directly in line with the femur.

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ANATOMY

TABLE 20-2

Muscles of the Knee: Actions, Nerve Supply, and Nerve Root Derivation

THE EXTREMITIES

Action

Primary Muscles

Peripheral Nerve Supply

Nerve Root Derivation

Flexion of knee

Biceps femoris Semimembranosus Semitendinosus Gracilis Sartorius Popliteus Gastrocnemius Tensor fascia latae

Sciatic Sciatic Sciatic Obturator Femoral Tibial Tibial Superior gluteal

L5, S1–2 L5, S2–2 L5, S1–2 L2–3 L2–3 L4–5, S1 S1–2 L4–5

Extension of knee 

Rectus femoris Vastus medialis Vastus intermedius Vastus lateralis Tensor fascia latae

Femoral Femoral Femoral Femoral Superior gluteal

L2–4 L2–4 L2–4 L2–4 L4–5

Internal rotation of flexed leg (non–weight-bearing) 

Popliteus Semimembranosus Semitendinosus Sartorius Gracilis

Tibial Sciatic Sciatic Femoral Obturator

L4–5 L5, S1–2 L5, S1–2 L2–3 L2–3

External rotation of flexed leg (non–weight-bearing)

Biceps femoris

Sciatic

L5, S1–2

Reproduced with permission from Magee DJ. Orthopaedic Physical Assessment. 2nd ed. Philadelphia, PA: WB Saunders; 1992.

Vastus Lateralis The VL (Fig. 19-7) is composed of two functional parts: the VL and the vastus lateralis oblique (VLO). The VL has a line of pull of about 12–15 degrees to the long axis of the femur in the frontal plane, whereas the VLO has a pull of 38–48 degrees.

Vastus Medialis The vastus medialis (Fig. 19-7) is composed of two parts that are anatomically distinct: the vastus medialis obliquus (VMO) and the vastus medialis proper or longus (VML). While there is some conjecture as to whether these are separate entities, most authors agree that the two components have differing functions due to their fiber orientation, attachments, and thus angle of force on the patella.6,29 The VML appears to have little biomechanical significance unlike its counterpart, the VMO.

932

Vastus Medialis Obliquus. The VMO arises from the adductor magnus tendon. The insertion site of the normal VMO is the medial border of the patella, approximately onethird to one-half of the way down from the proximal pole. If the VMO remains proximal to the proximal pole of the patella and does not reach the patella, there is an increased potential for malalignment.8 The vector of the VMO is medially directed, and it forms an angle of 50–55 degrees with the mechanical axis of the leg. This oblique alignment provides a mechanical advantage for stabilizing the patella, which counterbalances the larger crosssectional area and thus the force-producing capacity of the VL.6 The VMO is least active in the fully extended position and

Dutton_Ch20_p0922-p1023.indd 932

plays little role in extending the knee, acting instead to centralize the patella within the trochlea and enhancing the efficiency of the VL.6 It is active in this function throughout the whole range of extension.

CLINICAL PEARL The VMO, which is frequently innervated independently from the rest of the quadriceps by a separate branch of the femoral nerve, is the first muscle of the quadriceps group to atrophy and the last to rehabilitate.30,31 Vastus Medialis Longus. The VML originates from the medial aspect of the upper femur and inserts anteriorly into the quadriceps tendon, giving it a line of action of approximately 15–17 degrees off the long axis of the femur in the frontal plane.

Hamstrings As a group, the hamstrings primarily function to extend the hip and to flex the knee. The hamstrings are innervated by branches of the sciatic nerve.

Semimembranosus Muscle The semimembranosus muscle (Fig. 19-8) arises from the lateral facet of the ischial tuberosity and the ischial ramus. This muscle inserts into the posteromedial aspect of the medial tibial condyle and has a key expansion that reinforces the

10/07/19 2:37 PM

Gracilis m. Semimembranosus m.

Semitendinosus Muscle Semitendinosus m.

Biceps femoris m. Plantaris m.

Gastrocnemius m.

Biceps Femoris The biceps femoris (see Fig. 19-8) muscle is a two-headed muscle. The longer of the two heads arises from the inferomedial facet of the ischial tuberosity, whereas the shorter head originates from the lateral lip of the linea aspera of the femur. The muscle inserts on the lateral tibial condyle and the fibular head. The biceps femoris functions to extend the hip, flex the knee, and externally rotate the tibia. The superficial layer of the common tendon has been identified as the main force creating external tibial rotation and controlling the internal rotation of the femur.14 The pull of the biceps on the tibia retracts the joint capsule and pulls the iliotibial tract posteriorly, keeping it tight throughout flexion.

Fibularis brevis m. Flexor digitorum longus m.

The gastrocnemius originates from above the knee by two heads, each head connected to a femoral condyle and to the joint capsule (Fig. 20-4). Approximately halfway down the leg, the gastrocnemius muscles merge to form an aponeurosis. As the aponeurosis gradually contracts, it accepts the tendon of the soleus, a flat, broad muscle deep to the gastrocnemius. The aponeurosis and the soleus tendon end in a flat tendon called the Achilles tendon, which attaches to the posterior aspect of the calcaneus. The two heads of the gastrocnemius and the soleus are collectively known as the triceps surae (see Chapter 21). Although the primary function of the gastrocnemius– soleus complex is to plantar flex the ankle and to supinate the subtalar joint, the gastrocnemius also functions to flex or extend the knee, depending on whether the lower extremity is WB or not. It has been proposed that weakness of the gastrocnemius may cause knee hyperextension. In addition, it has been theorized that the gastrocnemius acts as an antagonist to the ACL, exerting an anteriorly directed pull on the tibia throughout the range of knee flexion–extension motion, particularly when the knee is near extension.

Popliteus The popliteus originates from the lateral femoral condyle near the LCL. The muscle has several attachments, including

Dutton_Ch20_p0922-p1023.indd 933

Soleus m. Flexor hallucis longus m.

Achilles tendon Medial malleolus Tibialis posterior m.

Gastrocnemius

The Knee Joint Complex

The semitendinosus muscle (see Fig. 19-8) arises from the upper portion of the ischial tuberosity via a shared tendon with the long head of the biceps femoris. From there, it travels distally, becoming cord-like about two-thirds of the way down the posteromedial thigh. Passing over the MCL, it inserts into the medial surface of the tibia and deep fascia of the lower leg, distal to the gracilis attachment, and posterior to the sartorius attachment. These three structures are collectively called the pes anserinus (“goose foot”) at this point. Like the semimembranosus, the semitendinosus functions to extend the hip, flex the knee, and internally rotate the tibia.

Iliotibial tract

ANATOMY

posteromedial corner of the knee capsule. The semimembranosus pulls the meniscus posteriorly, and internally rotates the tibia on the femur, during knee flexion, although its primary function is to extend the hip and flex the knee.

Flexor digitorum longus m.

Fibularis longus m. Lateral malleolus Calcaneus bone Fibularis brevis m. Fibularis longus m.

Flexor hallucis longus m.

FIGURE 20-4  Gastrocnemius muscle.

the lateral aspect of the lateral femoral condyle, the posteromedial aspect of the head of the fibula, and the posterior horn of the lateral meniscus.1 The larger base of this triangular muscle inserts obliquely into the posterosuperior part of the tibia above the soleal line. The muscle has several important functions, including the reinforcement of the posterior third of the lateral capsular ligament and the unlocking of the knee during flexion from terminal knee extension.1 It performs the latter task by internally rotating the tibia on the femur (a good example of an arcuvial muscle), preventing impingement of the posterior horn of the lateral meniscus by drawing it posteriorly, and, with the PCL, preventing a posterior glide of the tibia. Since knee joint injury frequently involves some component of transverse-plane rotation and the popliteus muscle

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ANATOMY

TABLE 20-3

Hip Adductors Involved in Knee Stability

THE EXTREMITIES

Muscle

Proximal Attachment

Distal Attachment

Innervation

Adductor longus

Pubic crest and symphysis

By an aponeurosis to middle third of linea aspera of femur

Obturator nerve, L3

Adductor magnus

Inferior ramus of pubis, ramus of ischium, and inferolateral aspect of ischial tuberosity

By an aponeurosis to linea aspera and adductor tubercle of femur

Obturator nerve and tibial portion of sciatic nerve, L2–4

Gracilis

Thin aponeurosis from medial margins of Upper part of medial surface of tibia, below tibial condyle and lower half of body of pubis, whole of just proximal to tendon of inferior ramus, and joining part of ramus semitendinosus of ischium

has been described as an important, primary, dynamic, transverse-plane, rotatory knee joint stabilizer, an understanding of its function in relation to other P-L knee joint structures is important.32 Attached to the popliteus tendon is the popliteofibular ligament, which forms a strong attachment to the popliteal tendon and the fibula. This ligament adds to P-L stability. A medial portion of the popliteus penetrates the joint, becoming intracapsular with the lateral meniscus. This part of the popliteus tendon is pain sensitive, and an injury here can often mimic a meniscal injury on the lateral aspect of the joint line. Differentiation between these two lesions can be elucidated with the reproduction of pain with resisted flexion in an extended and externally rotated position of the tibia if the popliteus is involved.

Obturator nerve, L2

patellar. Posteriorly, it is attached to the tendon of the biceps femoris. Laterally, it blends with an aponeurotic expansion from the VL (see Chapter 19). Like the patellar tendon, the ITB can be viewed as a ligament or a tendon. Its location adjacent to the center of rotation of the knee allows it to function as an anterolateral stabilizer of the knee in the frontal plane and to both flex and extend the knee.1 During stationary standing, the primary function of the ITB is to maintain knee and hip extension, providing the thigh muscles an opportunity to rest. While walking or running, the ITB helps maintain flexion of the hip and is a major support of the knee in squatting from full extension until 30 degrees of flexion. In knee flexion greater than 30 degrees, the iliotibial tract becomes a weak knee flexor, as well as an external rotator of the tibia.

Hip Adductors The hip adductors, which play an indirect role in the medial stability of the knee (Table 20-3), are described in Chapter 19. The exception to this is the two-joint gracilis muscle, the third member of the pes anserinus group, which in addition to adducting and flexing the hip, assists in flexion of the knee and internal rotation of the lower leg.

Tensor Fascia Latae The tensor fascia latae (TFL) arises from the outer lip of the iliac crest and the lateral surface of the anterior superior iliac spine (ASIS) (Fig. 19-5). Over the flattened lateral surface of the thigh, the fascia latae thickens to form a strong band, the iliotibial tract. When the hip is flexed, the TFL is anterior to the greater trochanter and helps maintain the hip in flexion. As the hip extends, the TFL moves posteriorly over the greater trochanter to assist with hip extension. The TFL is also a weak extensor of the knee, but only when the knee is already extended. The muscle is innervated by the superior gluteal nerve, L4–L5.

Iliotibial Band (Tract)

934

The ITB or tract begins as a wide covering of the superior and lateral aspects of the pelvis and thigh in continuity with the fascia latae (Figs. 20-4 and 19-5). It inserts distal and lateral to the patella at the tubercle of Gerdy on the lateral condyle of the tibia. Anteriorly, it attaches to the lateral border of the

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MAJOR NERVES AND BLOOD VESSELS The posterior structure of the knee joint is a complex of nerves and blood vessels. The knee joint is innervated by the posterior articular branch of the posterior tibial nerve, which is formed from all five anterior divisions (L4, L5, and S1–S3) of the sacral plexus (see below), and the terminal branches of the obturator and femoral nerves.23 The course and distribution of the femoral nerve are described in Chapter 3. The lateral portion of the capsule is innervated by the recurrent peroneal branch of the common fibular (peroneal) nerve, which is formed by the upper four posterior divisions (L4, L5, and S1, S2) of the sacral plexus (see below). The saphenous nerve is the largest cutaneous branch of the femoral nerve (L2–L4). It leaves the subsartorial canal approximately 8–10 cm above the medial condyle of the knee and gives off branches to the medial aspect of the knee. Entrapment of the saphenous nerve during its course here can occur because of direct trauma, genu valgus, or knee instability, resulting in saphenous neuritis. The sciatic nerve (see Chapter 3) provides motor branches to the hamstrings and all muscles below the knee.33 It also provides the sensory innervation to the posterior thigh and entire leg and foot below the knee (except the medial aspect, which is innervated by the saphenous nerve).33 The major blood supply to this area comes from the femoral (see Chapter 19), popliteal, and genicular arteries.

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The common fibular (peroneal) nerve is a component of the sciatic nerve as far as the upper part of the popliteal space. At the apex of the popliteal fossa, the common fibular (peroneal) nerve begins its independent course, descending along the posterior border of the biceps femoris, before traveling diagonally across the posterior aspect of the knee joint to the upper external portion of the leg near the head of the fibula. Sensory branches are given off in the popliteal space. These include the superior and inferior articular branches to the knee joint and the lateral sural cutaneous nerve. The latter nerve joins the medial calcaneal nerve (from the tibial nerve) to form the sural nerve, supplying the skin of the lower posterior aspect of the leg, the external malleolus, and the lateral side of the foot and fifth toe.1 The common fibular (peroneal) nerve curves around the lateral aspect of the fibula toward the anterior aspect of the bone, before passing deep to the two heads of the fibularis (peroneus) longus muscle, where it divides into three terminal branches: the recurrent articular, and the superficial and deep fibular (peroneal) nerves. The recurrent articular nerve accompanies the anterior tibial recurrent artery, supplying branches to the proximal tibiofibular and knee joints, and a twig to the tibialis anterior muscle.

Tibial Nerve The tibial nerve, the larger of the two branches of the sciatic nerve, begins its own course in the upper part of the popliteal space. It descends vertically through this space, passing between the heads of the gastrocnemius muscle to the posterior aspect of the leg, and to the posteromedial aspect of the ankle, where its terminal branches serve the foot and ankle (see Chapter 21). The tibial nerve supplies the gastrocnemius, plantaris, soleus, popliteus, tibialis posterior, flexor digitorum longus, and flexor hallucis longus muscles. Articular branches pass to the knee and ankle joints.

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As intermediate joints, the tibiofemoral joint and the PFJ depend on the appropriate mechanical behavior of the hip and ankle to maintain their proper dynamic alignment.36

Tibiofemoral Joint The tibiofemoral joint, or knee joint, is a ginglymoid, or modified hinge joint, which has six degrees of freedom. For example, during gait it rotates about the sagittal, transverse, and coronal axes (i.e., osteokinematics), and translates in the sagittal, transverse, and coronal planes (i.e., arthrokinematics). The bony configuration of the knee joint complex is geometrically inappropriate and lends little inherent stability to the joint. Joint stability is, therefore, reliant on the static restraints of the joint capsule, ligaments, and menisci, and the dynamic restraints of the quadriceps, hamstrings, and gastrocnemius. Since the ligaments share tensile load-carrying functions with the musculotendinous units, these structures can be considered to complement each other’s functions directly. The PCL is located very near the long axis of tibial rotation and has been described as the main stabilizer of the knee. The most common knee motions consist of flexion and extension in the sagittal plane, coupled with other motions such as varus and valgus motions, and external and internal rotation. This is because the longitudinal axis of the knee is not perpendicular to the sagittal plane but lies along a line that connects the origins of the collateral ligaments on the medial and lateral femoral epicondyles. All the motions about the tibiofemoral joint consist of a rolling, gliding, and rotation of the femoral condyles and the tibial plateaus (Fig. 20-5). This rolling, gliding, and rotation occur almost simultaneously, albeit in different directions, and serve to maintain joint congruency.

The Knee Joint Complex

Common Fibular (Peroneal) Nerve

BIOMECHANICS

BIOMECHANICS

Popliteal. Before bifurcating into the anterior and posterior tibial arteries, the popliteal artery normally courses beneath and between the medial and lateral heads of the gastrocnemius, adjacent to the plantaris and popliteus muscles, and through the tendinous arch of the soleus.34,35 Alteration of these normal structural relationships can cause compression of the popliteal artery—popliteal artery entrapment syndrome (see Chapter 5). ▶▶ Genicular. The descending genicular artery arises from the femoral artery, just before it passes through the adductor hiatus and immediately divides into the saphenous branch of descending genicular artery and the articular branches of descending genicular artery. The superior medial genicular artery and the superior lateral genicular artery both arise from the popliteal artery. The middle genicular artery is a small branch of the popliteal artery that originates inferior or distal to both of the superior genicular arteries. Arising from the middle genicular artery are the inferior medial and inferior lateral genicular arteries. ▶▶

Flexion and extension occur with a mediolateral translation around a mediolateral axis. In the relaxed standing position, with the knee straight or slightly flexed, the vector force is behind the knee; therefore, there is a tendency for further knee flexion unless the quadriceps contracts. ▶▶ A varus–valgus angulation occurs with anteroposterior translation around an anteroposterior axis. ▶▶ External and internal rotation of the joint occurs with superior–inferior translation around a superoinferior axis and transverse plane. The available range of motion (ROM) in rotation is dependent on the flexion– extension position of the knee.37 The amount of rotation progressively increases from no rotation at the terminal extension to 70 degrees of rotation (40 degrees of external rotation and 30 degrees of internal rotation) available at 90 degrees of flexion. The amount of available rotation decreases as further flexion occurs. ▶▶

During the initial 30 degrees of knee flexion, the LCL provides a greater contribution to resisting tibial varus, and the PMTC provides a greater contribution to resisting tibial external rotation and posterior translation.32,38 For flexion to be initiated from a position of full extension, the knee joint

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EXT

EN

SI

N

ROL

O

Quadriceps femoris

L

BIOMECHANICS

Screw-home rotation

Femur

S L ID E

THE EXTREMITIES

Patellar ligament

RO L L SL ID E

Tibia

EXTENSION

Screw-home rotation

A

Tibial-on-femoral extension

B

Femoral-on-tibial extension

FIGURE 20-5  The arthrokinematics of knee motions.

936

must first be “unlocked.” As mentioned previously, the service of locksmith is provided by the popliteus muscle, which acts to internally rotate the tibia with respect to the femur, enabling flexion to occur. During flexion of the knee, the femur rolls posteriorly and glides anteriorly, with the opposite motion occurring during extension of the knee. This arrangement resembles a twin wheel, rolling on a central rail. Available knee flexion can vary between 120 and 160 degrees, depending on the position of the hip and the girth of the soft tissues around the leg and the thigh. From 30 to 5 degrees of WB knee extension (moving toward full knee extension), the lateral condyle of the femur, together with the lateral meniscus, becomes congruent, moving the axis of movement more laterally. The tibial glide now becomes much greater on the medial side, which produces internal rotation of the femur, and the ligaments, both extrinsic and intrinsic, start to tighten near terminal extension. At this point, the cruciate ligaments become crossed and are tightened. In the last 5 degrees of extension, rotation is the only movement accompanying extension. This rotation is referred to as the “screw home” mechanism and is a characteristic motion in the normal knee, in which during terminal knee extension the tibia externally rotates relative to the femur (Fig. 20-3). This motion is known to be a complex function of surface geometry of the menisci, tension in the ligamentous structures, and the action of muscles. This external rotation of the tibia through swing into stance allows for the tibia and foot to be in the correct alignment at initial contact.39 Interestingly, the screw home mechanism is reduced in ACL-deficient knees, which could be attributed to a reduction in passive tension developed during terminal stance, thereby influencing the sensation of knee instability in these individuals.40

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Knee hyperextension is usually available from 0 to 15 degrees.41 During knee hyperextension, the femur does not continue to roll anteriorly but instead tilts forward. This creates anterior compression between the femur and the tibia. In the normal knee, bony contact does not limit hyperextension as it does at the elbow. Rather, hyperextension is checked by the soft-tissue structures. When the knee hyperextends, the axis of the thigh runs obliquely inferiorly and posteriorly, which tends to place the ground reaction force anterior to the knee. In this position, the posterior structures are placed under tension, which helps to stabilize the knee joint, negating the need for quadriceps muscle activity.

CLINICAL PEARL The transition from NWB to WB has been found to produce a threefold increase of anterior translation of the tibia relative to the femur in the ACL-deficient knee compared with the contralateral normal knees.42

The normal capsular pattern of the knee joint is a gross limitation of flexion and slight limitation of extension. The ratio of flexion to extension is roughly 1:10; thus, 5 degrees of limited extension corresponds to a 45–60-degree limitation of flexion. The causes of a capsular pattern in the knee are the same as for any other joint. These include traumatic arthritis, rheumatoid and reactive arthritis, osteoarthrosis, monarticular and steroid-sensitive arthritis, crystal synovitis or gout, hemarthrosis, and septic arthritis. Open-kinetic chain (OKC) and closed-kinetic chain (CKC) exercises have different effects on tibial translation and ligamentous strain and load:

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Patellofemoral Joint

1. Static restraints. There is evidence to support the relationship between femoral and tibial alignment and PFJ mechanics under static conditions. For example, increased knee abduction has been linked to increased PFJ stress,45 and increased internal femoral rotation with respect to the tibia has been shown to be related to decreased patellofemoral contact area46 and increased PFJ stress.47 Lateral passive support is provided by the fibrous superficial and deep lateral retinacula. Fibrous expansions from the VL and the ITB contribute to these retinacula, with additional lateral support provided by the distal component of the ITB, and the contact of the patella with the lateral edge of the patellar groove.6 Since most of the lateral retinaculum arises from the ITB, excessive lateral tracking may occur if the ITB is adaptively shortened.6 a. The appropriate tension on the medial and lateral structures ensures patellar tracking through the groove. Inappropriate tensioning may result in

TABLE 20-4

 atella–Femur Contact During Range of P Knee Flexion

Knee Range of Flexion (Degrees)

Facet Contact

0

No contact

15–20

Inferior pole

45

Middle pole

90

All facets

Full flexion (135 degrees)

Odd facet and lateral aspect

Data from Goodfellow J, Hungerford DS, Zindel M. Patello-femoral joint mechanics and pathology. 1. Functional anatomy of the patello-femoral joint. J Bone Joint Surg Br. 1976 Aug;58(3):287–290; Aglietti P, Insall JN, Walker PS, et al. A new patella prosthesis. Design and application. Clin Orthop Relat Res. 1975;(107):175–187.

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The Knee Joint Complex

The PFJ is susceptible to orthopaedic injury because it is the least stable joint in the lower limb and forces that are multiple times body weight are applied rapidly through a wide ROM during activities of daily living ADLs.43 The patella is an inactive component of the knee extensor mechanism. In view of the frequent problems associated with the PFJ, it is remarkable that, for much of the time, the articulating surfaces of this joint are not even in contact.44 Indeed, there is no bone-to-bone contact with the femur in full knee extension, or during standing or walking on level ground (Table 20-4).8 As the knee flexes, a number of forces act upon this joint. To assist in the control of the forces around the PFJ, there are a number of static and dynamic restraints:

excessive pressure on the lateral PFJ surfaces (lateral patellofemoral pressure syndrome) or medial subluxation of the patella from the groove. b. The PFJ is intrinsically unstable because the tibial tubercle lies lateral to the long axis of the femur, and the quadriceps muscle and the patella are, therefore, subject to a laterally directed force. The causes of insufficient engagement include ■■ an abnormally high patella; ■■ patellar dysplasia; and ■■ a poorly developed patellar groove (trochlea). The trochlea acts as a lateral buffer to the patella. If the patella fails to engage securely in the patellar groove at the start of flexion, it slips laterally, and as flexion continues, it can dislocate completely or slip back medially to its correct position. Sometimes the patella engages correctly at the start of the flexion but subluxes or dislocates as flexion proceeds. This disengagement may be the result of a defective lateral trochlear margin, an unusually shallow groove, or malalignment (if excessive genu valgus is present, the laterally directed force applied to the patella is greater).

BIOMECHANICS

During active OKC knee extension, the shear component produced by unopposed contraction of the quadriceps depends on the angle of knee flexion, increasing as the knee flexion angle increases. ▶▶ During CKC exercises for the lower extremity, the flexion moment arms of the knee and the hip increase as a squat is performed. ▶▶

c. Passive restraints to the translation of the patella are provided by the medial patellofemoral ligament, part of a joint capsule thickening formed by itself and the patellomeniscal and patellotibial ligaments. d. Medial retinaculum. As the medial retinaculum is not as robust as its lateral counterpart, it is thought to be less significant in influencing patellar tracking. 2. Dynamic restraints. As the PFJ is inherently unstable, it relies heavily on active stabilization via the muscular system. a. The primary dynamic restraints of the PFJ are the quadriceps muscle, particularly the VMO, and the extensor mechanism in general. The activity of the VMO increases as the torque around the knee increases, and it provides the only dynamic medial stability for the patella.14 However, the muscle vector of the VMO is more vertical than normal when a patellar malalignment is present, making it less effective as a dynamic stabilizer. The timing of the VMO contractions relative to those of other muscles, especially the VL, also appears to be critical and has been found to be abnormal with patellar malalignment.6

CLINICAL PEARL The tension provided by the dynamic restraints of the PFJ can prevent the patella from slipping laterally. However, excessively tight lateral structures or deficient medial structures may increase the laterally directed forces. This may result in maltracking of the patella or possible subluxation. The lateral structures (VL, lateral retinaculum, and ITB) may be tight from fibrosis of the VL or adaptively shortened.6 The medial structures (medial retinaculum) may be loose after injury to the medial retinaculum, from stretching after repeated dislocations, or from severe wasting of the vastus medialis.

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BIOMECHANICS THE EXTREMITIES

b. Neuromuscular control. Deficits in the timing of muscle activity have been identified in a number of musculoskeletal conditions.48 A study by Cowan et al.,48 which found that on average the onset of electromyographic (EMG) activity of the VL occurred before that of VMO in subjects with patellofemoral pain syndrome (PFPS), appears to lend support to this theory. Thus, specific retraining of the VMO is believed to improve patellar tracking.48 c. The integrity of the links of the kinematic chain. Hip muscle weakness49 and excessive foot pronation50 have been proposed to result in patellofemoral pain (PFP). There are a number of other factors that may impact on the PFJ including structures both proximal and distal to the joint6: Proximal. These include femoral internal rotation, altered hip motor control, increased apparent knee valgus, and in adequate flexibility of the hamstrings, ITB and tensor fascia lata. ▶▶ Distal. These include increased tibial rotation, pronated foot type, and inadequate flexibility of the gastrocnemius. ▶▶

Finally, in addition to the factors previously mentioned, there are two anatomical factors that can negatively impact the PFJ, the quadriceps angle and the alignment angle.

Quadriceps Angle The quadriceps (Q) angle can be described as the angle formed by the bisection of two lines, one line drawn from the ASIS to the center of the patella, and the other line drawn from the center of the patella to the tibial tubercle (Fig. 20-6). The angle is a measure of the tendency of the patella to move laterally when the quadriceps muscles are contracted.14 The Q-angle increases with knee extension. Various normal values for the Q-angle have been reported. The most frequent ranges cited are 8–14 degrees for males

and 15–17 degrees for females.14 The discrepancy between males and females allegedly results from the wider pelvis of the female, although this has yet to be proven. Indeed, it is not even clear that, on average, women have a significantly greater Q-angle. Angles of greater than 20 degrees are considered abnormal and may be indicative of potential displacement of the patella.6 The Q-angle can vary significantly with the degree of foot pronation and supination, and when compared with measurements made in the supine position. Confusing this issue is that the Q-angle is increased in patients with a lateralized tibial tuberosity, but it can be falsely normal when the patella is laterally displaced.8

CLINICAL PEARL It has been theorized that increased frontal plane hip motion may affect the lateral forces acting on the patella by increasing the “dynamic” quadriceps angle.51 Although this measurement has been used to evaluate and treat PFJ pathology, few studies have examined its reliability. Greene et al.52 evaluated the interobserver and intraobserver reliability of the Q-angle measurement comparing clinically derived Q-angle measurements with radiographically derived measurements. A reliability analysis was performed using intraclass correlation coefficients (ICCs). For interobserver measurements, the ICCs ranged from 0.17 to 0.29 for the four variables evaluated (right and left, extension and flexion). For intraobserver measurements, the ICCs ranged from 0.14 to 0.37. The average ICC between the clinically and radiographically derived measurements ranged from 0.13 to 0.32, which demonstrates poor interobserver and intraobserver reliability of the Q-angle measurement and poor correlation between clinically and radiographically derived Q-angles. One imaging process somewhat analogous to the Q-angle is the tibial tubercle-trochlear groove (TT-TG) distance, which may be measured with advanced 3D imaging (CT or magnetic resonance imaging [MRI]).5 A distance of 9–11 mm is generally considered normal for adults, while a distance of greater than 20 mm or greater than 15 mm is pathological depending on the population studied.53–55

CLINICAL PEARL Although an increased Q-angle is traditionally associated with valgus knees, some of the highest Q-angles are found in patients with a combination of genu varus and proximal tibial torsion. 25°

Alignment Angle 15°

Normal

938

FIGURE 20-6  The Q-angle.

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Abnormal

The A-angle, an assessment of the relationship between the patella and the tibial tuberosity, is another measurement that has been used to evaluate and treat PFJ pathology and as a quantitative measurement of patellar alignment. The A-angle is defined as the relationship between the longitudinal axis of the patella and the patellar tendon or the patella’s orientation

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The amount of contact between the patella and the femur appears to vary according to a number of factors, including (1) the angle of knee flexion, (2) the location of contact, (3) the surface area of contact, and (4) the PFJ reaction force (PJRF). This knowledge is particularly important when prescribing OKC and CKC exercises (see Intervention Strategies section). Each of these factors is discussed separately.

Angle of Knee Flexion As knee flexion proceeds, the quadriceps vector becomes more perpendicular, and the force on the patella gradually increases (Fig. 20-7). This increasing force is somewhat dissipated by the increased patellofemoral contact with increasing flexion (see later discussion). However, because the force increases more rapidly than the surface area, the stress on the patella increases significantly with flexion. At 20–30 degrees flexion, the patella articular surface is most constrained by the walls of the trochlea groove. Any muscle imbalance between the lateral and medial quadriceps muscles can affect

Location of Contact In the normal knee, as the knee flexes from 10 to 90 degrees, the contact area shifts gradually from the distal to the proximal pole of the patella.6 At full extension, the patella is not in contact with the femur but rests on the supratrochlear fat pad. From full extension to 10 degrees of flexion, the tibia internally rotates, allowing the patella to move into the trochlea.14 This brings the distal third of the patellar into contact with the femur. From 10 to 20 degrees of flexion, the patella contacts the lateral surface of the femur on the inferior patellar surface. The middle surfaces of the inferior aspect of the patellar come into contact with the femur at around 30–60 degrees of flexion, at which point the patella is well seated in the groove. As the knee continues to flex to 90 degrees; the patella moves laterally, and the area of patella contact moves proximally. At 90 degrees of knee flexion, the entire articular surface of the patella (except the odd facet) is in contact with the femur.14 Beyond 90 degrees, the patella rides down into the intercondylar notch. At this point, the medial and lateral surfaces of the patella are in contact with the femur, and the quadriceps tendon articulates with the patellar groove of the femur. At approximately 120 degrees of knee flexion, there is no contact between the patella and the medial femoral condyle. At 135 degrees of knee flexion, the odd facet of the patella makes contact with the medial femoral condyle.14

The Knee Joint Complex

Patella–Femur Contact and Loading

the patellar alignment and distribution of pressure in the lower flexion angles of less than 60 degrees. This can produce a rotation of the patella in the coronal plane.6 At higher flexion angles, imbalances are likely to produce a tilt of the patella in the sagittal plane.6

BIOMECHANICS

to the tibial tubercle. The angle is created by drawing imaginary lines through the patella longitudinally and from the tibial tuberosity to the apex of the inferior pole of the patella. An A-angle greater than 35 degrees is often cited as a cause of patellar pathomechanics. However, there has been little research on the reliability of this quantitative technique, and there is also a lack of research in determining if this angle differs significantly between individuals with patellofemoral dysfunction and those without.

Deep squat

Partial squat

QT JF QT P-L

JF

P-L

A

Extension mechanism

B

Body weight and load

C

Body weight and load

Body weight and load

FIGURE 20-7  The relationship between the depth of the squat position and the compression force within the patellofemoral joint.

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BIOMECHANICS

Surface Area of Contact Knowledge of the patellofemoral contact pattern is useful for determining the limits of motion when patients with patellofemoral symptoms perform OKC and CKC exercises.

Patellofemoral Joint Reaction Force

THE EXTREMITIES

The PJRF is a function of quadriceps and patellar tendon tension and of the angle formed between the quadriceps and patellar tendon. These forces are caused by the increase in patellar and quadriceps tendon tension and the increase in the acuity of the Q-angle that occurs during knee flexion.14

CLINICAL PEARL A recently proposed theory56 describes a collection of altered kinematics—increased hip adduction and internal rotation, increased knee valgus, and increased external tibial rotation—collectively referred to as the dynamic knee valgus—that combine to result in an excessive medial collapse of the lower extremity during various functional activities.43 These altered kinematics theoretically increase the Q-angle and subsequent lateral forces on the patella and joint contact pressure.51 The findings from a controlled laboratory study by Salsich et al.57 recommend avoiding dynamic knee valgus during the rehabilitation programs with PFP, as this movement pattern is associated with increased pain.

Patellar Tracking Patellar tracking, specifically patellar maltracking and its relation to dysfunction, continues to be the subject of many studies.58 In the normal knee, the patella glides in a sinuous path inferiorly and superiorly during flexion and extension, respectively, covering a distance of 5–7 cm with respect to the femur.58 A concave, lateral, C-shaped curve is produced by the patella as it moves from approximately 120 degrees of knee flexion toward approximately 30 degrees of knee extension. The lateral curve produces a gradual medial glide of the patella from 45 to 15 degrees of knee flexion in the frontal plane and a medial tilt (from 45 to 0 degrees of knee extension) in the sagittal plane. Further extension of the knee (between 15 and 0 degrees) produces a lateral glide of the patella in the frontal plane and a lateral tilt in the sagittal plane. One proposed mechanism for abnormal patellar tracking is an imbalance in the activity or tension of the medial and lateral restraints. The cause of the imbalance tends to be hypertonus of the VL, or an excessively tight TFL or ITB. Other joints within the lower kinetic chain can also influence the tracking of the patella.

Jumping and Landing Jumping and landing involve a number of recognized kinematic phases, which include the following59: ▶▶

940

Preparatory phase. During this phase, which places the muscles on a stretch to provide a more explosive contraction, the individual flexes at the hips, knees, and

Dutton_Ch20_p0922-p1023.indd 940

ankles. This is accomplished by an eccentric contraction of the gastroc-soleus and quadriceps, as well as control of the back extensors to maintain trunk position. ▶▶ Takeoff phase. The power necessary for this is generated through the plantar flexors, knee extensors, hip extensors, and back extensors. Forward and upward movement of the upper body increases the momentum. ▶▶ Landing phase. During this phase, the generated forces must be dissipated which is usually accomplished by returning to a flexed position. Abductor strength has been correlated with landing kinematics, more so in females than males.60

Kicking The popularity of the game of soccer in the US has grown exponentially over the past two decades and, as kicking is the defining action of the game, a knowledge of kicking mechanics has become really important. The components of the soccer kick can be broken down into the following phases59,61,62: ▶▶

The angle of approach. The angle of approach can alter peak ball velocity.

Plant limb position. The position of the plant limb not only affects the direction of the kick, but also the velocity and trajectory of the kick. There is a strong correlation between single-leg balance and kicking accuracy, but not with the velocity of the kick.63 ▶▶ Swing limb loading. This phase is analogous to the cocking phase of throwing, and it is here that the hip flexors and knee extensors are on a stretch to store elastic energy. This phase may be affected by foot placement of the stance leg due to the hips being allowed to adopt a more open or closed position. ▶▶ Hip flexion/knee extension. During this phase, the individual attempts to release the stored elastic energy from the previous phase in a controlled manner depending on the intent. The speed created in this phase may be achieved by rotational hip speed combined with both hip flexor and knee extensor muscular strength. In a 2006 study of kicking a football, MRI signal changes of 30% in the adductor longus and 49% in the gracilis were found in the kicking leg following 100 kicks.64 ▶▶ Foot contact. During this phase, the foot and ankle of the kicking leg are placed in a plantar flexed position, and the hip and knee of the kicking leg rapidly flex and extend, respectively. ▶▶ Follow-through. During this phase, the kicking leg continues to move forward, relying on the hamstrings and trunk for deceleration. ▶▶

CLINICAL SIGNIFICANCE OF OKC AND CKC ACTIVITIES As previously discussed, in relation to the lower kinetic chain, which includes the lumbar spine, pelvic joints, hip, knee, foot, and ankle joints, the motions that occur during activities can be described as CKC or OKC motions.

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A closed-chain motion at the knee joint complex occurs when the knee bends or straightens while the lower extremity is WB, or when the foot is in contact with any firm surface. An open-chain motion occurs when the knee bends or straightens when the foot is not in contact with any surface.

Closed-Kinetic Chain Motion Tibiofemoral Joint During CKC knee flexion, the femoral condyles roll backward and glide forward on the tibia. During CKC knee extension, the femoral condyles roll forward and slide backward. During CKC knee flexion, as the femur rolls posteriorly, the distance between the tibial and femoral insertions of the ACL increases. Since the ACL cannot lengthen, it guides the femoral condyles anteriorly.14 In contrast, during CKC extension of the knee, the distance between the femoral and tibial insertions of the PCL increases. Since the PCL cannot lengthen, the ligament pulls the femoral condyles posteriorly as the knee extends.14 It would appear that CKCEs are only beneficial if performed in a restricted range, with some studies demonstrating that CKCEs at greater than 30 degrees of knee flexion can exacerbate patellofemoral problems.6

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During CKCEs, the flexion moment of the arm increases as the angle of knee flexion increases. In addition, the joint-reaction force increases proportionately more during knee flexion than the magnitude of the contact area.6 Thus, the articular pressure gradually increases as the knee flexes from 0 to 90 degrees, with maximum values occurring at 90 degrees of flexion.14 However, because this increasing force is distributed over a larger patellofemoral contact area, the contact stress per unit area is minimized. From 90 to 120 degrees of flexion, the articular pressure remains essentially unchanged because the quadriceps tendon is in contact with the trochlea, which effectively increases the contact area.14 Thus, for the PFJ, CKCEs are performed in the 0–45-degree range of flexion, with caution used when exercising between 90 and 50 degrees of knee flexion, where the PJRFs can be significantly greater.

Open-Chain Motion Tibiofemoral Joint

The Knee Joint Complex

Since the knee joint complex is an integral part of the lower kinetic chain, movement at any portion of the kinetic chain will influence knee joint mechanics, necessitating an examination of the entire chain as part of a comprehensive assessment. Kinetic chain exercises need to be monitored carefully to detect the influence of any abnormal motion that occurs in one portion of the segment on the remaining portions of the kinetic chain.14 For example, normal biomechanics dictates that the tibiofemoral joint extends during midstance as the body traverses the fixed foot. Excessive pronation in either magnitude or duration prevents the knee joint from acquiring the necessary external rotation of the tibia for this extension, which in turn may affect patellar tracking. Another example occurs during the descending phase of a squat, which requires simultaneous flexion at the hip and knee, and dorsiflexion at the ankle. If ankle dorsiflexion motion is limited, subtalar joint pronation will increase to compensate for the lack of dorsiflexion.14 This increased pronation, which is coupled with internal rotation of the lower extremity, results in an increase in the functional Q-angle and may contribute to persistent PFP. Whether the motion at the knee joint complex occurs as a CKC or OKC has implications on the biomechanics and the joint compressive forces induced. A significant number of studies have examined the biomechanics of the knee during OKC and CKC activities and have attempted to quantify and compare cruciate ligament tensile forces, tibiofemoral compressive forces, and muscle activity about the knee during these activities.

Patellofemoral Joint

BIOMECHANICS

CLINICAL PEARL

During OKC flexion, the tibia rolls and glides posteriorly on the femur, while during extension the opposite occurs. OKC knee extension involves a conjunct external rotation of the tibia, while OKC knee flexion involves a conjunct internal rotation of the tibia. OKC activities produce shear forces at the tibiofemoral joint in the direction of tibial movement. For example, OKC knee extension produces anterior shear stresses. Open-kinetic chain exercise (OKCE) is preferred over closed-kinetic chain exercise (CKCE) if minimal PCL tensile force is desired. Since PCL tension generally increases with knee flexion, knee ROMs that are less than 60 degrees will minimize PCL tensile force. The higher compressive forces that occur during the beginning and end ranges of knee flexion in OKCE may serve to unload some of the tensile force in these respective cruciate ligaments. Both OKCEs and CKCEs appear equally effective in minimizing ACL tensile force, except during the final 25 degrees of knee extension in OKCEs. OKC flexion, resulting from an isolated contraction of the hamstrings, reduces ACL strain throughout the ROM, but increases the strain on the PCL as flexion increases from 30 to 90 degrees.14

CLINICAL PEARL It may be prudent to exclude the final 25 degrees of knee extension range for the patient using OKCE for rehabilitation immediately following an ACL injury.14

Patellofemoral Joint In an OKC activity, the forces across the patella are their lowest at 90 degrees of flexion. As the knee extends from this position, the flexion moment arm (contact stress/unit) for the knee increases, peaking between 35 and 40 degrees of flexion,

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EXAMINATION

while the patella contact area decreases.14 This produces an increase in the PJRF at a point when the contact area is very small. At 0 degrees of flexion (full knee extension), the quadriceps force is high, but the contact stress/unit is low. Thus OKCEs for the PFJ should be performed from 25 to 90 degrees of flexion (60–90 degrees if there are distal patellar lesions), or at 0 degrees of extension (or hyperextension) from a point of view of cartilage stress.6 OKCEs are not recommended for the PFJ between 0 and 45 degrees of knee flexion, especially if there are proximal patellar lesions, as the PJRFs are significantly greater.6

THE EXTREMITIES

CLINICAL PEARL Increased tension in the PCL occurs at greater than 65 degrees of knee flexion in CKCE and at greater than 30 degrees with OKCEs. Therefore, it may be prudent to limit knee flexion during both OKCE and CKCE to knee angles of less than 30 degrees following a PCL injury.

EXAMINATION The common pathologies for the knee joint complex are detailed after this section. An understanding of both is obviously necessary. Since the mention of the various pathologies occurs with reference to the examination, and vice versa, the reader is encouraged to switch between the two discussions.

History With the vast number of specific tests available for the knee joint complex, it is tempting to overlook the important role of the history, which can detail both the chronology and mechanism of events. The diagnosis of most tibiofemoral and PFJ disorders often can be made on the basis of a thorough history and physical examination alone. The patient’s family history, medical history, and history of the present knee problem TABLE 20-5

are necessary for a complete diagnosis. A medical screening questionnaire for the knee, leg, ankle, and foot region is provided in Table 20-5. In addition to those questions outlined in “History” section in Chapter 4, the clinician should determine the following:

Chief Complaint It is important to elucidate the exact nature and location of the patient’s chief complaint. Does the complaint relate to pain or instability, or both? If the chief complaint is pain, is there a history of recent trauma?

Onset of Symptoms Questions about the onset of symptoms (traumatic versus insidious) are, as with any joint, important. Acute injuries are often traumatic and can be associated with both pain and instability. Reports of immediate pain associated with an inability to weight bear can indicate a muscle, ligament, or fracture injury and should be related to the patient’s current complaints to identify the likely cause. As always, an insidious onset of pain should alert the clinician to the possibility of a serious condition. Pain in the knee can be referred from the hip, the back, and the sacroiliac joint. Complaints of shooting pain, burning pain, and pain that travels down the thigh should be carefully investigated using a lumbar screen to rule out radicular symptom production. A gradual, nontraumatic onset of knee pain could also indicate PFJ dysfunction or symptomatic degenerative joint disease (DJD) of the knee joint complex. The characteristic clinical features in an uncomplicated osteoarthritis (OA) of the knee joint are a dull and aching pain that occurs at the end of the day or after prolonged periods of standing or walking. As the disease progresses, there is pain and stiffness on rising in the morning, which eases with activity or rest, and a limitation of movement in a capsular pattern.

Mechanism of Injury The clinician should determine how exactly the injury happened—was it a traumatic blow, a contact injury, a

Medical Screening Questionnaire for the Knee, Leg, Ankle, and Foot Region

  Have you recently had a fever? Have you recently taken antibiotics or other medicines for an infection? Have you had a recent surgery? Have you had a recent injection to one or more of your joints? Have you recently had a cut, scrape, or open wound? Have you been diagnosed as having an immunosuppressive disorder? Do you have a history of heart trouble? Do you have a history of cancer? Have you recently taken a long car ride, bus trip, or plane flight or been bedridden for any reason? Have you recently begun a vigorous physical training program? Do you have growing, hip, thigh, or calf aching or pain that increase with physical activity, such as walking or running? Have you recently sustained a blow to your shins or any other trauma to either of your legs?

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Yes

No  

Reproduced with permission from Wilmarth MA. Medical Screening for the Physical Therapist. Orthopaedic Section Independent Study Course 14.1.1. La Crosse, WI: Orthopaedic Section, APTA, Inc.; 2003.

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Varus force.  A history of a varus force with rotation can involve the LCL, the P-L capsule, and the PCL. ▶▶ Hyperextension.  A hyperextension force can result in ACL injuries and associated medial meniscal tears. Complaints of buckling or giving way after the injury can reinforce a suspicion of ligamentous involvement. ▶▶ Flexion.  During flexion, as the tibia internally rotates, the posterior horn of the medial meniscus is pulled toward the center of the joint. If excessive, this movement can produce a traction injury of the medial meniscus, tearing it from its peripheral attachment and producing a longitudinal tear of the substance of the meniscus.65 ▶▶ Flexion with a posterior translation.  This mechanism can result in a PCL injury. ▶▶ Twisting force.  Meniscal injuries are usually associated with a torsional force that combines compression and rotation, often in activities that require cutting maneuvers. In addition, the ACL often is injured during traumatic twisting injuries in which the tibia moves forward with respect to the femur, often accompanied by valgus stress.65 No direct blow to the knee or leg is required, but the foot is usually planted, and the patient may remember a “popping” sensation at the time of the injury. Similar to the ACL, PCL injuries often occur during twisting with a planted foot in which the force of the injury is directed posteriorly against the tibia with the knee flexed.65 ▶▶ Overuse.  A patellar injury is most often a result of overuse. Typically, there is an associated 4–6-week training program change.

The location of the symptoms may afford the clinician clues as to the cause. Initially, the clinician should consider the anatomical structures underlying the area of pain to ascertain the cause. Medial knee pain can be caused by a spectrum of possibilities ranging from localized musculoskeletal to nonmusculoskeletal pathology (Table 20-6).67 For example, medial meniscal lesions frequently result in posterior medial joint line pain and mild medial joint line pain. Medial knee pain also may suggest an MCL injury. MCL injury can produce pain at the medial femoral condyle, medial joint line, or proximal tibia. Lateral joint line pain may be caused by an

TABLE 20-6 Cause

Condition

Local musculoskeletal 

Patellofemoral syndrome Medial meniscus tear Patellar tendinitis Lateral patellar subluxation Pes anserine tendinitis Pes anserine bursitis Vastus medialis strain Saphenous neuropathy Medial collateral ligament sprain Medial tibial plateau fracture Medial tibial plateau stress fracture Proximal tibia stress fracture

Tumors

Osteochondroma Chondroblastoma Giant cell tumor Osteoid osteoma Osteosarcoma Ewing sarcoma Chondrosarcoma Fibrosarcoma Pigmented villonodular synovitis (PVNS) Localized nodular synovitis (LNS)

Systemic disease

Thyroid disorder (Grave disease) Lymphoma Leukemia Myeloma

Vascular/ inflammatory

Rheumatoid arthritis Reiter syndrome Saphenous thrombophlebitis Deep vein thrombosis

▶▶

In many cases, there is no mechanism of injury. Nontraumatic knee complaints are a very common cause of pain and functional impairments in patients.66 Knee OA is the most common nontraumatic knee complaint.

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Differential Diagnosis of Medial Knee Pain

The Knee Joint Complex

Direct trauma.  A direct blow to the anterior aspect of the knee may cause a patellar injury. Repetitive microtrauma to the patella may also be a factor. ▶▶ Valgus force.  A history of a valgus force to the knee without rotation could indicate damage to the medial meniscus, MCL, epiphyseal plate, or patellar dislocation– subluxation. A history of a valgus force with rotation could indicate damage to the ACL, or the posteromedial capsule (the so-called unholy triad). ▶▶

Location of Symptoms

EXAMINATION

noncontact injury, or did the patient fall? The position of the joint at the time of the traumatic force dictates which anatomic structures are at risk for injury; hence, an important aspect of obtaining the patient’s history for acute injuries is to allow him or her to describe the position of the knee and direction of forces at the time it was injured. The direction the patient was turning to and the direction of the blow help to determine the structures likely affected.65 Twisting injuries can result in injuries to the ligaments or meniscus. Contact injuries can result in deep bone bruising, muscle contusions, and ligamentous or meniscal injury when combined with twisting or hyperextension. The primary mechanisms of injury in the knee are direct trauma, a varus or valgus force (with or without rotation), hyperextension, flexion with posterior translation, a twisting force, and overuse.

Remote Hip dysplasia neuromusculoskeletal Lumbosacral pathology Obturator neuropathy Reproduced with permission from Rosenthal MD, Moore JH, DeBerardino TM. Diagnosis of medial knee pain: atypical stress fracture about the knee joint. J Orthop Sports Phys Ther. 2006 Jul;36(7):526–534.

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EXAMINATION

LCL injury. Localized swelling over specific knee structures, such as the MCL or the LCL, also may accompany the pain. Midlateral joint line pain often is caused by a lateral meniscal lesion. PFJ pain usually is anterior, radiating medially and laterally, but primarily in, around, or under the patella. Posterior knee pain may be secondary to joint effusion producing distention of the posterior capsule, a mild strain of one of the gastrocnemius muscles or a PCL tear. Posterior knee pain accompanied by snapping could indicate a Baker cyst.

THE EXTREMITIES

Behavior of Symptoms Symptoms that are not alleviated with rest could indicate a nonmechanical source, or a chemically induced source, such as an inflammatory reaction. A hot and swollen joint without a history of trauma should provoke suspicions about hemophilia, rheumatoid arthritis, an infection, or gout.

Quality of the Symptoms Deep knee pain may indicate damage to one of the cruciate ligaments. Generalized pain in the knee region is characteristic of referred pain, or pain from a contusion or partial tear of a muscle or ligament. Often a patient with a chronic condition has several complaints, and a historical investigation can help identify the original cause. Patients do not always recognize the significance that an old injury may play in their current condition, but these options must be considered if the clinician is unable to make a diagnosis with the information available.

Reports of Swelling In the presence of trauma, the main thrust of the history should be to establish whether the patient experienced an effusion or hemarthrosis (the assessment of swelling is described in “Observation” section.) An effusion is a method by which the joint reacts to stress and usually takes several hours to accumulate. The effusion can result from blood filling the joint or from an increased production of synovial fluid. The time frame of onset provides the clinician with clues as to the nature of the effusion. Synovial effusion usually takes 6–12 hours to develop and produces a dull, aching pain as the joint capsule is distended. By contrast, an acute hemarthrosis is usually well formed after 1–2 hours, leaving a very tense and inflamed knee. The two diagnoses that represent over 80% of the causes of an acute tense hemarthrosis are an ACL tear and patellar dislocation. Other causes of an intraarticular effusion include MCL rupture and intra-articular fracture. Patients with a meniscal lesion often report repetitive episodes of effusion.

Reports of Joint Noise

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Reports of grinding, popping, and clicking in the knee with a particular maneuver are common but may not be related to a pathologic process. However, reports of a “pop” involving sudden rotation of the femur or tibia may indicate damage to the ACL, MCL, coronary ligament, or meniscus, or an osteochondral fracture. Sprains to the ligaments of the knee are often more painful than complete ruptures because the latter have no intact fibers from which pain of a mechanical

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origin can occur. Instability of the knee often is described as a sensation of “giving way,” sliding, or buckling. Sharp, catching pain usually indicates a mechanical problem.

Aggravating Positions or Activities Questions should be asked to determine whether certain kinds of activities bring on the symptoms. For example, the pain may be noticed after resting or after certain activities. Morning pain and stiffness that lessens with activity or movement may indicate a degenerative joint complaint. Complaints of locking or pseudolocking during active or passive flexion and extension can highlight a dysfunctional structure. True locking of the knee is rare; however, loose bodies can cause recurrent locking or the sensation of something catching or getting in the way of movement. “Locking” that occurs with extension could indicate a lesion of the meniscus, a hamstring muscle spasm or an entrapment of the cruciate ligament. “Locking” that occurs with flexion could indicate a lesion to the posterior horn of the medial meniscus. With patellar irritability, there is no true mechanical blocking, although there may be stiffness, grating, or rapid movement inhibition.

Impact on Function The clinician should determine which functional activities reproduce the pain or exacerbate the symptoms. The following statements should be viewed as generalizations, as there are always exceptions. WB activities involving a twisting WB load (e.g., getting in and out of a car with low seats) tend to aggravate a meniscal lesion. ▶▶ PFJ pain often develops as a result of extended activity, such as in the middle of a long run or bike ride, continues into the evening or night, and can disturb sleep. ▶▶ Walking upstairs or downstairs is usually difficult for patients with knee pathology. Usually, patients with a meniscal lesion complain of increased pain with stair climbing, whereas patients with a PFJ lesion complain of increased pain when descending stairs. ▶▶ Patients with a meniscal lesion or PFP rarely can do a full squat without pain. ▶▶ Complaints of pain with kneeling activities are more likely to indicate a patellofemoral lesion than a meniscal lesion. ▶▶ Sitting tends to provoke more symptoms in patients with patellofemoral dysfunction than it does in those with meniscal or ligamentous lesions. ▶▶

Anterior Knee Pain Due to the prevalence of patellofemoral-related disorders, there is a significant temptation to cut corners with a patient who presents with anterior knee pain, and to proceed directly to the diagnosis of PFP. However, this should be avoided, especially in light of the fact that the literature is replete with descriptions of physical examination techniques for the evaluation of the PFJ. Much of the confusion arises from the fact that patellofemoral disorders often lack any objective and identifiable structural failure.

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The differential diagnosis of anterior knee pain (see Chapter 5) should include tears of the menisci, medial synovial plica syndrome, inflammatory or degenerative arthritis, tumors of the joint, ligament injuries that mimic patellar instability, osteochondritis dissecans of the medial femoral condyle (see Chapter 30), prepatellar bursitis, patellar tendinopathy, inflammation of the patellar fat pad, and Sinding–Larsen–Johansson syndrome.6

Systems Review Knee pain and dysfunction can arise from multiple sources. Knee pain that has gradually worsened over time should lead to an evaluation of systemic illness and overuse complications such as tendinopathy. A subjective complaint of stiffness may imply swelling, and the joint mobility and effusion should be assessed. Complaints of weakness should be followed by an examination of the patient’s strength and gait pattern. The clinician needs to consider the likelihood of a specific diagnosis based on age. For example, a slipped capital femoral epiphysis (SCFE) is less likely to be the cause of a recent onset

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TESTS AND MEASURES

The Knee Joint Complex

Classically, the pain from PFJ dysfunction is anterior, but it also can be medial, lateral, or popliteal (posterior). Particular activities can help with differential diagnosis. Pain from rotational malalignment of the patella is typically exacerbated by activity and relieved by rest. Complaints of pain that occur when a patient arises from a seated position, negotiates stairs, or squats are associated with patellofemoral dysfunction. The so-called movie-theater sign—pain with prolonged sitting— traditionally has been associated with patellar pain from any source. Venous congestion and stretching of painful tissues are potential explanations for this symptom. Activities that involve eccentric loading of the knee, and increased hill work with running, tend to provoke patellar tendinopathy, whereas inferior patellar pain following vigorous kicking, flip turns in swimming, or delivery of a fast ball in cricket would tend to implicate the fat pad. The fat pad also may be irritated with the straight leg raise exercise. If a patellofemoral disorder is suspected, the clinician should look for evidence of an anatomical variant and/or a biomechanical dysfunction involving the lower quadrant. These anatomical variants can occur in any of the following joints: hip, patellofemoral, tibiofemoral, subtalar, intertarsal, or any combination of these joints. Examples of biomechanical dysfunctions that can cause patellofemoral disorders include excessive femoral anteversion, excessive genu valgum, excessive tibial external rotation, excessive pronation, and VMO dysplasia. Edema rarely is reported with insidious onset overuse injuries, except in the case of plical irritation, ITB friction syndrome (ITBFS), irritation of the pes anserine or Osgood– Schlatter disease. Following the history, a hypothesis is made, and this hypothesis is then tested with the physical examination. Ideally, the clinician is able to process and identify responsible structures for the patient’s complaints and the history of injury to aid in the differential diagnosis.

of pain in a 40-year-old fully developed man that it would be in an adolescent. Knee pain can be referred to the knee from the lumbosacral region (L3–S2 segments) or from the hip. For example, A-M pain can be referred from the L2 and L3 spinal levels, whereas P-L knee pain can be referred from the L4, L5, and S1 to S2 levels. The peripheral nerves are also capable of referring pain to this area. Medial knee pain having a burning quality could indicate saphenous nerve neuritis. A family history of knee problems, rheumatoid arthritis, or OA may need further investigation with a laboratory work-up or x-ray films. Pain that is constant and burning in nature should alert the clinician to the possibility of complex regional pain syndrome (CRPS), gout, or radicular pain. Intermittent pain usually indicates a mechanical problem (meniscus). The health intake questionnaire should be designed to provide evidence of undiagnosed systemic problems that relate to the knee dysfunction (e.g., Lyme disease). Chapter 5 describes some of the more common causes of referred knee pain and causes of a more serious nature.

EXAMINATION

CLINICAL PEARL

Observation The observation component of the examination begins as the clinician meets the patient and ends as the patient is leaving. This informal observation should occur at every visit.

Swelling or Effusion The amount of swelling present may provide the clinician with valuable information regarding the internal damage that may have resulted. Diffuse swelling indicates fluid in the joint or synovial swelling or both. An effusion can be detected by noticing the loss of the peripatellar groove and by palpation of the fluid. A perceptible bulge on the medial aspect suggests a small effusion; this sign may not be present with larger effusions. The swelling can be examined with the patient positioned in supine, in the following ways: ▶▶

Patellar ballottement/tap test.  Using one hand, the clinician grasps the patient’s thigh at the anterior aspect about 10 cm above the patella, placing the fingers medial and the thumb lateral. The patient’s knee is extended. With the other hand, the clinician grasps the patient’s lower leg about 5 cm distal to the patella, placing the fingers medial and the thumb lateral. The proximal hand exerts compression against the anterior, lateral, and medial aspects of the thigh and, while maintaining this pressure, slides distally. The distal hand exerts compression in a similar way and slides proximally (Fig. 20-8). Using the index finger of the distal hand, the clinician now taps the patella against the femur. In the normal knee joint with minimal free fluid, the patella moves directly into the femoral condyle, and there is no tapping sensation underneath the clinician’s fingertips. However, in the knee with excess fluid, the patella is “floating”; thus, ballottement causes the patella to tap directly against the femoral condyle. This sensation

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EXAMINATION

with MRI and ultrasound have demonstrated strong validity, manual measurements using measuring tape are not sensitive enough unless the atrophy is severe.69 The formal observation of the patient is divided into three sections: standing and walking, seated, and lying examinations.

Patient Standing

THE EXTREMITIES

FIGURE 20-8  Patellar ballottement test.

is transmitted to the clinician’s fingertips. A positive test is indicative of a significant synovial effusion or hemarthrosis in the knee joint. However, sometimes, this test can produce false-positive results. When this is the case, the uninvolved side usually tests positive as well. ▶▶ Stroke test.  The patient is positioned in supine, with the knee extended. Using the web space between the forefinger and thumb, the clinician strokes the medial aspect of the knee in an attempt to milk the fluid into the lateral compartment. The test can be graded as follows68: ■■ 0—No wave produced on downstroke. ■■ Trace—small wave on medial side with downstroke. ■■ 1+—Large bulge on medial side with downstroke. ■■ 2+—Effusion spontaneously returns to the medial side after upstroke (no downstroke necessary). ■■ 3+—So much fluid that it is not possible to move the effusion out of the medial aspect of the knee. ▶▶

Fluid Wave Test.  This test is used when there is minimal effusion (50% of lateral border can be palpated but posterior surface cannot; 2 if 3 > 4 > 5. ▶▶ Index minus.  With this type, the second metatarsal is longer than the first and third metatarsals. The fourth and fifth metatarsals are progressively shorter than the third, so that 1 < 2 > 3 > 4 > 5. ▶▶

Stability of the MTP joints is primarily provided by a musculocapsular ligamentous complex anteriorly (plantarly), and medially and laterally by the medial and lateral collateral ligaments, respectively.

First MTP Joint The first MTP joint is the articulation between the head of the first metatarsal and the proximal phalanx. Although there is some anatomic variation from patient to patient, the first MTP joint is typically a cam-shaped, bicondylar-hinged joint that has 2 degrees of freedom. The first MTP joint has little inherent stability because the proximal phalanx has a fairly shallow cavity in which the metatarsal head articulates. The joint is stabilized posteriorly (dorsally) by the capsule and expansion of the extensor hallucis tendon. Fan-shaped medial and lateral collateral ligaments provide valgus and varus stability, respectively. The plantar surface of the capsule is reinforced by a fibrocartilaginous plate, called the plantar accessory ligament. In addition, the MTP joint is dynamically stabilized by the short flexor complex (FHB and the two sesamoids embedded in the FHB tendons), the adductor hallucis, and the abductor hallucis tendons.

CLINICAL PEARL The sesamoids are contained within the tendon of the FHB and serve to increase the lever arm for flexion of the MTP joint, analogous to the function of the patella in knee extension. The sesamoids are connected distally to the base of the proximal phalanx by extensions of the FHB called the plantar

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Soleus m.

Tibialis anterior m.

Inferior extensor retinaculum

Tibialis anterior tendon

Metatarsal

Flexor digitorum longus m. Tibialis posterior m. Flexor hallucis longus m. Posterior tibial a. Tibial n.

Metatarsalphalangeal joint

Achilles tendon

Distal phalange Calcaneus

Lower Leg, Ankle, and Foot

Superior extensor retinaculum

ANATOMY

Tibia

Flexor retinaculum Proximal phalange

Plantar aponeurosis

Interphalangeal joint

Lateral plantar a. and n. Medial plantar a. and n.

FIGURE 21-4  Medial aspect of the ankle and foot. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

plate. Typically, the sesamoids are anterior (plantar) to the medial and lateral condyles of the metatarsal pad. The sesamoids are separated on the anterior (plantar) aspect of the first metatarsal head by a cresta, which helps to stabilize the sesamoids, and are connected to one another by the intersesamoidal ligament. The abductor hallucis inserts into the medial sesamoid, and the adductor hallucis inserts into the lateral sesamoid. The FHL (Fig. 21-4) pierces the two heads of the FHB muscle to run just anterior (plantar) to the intersesamoidal ligament. While there are many conditions that can affect first ray function, the most prevalent include progressive first MTP joint degeneration, hallux abducto-valgus (HAV), hallucal sesamoid syndrome, flexor hallucal longus tendinopathies, turf toe, metatarsalgia, and interdigital neuroma.6

INTERPHALANGEAL The IP joints are classified as condyloid synovial joints. The hallux has two phalanges; whereas each of the remaining toes has three (see Fig. 21-1). The IP joints are classified as simple, synovial, modified sellar joints. The saddle-shaped articular fossa of the head of the proximal phalanx articulates with the

Dutton_Ch21_p1024-p1120.indd 1035

base of the intermediate phalanx. This in turn receives the smaller and flatter distal phalanx.

ACCESSORY OSSICLE An accessory ossicle (accessory bone) is an anomalous bone that fails to unite during developmental ossification. Common locations include the fibular malleolus, tibial malleolus, navicular, and talus. The accessory navicular is the most common accessory bone in the foot.8 It occurs on the medial, anterior (plantar) border of the navicular, at the site of the tibialis posterior tendon insertion. The posterior aspect of the talus often exhibits a separate ossification center, appearing at 8–10 years of age in girls and 11–13 years of age in boys. Fusion usually occurs 1 year after its appearance.8 When fusion does not occur, a drawer sign is formed (see Chapter 5).

CLINICAL PEARL An accessory bone can be differentiated from a fracture radiographically, as an accessory bone will have rounded edges whereas a fracture will have sharp edges.

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ANATOMY

PLANTAR FASCIA/PLANTAR APONEUROSIS

THE EXTREMITIES

The terms plantar fascia and plantar aponeurosis (Fig. 21-4) are often used interchangeably, although strictly speaking only the central part of the plantar fascia is extensively aponeurotic. The plantar fascia is the investing fascial layer of the anterior (plantar) aspect of the foot that originates from the os calcis and inserts through a complex network to the anterior (plantar) forefoot. It is a tough, fibrous layer, composed histologically of both collagen and elastic fibers. The plantar fascia is often regarded as being analogous to the palmar fascia of the hand. However, unlike the fascial layer of the palm, which is generally thin, the plantar fascia is a thick structure, and not only serves a supportive and protective role, but is also intricately involved with the weight-bearing function of the foot. The load to failure of the plantar fascia is estimated in the range of 1000 N.21,22 The plantar fascia is divided into three major areas: a central portion and medial and lateral sections, each oriented longitudinally on the anterior (plantar) surface of the foot.8 Central portion.  The central portion is the major portion of the plantar fascia both anatomically and functionally. This portion is the thickest and the strongest and is narrowest proximally where it attaches to the medial process of the calcaneal tuberosity, proximal to the flexor digitorum brevis (FDB). This attachment site is often involved in a condition called plantar heel pain (see “Intervention Strategies” section); however, pain can occur anywhere in the structure. The central portion envelops the FDB muscle on both sides, forming the medial and lateral intermuscular septums, which anchor the plantar fascia to the deep plantar pedis. Due to the anatomical connections of the central portion, dorsiflexion of the toe slides the plantar pads distally, placing tension on the plantar aponeurosis. The central portion of the fascia primarily functions as a dynamic stabilizer of the medial longitudinal arch during weightbearing activities. ▶▶ Lateral and medial portions.  The smaller and thinner lateral and medial portions are thin and cover the undersurface of the abductor digiti minimi and abductor hallucis muscles, respectively.

▶▶

Truss. In the truss system of the foot, the triangular unit is the medial longitudinal arch with the ankle joint functioning as the apex of the triangle, the calcaneus and talus are the posterior struts, and the first ray is the anterior strut. The plantar fascia stabilizes the two rigid struts inferiorly by limiting the ability of the struts to spread apart.

During the initial contact, and during the first half of the stance phase of the gait cycle (see Chapter 6) with the toes in neutral, the plantar fascia relaxes, flattening the arch. This allows the foot to accommodate to irregularities in the walking surface and to absorb shock. As the foot proceeds from midstance to terminal stance, the foot pressure migrates anteriorly and the toes dorsiflex and, through its attachments to the toes via the plantar plate, the plantar fascia tightens. The tension in the plantar fascia is directly related to dorsiflexion of the MTP of the toes.24 The plantar fascia is pulled over the metatarsal heads, causing the metatarsal heads to be depressed and the longitudinal arch to rise. During the swing phase of gait, the plantar fascia is under little tension and appears to serve no important functional role.

▶▶

With standing and weight-bearing, the plantar fascia plays a major role in the support of the weight of the body, by virtue of its attachments across the medial longitudinal arch. During the different phases of gait, the plantar fascia assumes different biomechanical functions, which have been described as a windlass mechanism or a truss mechanism: ▶▶

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Windlass. The windlass effect on the plantar fascia helps to reconstitute the medial longitudinal arch and generates a more rigid foot for propulsion during the toe-off portion of the gait cycle. The plantar fascia, which serves as the cable of the windlass mechanism, wraps around the head of the metatarsal, which serves as the cylinder of the windlass, and raises the medial longitudinal arch to attach to the medial tubercle of the calcaneus.23

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RETINACULA The extensor and fibular (peroneal) retinacula contribute to ankle and hindfoot stability primarily due to their anatomical orientation. There are four important ankle retinacula, which function to tether the leg tendons as they cross the ankle to enter the foot (Fig. 21-4). Inferior extensor retinaculum.  The inferior extensor retinaculum runs from the tip of the lateral malleolus to insert on the lateral calcaneus and sinus tarsi. It also blends with the inferior fibular retinaculum and may improve evertor muscle function. It consists of two parts: superior and inferior. The superior part functions to contain the tendons of the extensor digitorum longus (EDL), extensor hallucis longus (EHL), tibialis anterior, and fibularis (peroneus) tertius. The Y-shaped inferior part consists of an upper and a lower band, which prevent “bow-stringing” of the posterior (dorsal) tendons. ▶▶ Superior fibular (peroneal) retinaculum.  The superior fibular retinaculum, which courses from the lateral malleolus to the calcaneus, parallel with the posterior fibers of the CFL,16 firmly tethers the fibularis (peroneus) longus and brevis tendons behind the fibular malleolus. ▶▶ Flexor retinaculum.  The flexor retinaculum provides a firm support structure for the flexor digitorum longus (FDL), FHL, tibialis posterior, and the neurovascular bundle. ▶▶

EXTRINSIC MUSCLES OF THE LEG AND FOOT Twenty-three muscles are involved with motion at the foot and ankle, 12 of which originate on the tibia or fibula, and 11 on the foot itself. For simplicity sake, the muscles of the leg

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Extrinsic Muscle Attachments and Innervation Proximal

Distal

Innervation

Gastrocnemius

Medial and lateral condyle of femur

Posterior surface of calcaneus through Achilles tendon

Tibial S2 (S1)

Plantaris

Lateral supracondylar line of femur

Posterior surface of calcaneus through Achilles tendon

Tibial S2 (S1)

Soleus

Head of fibula, proximal third of shaft, soleal line and midshaft of posterior tibia

Posterior surface of calcaneus through Achilles tendon

Tibial S2 (S1)

Tibialis anterior

Distal to lateral tibial condyle, proximal half of lateral tibial shaft, and interosseous membrane

First cuneiform bone, medial and plantar surfaces, and base of first metatarsal

Deep fibular (peroneal) L4 (L5)

Tibialis posterior

Posterior surface of tibia, proximal two-thirds posterior of fibula, and interosseous membrane

Tuberosity of navicular bone and tendinous expansion to other tarsals and metatarsals

Tibial L4 and L5

Fibularis (peroneus) longus

Lateral condyle of tibia, head, and proximal two-thirds of fibula

Base of first metatarsal and first cuneiform, lateral side

Superficial fibular (peroneal) L5 and S1 (S2)

Fibularis (peroneus) brevis

Distal two-thirds of lateral fibular shaft

Tuberosity of fifth metatarsal

Superficial fibular (peroneal) L5 and S1 (S2)

Fibularis (peroneus) tertius

Lateral slip from extensor digitorum longus

Tuberosity of fifth metatarsal

Deep fibular (peroneal) L5 and S1

Flexor hallucis longus

Posterior distal two-thirds fibula

Base of distal phalanx of great toe

Tibial S2 (S3)

Flexor digitorum longus

Middle three-fifths of posterior tibia

Base of distal phalanx of lateral four toes

Tibial S2 (S3)

Extensor hallucis longus

Middle half of anterior shaft of fibula

Base of distal phalanx of great toe

Deep fibular (peroneal) L5 and S1

Extensor digitorum longus

Lateral condyle of tibia proximal anterior surface of shaft of fibula

One tendon to each lateral four toes, to middle phalanx, and extending to distal phalanges

Deep fibular (peroneal) L5 and S1

and foot are divided into extrinsic muscles (those that originate at the tibia or fibula), and intrinsic (those that originate from the foot itself) muscles. The extrinsic muscles of the foot (Table 21-4) are further subdivided based on location into anterior, posterior superficial, posterior deep, and lateral compartments.

Anterior Compartment This compartment contains the dorsiflexors (extensors) of the foot. These include the tibialis anterior, fibularis tertius, EDL, and EHL (see Fig. 21-5).

CLINICAL PEARL Clinically, the loss of the ankle dorsiflexors is a common problem as a result of an isolated L4 nerve root compromise. The common sign of this weakness is a “foot slap” during gait which is evident by an accelerated plantar flexion of the ankle immediately following initial contact.11 The tibialis anterior muscle attachment, which is distal to the ankle joint on the plantar surface of the medial cuneiform

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Lower Leg, Ankle, and Foot

Muscle

ANATOMY

TABLE 21-4

and first metatarsal, indicates a role of this muscle at the subtalar joint and talonavicular joints. In addition to dorsiflexion of the foot, the tibialis anterior can produce a supination moment as its pull is medial to the subtalar joint, although its moment arm for supination is one-fifth the moment arm of the tibialis posterior muscle. The moment arm of the tibialis anterior muscle at the talonavicular joint is not well described but it is assumed to be a powerful dorsiflexor, and therefore, may play a role in forefoot control.11 The EDL balances the inversion component of the tibialis anterior to keep dorsiflexion in the sagittal plane, making it an open kinetic chain foot evertor. In addition, it powerfully extends the proximal phalanges of the four lateral toes and extends the middle and distal phalanges less intensely.25 The EHL functions to strongly extend the proximal phalanx of the great toe. In order to perform this function, the first dorsal interosseous muscle must synergistically fixate the proximal phalanx.25

Posterior Superficial Compartment This compartment, located posterior to the interosseous membrane, contains the calf muscles that plantar flex the

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ANATOMY

Biceps femoris m.

Vastus lateralis m. Iliotibial tract Patella Patellar ligament

THE EXTREMITIES

Head of fibula

and, according to electromyographic (EMG) studies, is the most active of the two while running. The soleus (Fig. 21-5), because it does not cross the knee joint, is subject to early disuse atrophy with undertraining and/or immobilization. Instead, the soleus muscle crosses only the ankle, specifically the talocrural joint and the talocalcaneal joint.25 It is enclosed between two layers of thick fascia, the aponeurosis of the Achilles tendon superficially, and a second layer deep to the soleus. Unusual in human muscle (most human skeletal muscle is estimated to be an even mix of slow and fast twitch fiber types), the soleus muscle is approximately 70% of the slow

Lateral tibial condyle

Gastrocnemius m. (lateral head) Fibularis longus m.

Tibialis anterior m.

Gastrocnemius m. (medial head)

Plantaris m.

Extensor digitorum longus m.

Soleus m.

Gastrocnemius m. (lateral head)

Biceps femoris m. Popliteus m.

Plantaris tendon Soleus m.

Extensor hallucis longus m.

Fibularis brevis m.

Extensor digitorum brevis m.

Lateral malleolus of fibula Achilles tendon

Fibularis tertius m. Fibularis brevis m.

Calcaneus bone

Fibularis longus m.

Flexor digitorum longus m. Flexor hallucis longus m.

Fibularis brevis m. Extensor digitorum longus m.

FIGURE 21-5  Lateral aspect of foot and ankle. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

foot. These include the gastrocnemius, soleus (see Fig. 21-5), and the plantaris muscle (Fig. 21-6). All three muscles converge to attach on to the Achilles tendon, which then inserts into the calcaneus.

Fibularis longus m.

Tibialis posterior m. Flexor digitorum longus m.

Calcaneus bone Fibularis brevis m. Fibularis longus m.

Flexor hallucis longus m.

Triceps Surae The triceps surae comprises the two heads of the gastrocnemius, which arise from the posterior aspects of the distal femur, and the soleus, which arises from the tibia and fibula, which combine to form the Achilles tendon. The medial head of the gastrocnemius is by far the largest component

FIGURE 21-6 Posterior superficial muscles. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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This compartment contains the flexors of the foot. These muscles course behind the medial malleolus. They include the tibialis posterior, FDL, and FHL (see Fig. 21-7). This group is thought to play a major role in supinating the subtalar joint.11

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Gastrocnemius m. (medial head)

Gastrocnemius m. (lateral head) Popliteus m. Biceps femoris m. Fibularis longus m.

Tibialis posterior m.

Flexor digitorum longus m.

Tibialis posterior m.

Flexor hallucis longus m.

Lower Leg, Ankle, and Foot

Deep Posterior Compartment

Plantaris m.

ANATOMY

twitch fiber type which would suggest the soleus is resistant to fatigue.11,26,27 In contrast, the gastrocnemius is approximately 54% fast twitch fiber type,27 which is more typical of human muscle.11 The gastrocnemius functions in closed kinetic chain activities to assist the other plantar flexors in controlling the forward sagittal plane rotation of the leg over the fixed foot during ambulation while also stabilizing the knee.25 By virtue of the calcaneocuboid joint, a plantar flexor moment is extended through the lateral two metatarsals.25 The large cross-sectional area of the soleus and gastrocnemius muscles, coupled with a large moment arm, make the triceps surae muscle capable of producing significant joint moments and powers at the ankle.11 The fibers from the gastrocnemius and soleus interweave and twist as they descend. There is an area of high stress 2–6 cm above the distal tendon insertion. A region of relative avascularity exists in the same area, which correlates well with the site of some Achilles tendon injuries, including complete spontaneous rupture. The plantaris muscle has its own tendon and contributes no fibers to the Achilles tendon. Achilles Tendon.  The Achilles tendon is the largest, thickest, and strongest tendon in the body.28 As the Achilles tendon comes from the posterior calf muscles, it courses distally to attach approximately three-quarters of an inch below the superior portion of the os calcis, on the medial aspect of the calcaneus. As the tendon fibers spiral 90 degrees instead of vertically, there is an increased potential for elongation and energy production. In fact, the tendon can stretch up to 4% before microscopic damage occurs; macroscopic rupture occurs at strain levels greater than 8%.29 Two bursae occur at the point of insertion of the Achilles tendon into the calcaneus. The retrocalcaneal bursa lies deep into the tendon, adjacent to the calcaneus. The superficial bursa of the tendo Achilles lies superficial to the distal portion of the tendon, between the tendon itself and the subcutaneous tissues but is not visible unless it is pathologically inflamed. Deeper to the Achilles tendon is the pre-Achilles fat pad, a triangular area of adipose tissue, also known as Kager’s triangle. Further anterior to this fat pad are the deep flexor tendons of the calf, predominantly the FHL, which overlies the posterior tibia and the talus. There is no synovial sheath surrounding the Achilles tendon. The peritendon covers the endotendon and is composed of a thin sheath, called the epitenon, and another fine outer sheath, the peritenon, composed of fatty areola tissue, which fills the interstices of the fascial compartment in which the tendon is situated. The peritenon is able to stretch 2–3 cm with tendon movement, which allows the Achilles tendon to glide smoothly. The plantar flexion moment arm of the Achilles tendon is approximately 4 cm and varies little across the full range of plantar flexion and dorsiflexion.30 This moment arm suggests a significant mechanical advantage in plantar flexing the calcaneus.11

Gastrocnemius and soleus mm.

Fibularis brevis m. Tibialis anterior m. Flexor hallucis longus m.

Flexor digitorum longus mm.

FIGURE 21-7  Posterior deep muscle compartment. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

The tibialis posterior muscle is arguably one of the most important determinants of optimal foot and ankle function as it is a key stabilizer of the leg, ankle, and foot. It originates from the posterior lateral surface of the tibia, medial two-thirds of the posterior fibula, interosseous membrane, intermuscular septa, and fascia. The myotendinous junction appears in the distal one-third of the leg from which it courses posteriorly to the medial malleolus in a separate fibroosseous groove and is held in place by the lancinate ligament (flexor retinaculum).31 The tendon of the tibialis posterior then courses posterior to the medial malleolus, thereby passing posterior to the axis of the talocalcaneal (tibiotalar) joint and medial to the subtalar joint.

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ANATOMY

As the tendon nears its insertion on the navicular tuberosity, it divides into three slips31:

THE EXTREMITIES

Anterior. The anterior slip is the largest of the three, is in direct continuation with the proximal tendon, and inserts on the navicular tuberosity. ▶▶ Middle. The middle slip continues distally as a tarsometatarsal extension and inserts on the plantar aspects of the intermediate and lateral cuneiforms, and the bases of metatarsals 2, 3, and 4. The middle slip also attaches on the plantar cuboid, covering the fibular canal through which the fibularis longus courses. The middle slip also serves as an origin for the Y-shaped FHB. ▶▶ Posterior. The posterior slip is recurrent and arises from the main tendon. It is oriented posteriorly and laterally, and inserts on the anterior portion of the sustentaculum tali. ▶▶

CLINICAL PEARL The tibialis posterior tendon is unique in the fact that it lacks a complete mesotenon and must receive its vascular supply through other channels, namely the posterior tibial artery, and the periosteum. The tibialis posterior is innervated by the tibial nerve, arising from the fifth lumbar and first sacral nerve roots.

CLINICAL PEARL In the open kinetic chain, the tibialis posterior functions to invert the subtalar and ankle joints, adduct the forefoot, and plantar flex the foot and ankle. As the tendon is located farthest medially from the axis of the subtalar joint, it creates a moment arm that allows the tendon to have a great degree of inversion force.31

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The primary function of the tibialis posterior muscle is to invert, adduct, and plantar flex the foot. It also provides support to the medial longitudinal arch. The tibialis posterior muscle at the subtalar joint has a moment arm that is 2.5–5 times larger than the other deep compartment muscles, which would tend to suggest that it is the dominant supinator of the subtalar joint.32 Because of the significant mechanical advantage, the tibialis posterior muscle has the potential to both strictly control hindfoot movement and influence the medial longitudinal arch by inverting the subtalar joint.11 The primary antagonist of the tibialis posterior muscle is the fibularis brevis muscle, although the former is more than two times stronger.31 The FDL originates from the posterior surface of the body of the tibia, medial to the tibial origin of the tibialis posterior. The tendon then passes behind the medial malleolus in a groove together with the tibialis posterior, but separated from the latter by a fibrous septum. It then travels superficial to the deltoid ligament of the ankle in an anterolateral direction into the sole of the foot, where it crosses inferior to the tendon of the FHL. It finally divides into four tendons, which insert into the bases of the last phalanges of the second, third, fourth,

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and fifth toes, as they each pass through an opening in the corresponding tendon of the FDB opposite the base of the first phalanx. The FDL functions to flex the phalanges of the lateral four toes and assists with plantar flexion of the foot.

CLINICAL PEARL The FHL and FDL tendons cross each other at a point called the Master Knot of Henry (approximately one thumb breadth lateral to the navicular tuberosity), a fibrous slip that envelops the FHL and FDL tendons. The Master Knot of Henry has several intertendinous connections and is often a source of pain.33 The FHL tendon courses distally from the posterior border of the fibula and interosseous membrane before traveling through a retinacular structure posterior to the ankle and subtalar joints. It continues between the medial and lateral tubercles of the talus to the sustentaculum tali. Distal to the sustentaculum tali, the FHL crossed dorsal to the FDL to the intersesamoidal ligament through a fibro-osseous tunnel, ultimately inserting on the distal phalanx of the hallux. The FHL flexes the great toe and also assists with plantar flexion of the foot.33

CLINICAL PEARL The deep posterior compartment muscles likely interact with the foot intrinsic muscles to control the raising and lowering of the medial longitudinal arch and plantar flex the forefoot and toes.11

Lateral Compartment The lateral compartment of the lower leg is innervated by the superficial fibular nerve (L4–S1). This compartment contains the fibularis (peroneus) longus and brevis (see Fig. 21-5). The fibular (peroneal) tendons lie behind the lateral malleolus in a fibro-osseous tunnel formed by a groove in the fibula and the superficial fibular (peroneal) retinaculum. The fibular (peroneal) retinaculum and the posterior CFL form the posterior wall of this tunnel. Distal to the lateral malleolus, the fibularis longus tendon sheath bifurcates around the fibular tubercle and through the inferior fibularis retinaculum. The os paronychium which is ossified in approximately 20% of individuals is located within the substance of the fibularis (peroneus) longus tendon at the level of the calcaneocuboid joint.34 The fibularis (peroneus) longus tendon, which forms a sling around the lateral and plantar aspects of the cuboid before inserting on the plantar aspect of the lateral first metatarsal base and medial cuneiform assist with calcaneocuboid joint stabilization.35 The fibularis (peroneal) muscles serve as both plantar flexors and evertors of the foot, although the fibularis (peroneus) longus produces about 1/10 the plantarflexor force and the gastrocnemius, and the fibularis brevis exerts half of the fibularis (peroneus) longus. The fibularis (peroneus) brevis also abducts the forefoot in the transverse plane, thereby serving as a support for the medial longitudinal arch. The fibularis muscles are known to pronate the

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CLINICAL PEARL

TABLE 21-5

Beneath the plantar aponeurosis–plantar fascia are the four muscular layers of the intrinsic muscles of the anterior (plantar) foot (Table 21-5), as well as the plantar ligaments of the rearand midfoot. The intrinsic muscles provide support to the foot during propulsion. Specifically, these muscles are synergists for proximal IP joint flexion (second-fifth digits), MTP joint flexion (first-fifth digits), and adduction and abduction of the MTP joints.11 In addition, this muscle group also plays an important function in arch support and propulsion during walking and running.36 The foot intrinsic muscles are

Intrinsic Muscles of the Foot

Muscle

Proximal

Distal

Innervation

Extensor digitorum brevis

Distal superior surface of calcaneus

Posterior (dorsal) surface of second through fourth toes and base of proximal phalanx

Deep fibular (peroneal) S1 and S2

Flexor hallucis brevis

Plantar surface of cuboid and third cuneiform bones

Base of proximal phalanx of great Medial plantar L4, 5 toe

Flexor digitorum brevis

Tuberosity of calcaneus

One tendon slip into base of Medial and lateral plantar L4–S2 middle phalanx of each of the lateral four toes

Extensor hallucis brevis

Distal superior and lateral surfaces of calcaneus Posterior (dorsal) surface of proximal phalanx

Lower Leg, Ankle, and Foot

The fibularis (peroneal) muscles have an important role in the rehabilitation of lateral ankle injuries because of the moment arms of these muscles toward pronation at the subtalar joint.11

INTRINSIC MUSCLES OF THE FOOT

ANATOMY

subtalar joint. The fibularis (peroneus) longus muscle is also a plantarflexor of the first metatarsal through its attachment to the base of the first metatarsal and medial cuneiform bones. The fibularis (peroneus) longus is counterbalanced by the tibialis posterior to stabilize the midtarsal joint.6

Deep fibular (peroneal) S1 and S2

Abductor hallucis Tuberosity of calcaneus and plantar aponeurosis

Base of proximal phalanx and medial side

Medial plantar L4, 5

Adductor hallucis Base of second, third, and fourth metatarsals and deep plantar ligaments

Proximal phalanx of first digit lateral side

Medial and lateral plantar L4–S2

Lumbricals

Medial and adjacent sides of flexor digitorum longus tendon to each lateral digit

Medial side of proximal phalanx and extensor hood

Medial and lateral plantar L4–S2

First

Base and medial side of third metatarsal

Base of proximal phalanx and extensor hood of third digit

 

Second

Base and medial side of fourth metatarsal

Base of proximal phalanx and extensor hood of fourth digit

Medial and lateral plantar L4–S2

Third

Base and medial side of fifth metatarsal

Base of proximal phalanx and extensor hood of fifth digit

 

Plantar interossei

Posterior (dorsal) interossei First

First and second metatarsal bones

Proximal phalanx and extensor   hood of second digit medially

Second

Second and third metatarsal bones

Proximal phalanx and extensor hood of second digit laterally

Medial and lateral plantar L4–S2

Third

Third and fourth metatarsal bones

Proximal phalanx and extensor hood of third digit laterally

 

Fourth

Fourth and fifth metatarsal bones

Proximal phalanx and extensor hood of fourth digit laterally

 

Abductor digiti minimi

Lateral side of fifth metatarsal bone

Proximal phalanx of fifth digit

Lateral plantar S1 and S2

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ANATOMY

typically described based on their anatomical position using a series of layers.

First Layer The first layer is the most anterior and superficial (plantar) and consists of the following: Abductor hallucis (Fig. 21-8).  This muscle arises from the medial process of the calcaneal tuberosity and inserts on the medial side of the base of the proximal phalanx of the great toe. It functions to flex and/or abduct the proximal phalanx of the great toe (depending on its variable anatomical insertion),37 and also helps to control pronation at the midtarsal joint. ▶▶ Abductor digiti minimi (see Fig. 21-8).  This muscle arises from the lateral process of the calcaneal tuberosity as well as the plantar aponeurosis and inserts into the lateral side of the base of the proximal phalanx of the little toe. ▶▶ Flexor digitorum brevis (see Fig. 21-8).  This muscle arises from the medial process of the calcaneal tuberosity, lateral to the abductor hallucis and deep into the central portion of the plantar fascia, and inserts into the middle phalanx of the lateral four toes. It functions to flex only the middle phalanx of the lateral four toes. ▶▶

THE EXTREMITIES

on the medial and lateral side of the proximal phalanx of the great toe. ▶▶ Flexor digiti minimi (see Fig. 21-8).  This muscle arises from the sheath of the fibularis (peroneus) longus, the base of the fifth metatarsal bone, and inserts into the lateral side of the base of the proximal phalanx of the little toe. ▶▶ Adductor hallucis (see Fig. 21-8).  This muscle arises via two heads: an oblique and a transverse head. The oblique head arises from the bases of the second, third, and fourth metatarsal bones and the sheath of the fibularis (peroneus) longus. The transverse head arises from the joint capsules of the second, third, fourth, and fifth MTP heads and the deep transverse metatarsal ligament. The adductor hallucis inserts on the lateral side of the base of the proximal phalanx of the great toe.

Fourth Layer ▶▶

Posterior (dorsal) interossei.  The four posterior (dorsal) interossei are bipennate, and they arise from adjacent sides of the metatarsal bones. The first inserts into the medial side of the proximal phalanx of the second toe. The second inserts into the lateral side of the proximal phalanx of the second toe. The third inserts into the lateral side of the proximal phalanx of the third toe, and the fourth inserts into the lateral side of the proximal phalanx of the fourth toe. The posterior (dorsal) interossei function to abduct the second, third, and fourth toes from an axis through the second metatarsal ray.

▶▶

Anterior (plantar) interossei (Fig. 21-8).  The three anterior (plantar) interossei are unipennate and arise from the bases and medial sides of the third, fourth, and fifth metatarsal bones. They insert into the medial sides of the bases of the proximal phalanges of the third, fourth, and fifth toes. The anterior (plantar) interossei function to adduct the lateral three toes.

Second Layer Flexor digitorum accessorius (quadratus plantae; Fig. 21-8).  This muscle arises from the calcaneal tuberosity via two heads. The medial head arises from the medial surface of the calcaneus and the medial border of the long plantar ligament, whereas the lateral head arises from the lateral border of the anterior (plantar) surface of the calcaneus and the lateral border of the long plantar ligament. The muscle terminates in tendinous slips, joining the long flexor tendons to the second, third, fourth, and occasionally fifth toes. ▶▶ Lumbricales.  There are four lumbricales (see Fig. 21-8), all of which arise from the tendon of the FDL. The first arises from the medial side of the tendon of the second toe, the second from adjacent sides of the tendons for the second and third toes, the third from adjacent sides of the tendons for the third and fourth toes, and the fourth from adjacent sides of tendons for the fourth and fifth toes. They insert with the tendons of the EDL and interossei into the bases of the terminal phalanges of the four lateral toes. The function of the lumbricales is to flex the MTP joint and extend the proximal IP (PIP) joint. ▶▶

Third Layer ▶▶

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Flexor hallucis brevis (Fig. 21-8).  This muscle arises from the medial part of the anterior (plantar) surface of the cuboid bone, the adjacent portion of the lateral cuneiform, and the posterior tibialis tendon and inserts

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Posterior (Dorsal) Intrinsic Muscle The posterior (dorsal) intrinsic muscles of the foot are the extensor hallucis brevis (EHB) and extensor digitorum brevis (EDB). The EHB inserts into the base of the proximal phalanx of the great toe, whereas the EDB inserts into the base of the second, third, and fourth proximal phalanges. Both of these muscles are innervated by the lateral terminal branch of the deep fibular (peroneal) nerve.

ARCHES OF THE FOOT The arches of the foot support the foot by three mechanisms38: The osseous relationship of the tarsal and metatarsal bones. ▶▶ Ligamentous support from the plantar aponeurosis and anterior (plantar) ligaments. ▶▶

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ANATOMY

Flexor digitorum brevis tendons (cut)

Lumbrical mm.

Flexor hallucis brevis mm.

Flexor hallucis longus tendon Lumbrical mm. Flex or digitorum longus tendon

Lateral plantar n., a., and v.

Medial plantar a., v., and n.

Lateral plantar n., a., and v.

Abductor digiti minimi m.

Flexor digitorum brevis m.

Flexor digiti minimi brevis m.

Abductor hallucis m.

Medial plantar a., v., and n. Abductor hallucis m. (cut)

Quadratus plantae m.

Posterior tibial n., a., and v. Flexor digitorum brevis m. (cut)

Calcaneus

A

Lower Leg, Ankle, and Foot

Flexor hallucis longus tendon

B

Proper plantar digital nn. and aa. Common plantar digital nn. Plantar metatarsal aa. Flexor digiti minimi brevis m. Deep plantar arterial arch

Lateral plantar n., a., and v.

Adductor hallucis m. Flexor hallucis brevis m.

Abductor hallucis m. (cut)

Plantar interossei mm.

Dorsal interossei mm.

Fibularis longus tendon

Medial plantar n., a., and v.

Tibialis posterior tendon

Long plantar ligament

Plantar calcaneonavicular (spring) ligament

C

D

FIGURE 21-8  Intrinsic muscles of the foot. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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ANATOMY

▶▶

Muscle support. There are three main arches: the medial longitudinal, the lateral longitudinal, and the transverse arches.

The Medial Longitudinal Arch

THE EXTREMITIES

The medial longitudinal arch plays an important role in foot function during weight-bearing activities. The arch comprises the calcaneus, talus, navicular, three cuneiforms, and the three medial metatarsals (including the two sesamoids). Although some of the integrity of the arch depends on the bony architecture, support is also provided by the ligaments and muscles, including the anterior (plantar) calcaneonavicular (spring) ligament, the plantar fascia, the tibialis posterior, fibularis (peroneus) longus, FDL, FHL, and fibularis (peroneus) longus. The soleus and gastrocnemius muscle group has also been noted to have an effect on the arch and can flatten it with adaptive shortening. Not only is the arch a major source of frontal plane motion of the foot, but it also is a major load-bearing structure. Analysis of the medial longitudinal arch has long been used by clinicians to make determinations about foot abnormalities, with a high arch indicating a supinated foot and a low or collapsed arch being associated with a pronated or flatfoot, respectively.39 Biomechanical models have suggested that damage to the plantar fascia results in lowering of the medial longitudinal arch and increased load on associated ligaments.11,40 In addition, studies have found a higher incidence of stress fractures, plantar heel pain, metatarsalgia, and lower extremity injuries, including knee strains and iliotibial band syndrome, in individuals with high arches, compared with those who have low arches. The role of muscle in controlling the medial longitudinal arches of the foot is controversial. A number of studies have shown that the foot intrinsic and extrinsic muscles, including the tibialis posterior and the Achilles tendon, are very active during gait and standing.41–43 However, muscle control alone is insufficient to balance the forces experienced during high demand tasks, so it is likely that a combination of passive and active mechanisms underlie control of the medial longitudinal arch.11

The Lateral Longitudinal Arch The lateral longitudinal arch, which is more stable and less mobile than the medial longitudinal arch, consists of the calcaneus, cuboid, and fourth and fifth metatarsals. The superior and deep longitudinal plantar ligament supports the calcaneocuboid and cubometatarsal joints, together with the fibularis (peroneus) brevis, longus, and tertius, and the abductor digiti minimi and FDB muscles.

The Transverse Arch

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The transverse arch forms the convexity of the posterior aspect of the foot and consists of metatarsal heads one through five, including the sesamoids (arch I); cuneiforms one through three and the cuboid (arch II); and the navicular and cuboid

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(arch III). The adductor hallucis, fibularis (peroneus) longus, posterior tibialis, and anterior tibialis all add dynamic support to this arch.

NAIL PLATE The nail plate is composed of keratinized squamous cells, bordered by proximal and lateral nail folds.44 The hyponychium lies between the distal portion of the nail bed and the distal nail fold and marks the transition to normal toe epidermis.44 Fingernail plates grow on average at a rate of 3 mm per month, and toenail plates grow at one-half to onethird that rate.44

NEUROLOGY The saphenous nerve, the largest cutaneous branch of the femoral nerve, provides cutaneous distribution to the medial aspect of the foot. Branches of the sciatic nerve provide the sensory and motor innervation of the foot and leg (see Chapter 3). The branches are the common fibular (peroneal) and tibial nerves. The common fibular (peroneal) nerve, in turn, divides into the superficial fibular (peroneal) and deep fibular (peroneal) nerves (Fig. 21-9). The tibial nerve divides into the sural, medial calcaneal, medial anterior (plantar), and lateral anterior (plantar) nerves.44

VASCULAR SUPPLY Two branches of the popliteal artery (see Chapter 20), the anterior tibial artery and the posterior tibial artery, form the main blood supply to the foot (Fig. 21-9).

Anterior Tibial Artery The anterior tibial artery supplies the anterior compartment of the leg and enters the posterior aspect of the foot under the superior and inferior retinacula as the posterior (dorsal) pedis artery. The posterior (dorsal) pedis artery gives rise to the arcuate artery and the first posterior (dorsal) and anterior (plantar) metatarsal artery, which serve the posterior aspect of the foot and the digits.

Posterior Tibial Artery The posterior tibial artery, which supplies the posterior and lateral compartments and 75% of the blood to the foot, enters the foot after traveling around the medial malleoli. At this point, the artery divides into the medial and lateral anterior (plantar) arteries, which serve the anterior (plantar) aspect of the foot. A main branch of the posterior tibial artery, the fibular (peroneal) artery, supplies the lateral compartment as well as many hindfoot structures.

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ANATOMY

Deep peroneal n. Superficial peroneal n.

Extensor retinaculum Deep branch

Superficial branch

Lateral plantar n., a., and v.

Extensor digitorum brevis m. Medial plantar n., a., and v. Tibial n. Posterior tibial a.

Deep peroneal n. Dorsal pedis a.

Lower Leg, Ankle, and Foot

Anterior tibial a.

Cutaneous branches of superficial fibular n.

Medial calcaneal n.

A

Lateral plantar n.

Sural n.

Tibial n.

Cutaneous branches of deep fibular n.

B

Medial plantar n.

Saphenous n.

Superficial fibular n.

Saphenous n.

Sural n. Deep fibular n.

FIGURE 21-9  Neurovascular supply of the ankle and foot. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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BIOMECHANICS

BIOMECHANICS Terminology Motions of the leg, foot, and ankle consist of single- and multiplane movements. The single-plane motions include the following:

THE EXTREMITIES

The frontal plane motions of inversion and eversion.  Eversion is a frontal plane motion of the talonavicular joint about an A-P axis, in which the medial aspect of the sole of the foot moves in an anterior (plantar) direction (Fig. 21-10). Inversion is a frontal plane motion of the foot about an A-P axis, in which the lateral aspect of the sole of the foot moves in an anterior (plantar) direction (Fig. 21-10). ▶▶ The sagittal plane motions of dorsiflexion and plantar flexion.  These movements at the subtalar, talonavicular, and forefoot joints occur in the sagittal plane about an M-L axis. Plantar flexion is a movement of the foot downward toward the ground, and dorsiflexion is a movement of the foot upward toward the tibia. ▶▶ The horizontal plane motions of adduction and abduction.  These motions of the talonavicular joint and forefoot occur in the transverse plane about a superoinferior axis. Abduction moves the forefoot laterally, whereas adduction moves the forefoot medially. ▶▶

The axes of rotation of each component joint of the anklefoot complex provides for movement in all three cardinal planes, a phenomenon called triplanar movement—a movement about an obliquely oriented axis through all three body planes.1 Triplanar motions occur at the talocrural, subtalar, and transverse tarsal joints and at the first and fifth rays. Pronation and supination are examples of triplanar motions. The three body plane motions in pronation are abduction in the transverse plane, dorsiflexion in the sagittal plane, and eversion in the frontal plane (Fig. 21-11). The three body plane motions in supination are adduction in the transverse plane, plantar flexion in the sagittal plane, and inversion in the frontal plane (Fig. 21-12). In pronation, the forefoot is rotated in such a manner so that the big toe moves downward, and little toe moves upward, whereas in supination, the reverse occurs.

CLINICAL PEARL Terms that describe movement of the foot and ankle typically end in the suffix “-ion” whereas terms ending in the suffixes “-ed,” “-us,” and “-um” commonly refer to positions of the foot and ankle.1 For example, “forefoot adduction” is the movement of the forefoot toward the midline about a superoinferior axis of rotation, while “forefoot adductus” is the static position of the foot in an adducted position.

Distal Tibiofibular Joint Although the two tibiofibular joints (proximal and distal) are described as individual articulations, they function as a pair. The movements that occur at these joints are primarily a result of the ankle’s influence. ▶▶

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Supination of the foot produces a distal and posterior glide of the head of the fibula.

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Pronation produces a proximal and anterior glide with an external rotation of the fibula. ▶▶ Plantar flexion of the foot produces a distal glide with a slight medial rotation of the fibula. ▶▶ Dorsiflexion of the ankle yields a proximal glide. The fibula rotates externally around its longitudinal axis. ▶▶

During these movements, however, it is the tibia that performs the greatest amount of movement, as it rotates around the fibula. This is probably a consequence of more body weight falling through the larger bone. During ipsilateral rotation, both the tibia and the fibula rotate laterally, but in relative terms, the tibia moves more laterally than the fibula, causing a relative anterior and superior glide of the fibular head on the tibia at the superior joint. During contralateral rotation, the tibia rotates more medially, producing a relative posterior and inferior fibular glide at the joint. The ligaments of the distal tibiofibular joint are more commonly injured than the ATFL. Injuries to the ankle syndesmosis most often occur as a result of forced external rotation of the foot or during internal rotation of the tibia on a planted foot.45 Hyperdorsiflexion may also be a contributing mechanism. The capsular pattern of this joint is likely pain with weightbearing dorsiflexion of the ankle, as this produces the greatest ligamentous tension (Table 21-1). For the same reason, the close-packed position is considered as weight-bearing dorsiflexion of the ankle.

CLINICAL PEARL Because of the interaction between the proximal and distal tibiofibular joints with the knee and the ankle function, the clinician should always assess the functional mobility of both these complexes when treating one or the other.   An abnormal position of the fibula (anterior or posterior relative to the tibia) at the distal tibiofibular joint has been reported to contribute to abnormal muscle function in patients after an ankle sprain.46,47

Talocrural Joint The talocrural, or tibiotalar, joint is classified as a synovial hinge or modified sellar joint. There is general agreement that motion between the tibia and the foot is a complex combination of talocrural and subtalar joint motion, which is limited by the shape of the articulations and soft-tissue interaction. Stability for this joint in weight-bearing is provided by the articular surfaces, while in non–weight-bearing, the ligaments appear to provide the majority of stability. Talocrural joint motion occurs around a functional axis that is obliquely oriented in both the frontal and transverse planes. The talocrural joint axis, which is rotated posteriorly by 6 degrees, has a tilt of approximately 10 degrees from horizontal in the frontal plane (i.e., superomedial to inferolateral) and it has an 18–20 degrees of obliquity in the transverse plane (i.e., anteromedial to posterolateral).48 The orientation of the talocrural joint axis can be roughly estimated clinically as a line that passes inferiorly from the medial malleolus to the lateral malleolus, with the adult distal leg being oriented vertically.48 The angle of inclination provides for the majority

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Interosseous membrane

Anterior muscular septum

Deep fibular n. (anterior tibial a. and v.) Tibia

Superficial fibular n.

Iliotibial tract Vastus medialis m.

Lateral compartment

Posterior intermuscular septum

Patella

Patellar ligament

Fibular a. and v. Transverse intermuscular septum

Tibial tuberosity

Posterior compartment (superficial part) Posterior compartment (deep part)

Deep fascia of leg

Pes anserinus (common insertion of sartorius, gracilis, and semitendinosus mm.)

Gastrocnemius m. (medial head)

A

Fibularis longus m.

Lower Leg, Ankle, and Foot

Tibial n. (posterior tibial a. and v.)

Fibula

BIOMECHANICS

Anterior compartment

Tibialis anterior m. Soleus m.

Tibia

Dorsiflexion

Extensor digitorum longus m. Plantar flexion

Extensor hallucis longus m. Medial malleolus

Fibularis tertius m.

Extensor hallucis brevis m. Interossei mm.

Eversion

B

Inversion

Extensor digitorum longus m.

C

Extensor hallucis longus m.

FIGURE 21-10  Ankle motions and related musculature. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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BIOMECHANICS

Theoretically, the capsular pattern of the ankle joint is more restriction of plantar flexion than dorsiflexion, although clinically this appears to be reversed (Table 21-1). The close-packed position is weight-bearing dorsiflexion, whereas the openpacked position is midway between supination and pronation.

CLINICAL PEARL

THE EXTREMITIES

The major contributors to stability of the ankle joint are the osseous congruency and fit of the articular surfaces when the joints are loaded, static ligamentous (anterior talofibular ligament, and CFL) and capsular restraints, and the surrounding musculotendinous units.50 FIGURE 21-11  Pronation in non–weight-bearing.

of talocrural motion to occur in the sagittal plane during plantar flexion and dorsiflexion (Fig. 21-10), although some motion also occurs in the frontal and transverse planes, particularly during plantar flexion.11 According to an MRI study49 that recorded ROM during non–weight-bearing movements, the reported range of plantar flexion was 41 degrees, dorsiflexion 16 degrees, abduction 5 degrees, adduction 14 degrees, eversion 7 degrees and inversion 3 degrees. The joint translations that occurred averaged 4 mm anterior for plantar flexion and 1 mm posterior for dorsiflexion.49 The maximum amount of dorsiflexion necessary at the talocrural joint during human gait is approximately 10 degrees of the normally available 20 degrees, and occurs during the stance phase, just prior to when the heel begins to rise. The trochlea of the saddle-shaped talus is wider anteriorly than posteriorly resulting in a tighter fit between the talus and ankle mortise when the ankle is in dorsiflexion. Due to this fit of the talus within the mortise, the talus is able to produce a slight separation of the tibial and fibula malleoli during the extremes of dorsiflexion and plantar flexion. In addition, because of this fit, the tibia follows the talus during weightbearing so that the talocrural joint externally rotates with supination and internally rotates with pronation. Conversely, the tibia internally rotates during pronation and externally rotates during supination. Passive stability to this joint is also provided from its lateral and medial collateral ligaments.

Subtalar Joint The axis of motion for the subtalar (talocalcaneal) joint, which is approximately 42 degrees from horizontal in the sagittal plane, and 16 degrees medial to the midsagittal plane referencing the anterior side of the joint.51,52 The subtalar joint axis of rotation creates a dominant frontal plane movement (i.e., inversion and eversion), with secondary movements available in the transverse and sagittal planes. This configuration allows the subtalar joint, together with the talocrural joint, to produce the triplanar motions of pronation/ supination, a motion that has been compared to a ship on the sea or an oblique mitered hinge. The various components of the triplanar motion at this joint vary according to whether the joint is weight-bearing or non–weight-bearing. During weight-bearing (closed-chain) activities, pronation involves a combination of calcaneal eversion (frontal plane motion), adduction (transverse plane motion), and plantar flexion (sagittal plane motion) of the talus and internal rotation of the tibia. These movements result in a lowering of the medial longitudinal arch. Closed-chain supination involves a combination of calcaneal inversion, abduction and dorsiflexion of the talus and external rotation of the tibia. These movements result in an elevation of the medial longitudinal arch. ▶▶ During non–weight-bearing (open chain) activities, pronation involves a combination of calcaneal eversion and abduction and dorsiflexion of the talus (see Fig. 21-11), whereas supination involves a combination of calcaneal inversion and adduction and plantar flexion of the talus (see Fig. 21-12). ▶▶

CLINICAL PEARL

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FIGURE 21-12  Supination in non–weight-bearing.

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Although the terms pronation and eversion are both widely used to refer to externally directly rotation of the foot segment around the functional axis of the subtalar joint, the term eversion is typically used in the context of an ankle ligament injury mechanism that involves outward displacement of the sole of the foot.53 Similarly, the term supination and inversion are both widely used to refer to internally directed rotation of the foot segment around the functional axis of the subtalar joint, but the term inversion is almost exclusively used to describe the inward displacement of the sole of the foot that produces a lateral ankle ligament injury.

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Mathematically, the STJN position is that angle at which the ratio of calcaneal inversion to eversion is approximately 2:1. Stability of the subtalar joint is provided by the CFL, the cervical ligament, the interosseous ligament, the LTCL, the fibulotalocalcaneal ligament (ligament of Rouviere), and the extensor retinaculum. The capsular pattern of this joint varies. In chronic arthritic conditions, there is an increasing limitation of inversion, but with traumatic arthritis, eversion appears most limited clinically. The close-packed position for this joint is maximum inversion, whereas the open-packed position is inversion/ plantar flexion (Table 21-1).

Transverse Joint Complex The function of the transverse tarsal joint complex (talonavicular, and calcaneocuboid joints) is to provide the foot with an additional mechanism for raising and lowering the arch and to absorb some of the horizontal plane tibial motion that is transmitted to the foot during stance. The calcaneocuboid joint is a plane synovial joint whereas the talonavicular joint is a synovial pivot joint.11

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When combined, motions around the two axes of the transverse tarsal joint complex which are limited by the plantar calcaneocuboid ligament (short plantar ligament), long plantar ligament, plantar calcaneonavicular ligament (spring ligament), bifurcate ligament, and the plantar aponeurosis, involve38:

Lower Leg, Ankle, and Foot

CLINICAL PEARL

Calcaneocuboid joint. The joint axes of rotation for the calcaneocuboid joint are inclined 52 degrees superior and 57 degrees medial, referencing the anterior side of the joint.1 This orientation yields a dominant transverse plane movement (i.e., abduction and adduction), with sagittal and frontal plane movements also available. The principal movement about the sagittal axis is internal/external rotation with the calcaneus process acting as a pivot. This rotational movement has been described as pronation/ supination, but inversion/eversion is used herein. The cuboid, which acts as a pulley for the fibularis (peroneus) longus tendon during gait, rotates as much as 25 degrees during inversion/eversion. ▶▶ Talonavicular joint. The joint axes of rotation of the talonavicular joint are inclined superior 15 degrees and medial 9 degrees, referencing the anterior side of the joint.1 This orientation creates a dominant frontal plane movement for the talonavicular joint (i.e., inversion and eversion), with a minor amount of transverse plane and sagittal plane movements available. ▶▶

BIOMECHANICS

The subtalar joint controls supination and pronation in close conjunction with the transverse tarsal joints of the midfoot. Subtalar joint supination and pronation are measured clinically by the amount of calcaneal or hindfoot inversion and eversion. In normal individuals, there is an inversion to eversion ratio of 2:3 to 1:3, which amounts to an average of approximately 20 degrees of inversion and 10 degrees of eversion. It is important to remember that variability of ROM across individuals is common when attempting to restore function to the subtalar joint.11 For normal gait, a minimum of 4–6 degrees of eversion and 8–12 degrees of inversion are required. During normal gait, the foot needs to pronate and supinate 6–8 degrees from the neutral position. If the foot pronates excessively, a compensatory internal rotation of the tibia may occur. This produces an increased amount of rotatory stress and dynamic abduction moment at the knee, which has to be absorbed through the peripatellar soft tissues at the knee joint. These stresses can force the patella to displace laterally and may result in patellofemoral dysfunction.2,54 In addition, a change in the position of the talus can affect the functional leg length. Subtalar supination may cause the leg to lengthen while subtalar pronation shortens the leg. Thus, the midposition of the subtalar joint, subtalar joint neutral (STJN), is considered the range at which the subtalar joint should act to prevent dysfunction. The STJN position is actually a measurement of the angle between a line that bisects the distal third of the lower leg and a line that bisects the calcaneus. The bisection of the calcaneus represents the position of the anterior (plantar) condyles because the calcaneus is almost perpendicular to the condyles. The angle between the bisections should be 0 degrees in the normal foot but is actually 2–3 degrees of varus (inverted in most subjects).

a rotational motion about a longitudinal axis into adduction/inversion and abduction/eversion,11 which can be observed in the elevation and depression of the medial arch of the foot during the stance phase of gait. Movements of the transverse tarsal joint complex into adduction and inversion result in less movement of the foot in the sagittal plane as the bones of the foot transform into a rigid lever. In contrast, movements of abduction and eversion result in greater movement of the foot in the sagittal plane as the foot transforms into a flexible lever. ▶▶ an oblique axis, producing the near sagittal motions of forefoot dorsiflexion and forefoot plantar flexion.11 ▶▶

Both axes are dependent on the position of the subtalar joint. When the subtalar joint is pronated, the two sets of axes are parallel to one another, allowing for the maximum amount of motion at the transverse tarsal joint complex. When the subtalar joint is supinated, the two sets of axes are in opposition, allowing only little motion to occur, thereby enhancing stability. This connection between supination and foot rigidity and pronation and foot flexibility has clinical significance. For example, patients with feet that are unable to pronate sufficiently may have syndromes associated with the inability to absorb impact forces whereas, patients with feet that are able to supinate sufficiently, may have syndromes associated with soft-tissue loading (i.e., tendon or ligament problems).11,55 During gait, the transverse tarsal joint complex has following two functions38: To permit adaptation of the foot to uneven terrain in the early stance. ▶▶ To provide a stable foot during terminal stance. ▶▶

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EXAMINATION

Theoretically, as a modified ovoid, the joint complex can sublux into dorsiflexion/plantar flexion, abduction/ adduction, with or without rotation. In practice, the most commonly found subluxations may be considered as inversion/ dorsiflexion or eversion/plantar flexion lesions. The capsular pattern of the transverse tarsal joint complex is a limitation of dorsiflexion, plantar flexion, adduction, and internal rotation (Table 21-1). The close-packed position for the transverse tarsal joint complex is supination (Table 21-1). The open-packed position is midway between the extremes of ROM.

THE EXTREMITIES

Cuneonavicular Joint The cuneonavicular joint has 1–2 degrees of freedom: plantar flexion/dorsiflexion, inversion/eversion. The capsular pattern of this joint is a limitation of dorsiflexion, plantar flexion, adduction, and internal rotation. The close-packed position is supination. The open-packed position is considered to be midway between the extremes of ROM (Table 21-1).

Intercuneiform and Cuneocuboid Joints Due to their very plane curvature, these joints have only 1 degree of freedom: inversion/eversion. The close-packed position for these joints is supination. The open-packed position is considered to be midway between the extremes of ROM (Table 21-1).

Cubometatarsal Joint The capsular pattern of this joint is a limitation of dorsiflexion, plantar flexion, adduction, and internal rotation. The close-packed position is pronation. The open-packed position is considered to be midway between the extremes of ROM (Table 21-1).

first MTP joint varies between 5 degrees varus and 15 degrees valgus. The function of the great toe is to provide for normal propulsion during gait and to provide stability to the medial aspect of the foot. The first MTP joint moves into extension during gait as a result of the heel lift, subtalar joint supination, and normal sesamoid function.56,57 Theoretically, motions occur in adduction and abduction around a superoinferior axis, and dorsiflexion and plantar flexion around an M-L axis. However, the amount of abduction and adduction of the joint is small compared to sagittal plane motion. Indeed, the most important motion at the first MTP is extension/dorsiflexion, which is coupled with inversion of the proximal joints of the first ray.58 During normal gait, the first MTP joint dorsiflexes approximately 60 degrees. During sprinting (running sports), squatting (football and baseball), and relevé (in dance), greater than 90 degrees of dorsiflexion is necessary. The first MTP is characterized by having a remarkable discrepancy between active and passive motion. The first ray of the foot consists of the first metatarsal and the first (medial) cuneiform bone. These two bones, along with the medial column of the foot, act as a functional unit, playing an important role in providing structural integrity to the foot during walking and running activities. An example is the late stance phase of walking when the ankle is plantar flexing to propel the center of mass of the body up and forward.11 Three extrinsic muscles of the foot insert at the base of the first ray: the anterior tibialis, posterior tibialis, and fibularis (peroneus) longus. The need for clinical assessment of the posterior (dorsal) mobility of the first ray is based on its functional role during weightbearing activities. Any disruption to its normal motion (hypo- or hypermobility) reduces the ability of the first ray to adequately stabilize the medial column of the foot and the longitudinal arch, increasing the potential for injury to the head of the first metacarpal.59

Cubonavicular Joint

IP Joints

The close-packed position for this joint is supination. The open-packed position is midway between the extremes of ROM (Table 21-1).

Each of the IP joints has 1 degree of freedom: flexion/extension. The capsular pattern is more limitation of flexion than of extension. The close-packed position is maximum extension (Table 21-1). The open-packed position is slight flexion.

Intermetatarsal Joints The close-packed position for these joints is supination. The open-packed position is midway between the extremes of ROM (Table 21-1).

MTP Joints The MTP joints have 2 degrees of freedom: flexion/extension and abduction/adduction. ROM of these joints is variable. The closed-packed position for the MTP joints is maximum extension. The capsular pattern for these joints is variable, with more limitation of extension than flexion. The openpacked position is 10 degrees of extension.

First MTP Joint 1050

The hallux and first MTP joint are important to foot function and frequently problematic.11 Normal alignment of the

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EXAMINATION The examination is used to identify static and dynamic, and structural or mechanical foot abnormalities. A successful examination depends on the clinician’s ability to select the most appropriate tests to address the patient-specific problem. The clinical diagnosis is based on an assessment of the changes in joint mobility and tissue changes at the foot and ankle and the effect these have on the function of the foot and ankle and the remainder of the lower kinetic chain. The exact form of the examination is very much dependent on the acuteness of the condition. For example, weight-bearing tests cannot be done if the patient cannot bear weight, and most stress tests will prove impossible if the joints cannot be taken to their full range. In these cases, the clinician must rely heavily on the history.

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With an acute lesion, the purpose of the examination is to try to determine if a serious injury might have occurred and whether there is a need to refer the patient back for further medical examination. Due to the acute pain and inflammatory state of the tissues in the acute stage, the physical examination may need to be modified and sometimes curtailed.

The primary purposes of the history are to do the following: Determine the patient’s chief complaint. ▶▶ Determine the mechanism of injury, if any. Information about the mechanism of injury should include when, where, how, and if an injury occurred. Details about the mechanism of injury allow the clinician to infer the pathologic status and structures involved, although it must be remembered that the patient’s recollection of the mechanism involved frequently does not necessarily correspond to the structures damaged. Most ankle sprains occur when the foot is plantar flexed, inverted, and adducted (Table 21-6). This same mechanism can also lead to a malleolar or talar dome fracture. A history involving sudden changes in training patterns may indicate an overuse injury. A dorsiflexion injury with associated snapping and pain on the lateral aspect of the ankle that rapidly diminishes may indicate a tear of the fibular (peroneal) retinaculum. If there is no traumatic event, the clinician must determine if there has been a change in exercise or activity intensity (e.g., increased mileage with runners), training surface, or changes in body weight or shoe wear (causal agents). In addition, the clinician must determine whether the symptoms vary with activity, type of terrain, or changes in position: ▶▶

■■

■■

■■

■■

■■

■■

▶▶

Complaints of cramping may accompany muscular fatigue or intermittent claudication from arterial insufficiency. Plantar heel pain associated with plantar fasciitis is typically associated with an insidious onset. Pain that is related to a certain time of day may indicate an activity-related problem or a condition such as plantar heel pain if the pain is felt when first bearing weight in the morning. Achilles tendinopathy is an overuse injury associated with an insidious onset of posterior calcaneal pain. Increased symptoms, when walking or running on uneven terrain as compared with an even terrain, may suggest ankle instability. Increased symptoms, when walking or running on hard surfaces, as compared with a softer surface, may suggest a lack of shock absorbency of the foot or shoe.

Determine the patient’s occupation, if any. The impact of the injury on the patient’s personal life, work, and athletic demands will largely direct the early intervention.

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TABLE 21-6

 xamination Sequence in the Presence of E a History of Inversion Trauma of the Foot and Ankle

History of Inversion Trauma Possible pathology/structure involved Ligamentous   Lesion of the anterior talofibular/calcaneofibular ligament   Lesion of the bifurcate ligament   Lesion of the cuboid-fifth metatarsal ligament   Lesion of the anterior tibiotalar and tibionavicular ligaments   Lesion of the tibiofibular interosseous ligament Articular   Traumatic arthritis of the talocrural joint (TCJ)   Traumatic arthritis of the subtalar joint (STJ)   Traumatic arthritis of the transverse tarsal joints (TTJ)   Posterior tibiotalar compression syndrome   Sinus tarsi syndrome   Tibio fibular syndesmosis instability Muscular   Tenosynovitis of the fibularis muscles   Tendinitis of the fibularis muscles   Rupture of the superior extensor retinaculum  Achillodynia   Tenosynovitis or tendinitis of the EHL   Tenosynovitis or tendinitis of the EDL Neurologic  Overstretching of common fibular nerve/superficial fibular/   deep fibular nerve Osseous   Avulsion fracture of the base of the fifth metatarsal   Fracture of the shaft of the fifth metatarsal   Avulsion fracture at the lateral calcaneus   Avulsion fracture at the cuboid   Fracture of the anterior calcaneal process   Osteochondral fracture of the talus   Fracture of the lateral tubercle of the talus   Navicular fracture   Talar neck fracture   Talar head fracture

Lower Leg, Ankle, and Foot

HISTORY



EXAMINATION

CLINICAL PEARL

Modified with permission from Winkel D, Matthijs O, Phelps V. Diagnosis and Treatment of the Lower Extremities. Philadelphia, PA: Lippincott Williams & Wilkins; 1997.

▶▶

■■

If painless ambulation is essential, then rigid immobilization (i.e., a cast) may be appropriate.

■■

If a rapid return to sports competition is of paramount importance, functional immobilization is preferred.

Determine the location and severity of the condition. Most often, the patient can point to the location of the pain. The site and severity of the pain can be measured using a body diagram and visual analog scale, respectively. The distribution of pain is important, and the clinician should determine whether the pattern is referred, associated with a structure, related to a dermatome or peripheral nerve, or systemic in nature.60 A stress fracture

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EXAMINATION THE EXTREMITIES

or tendinopathy typically has a localized site of pain, whereas diffuse pain is associated with compartment syndromes (see Chapter 5). ▶▶ Determine which activities and positions aggravate the symptoms. Information should be gleaned about whether activities aggravate the symptoms and if so, which. For example, pain with forced dorsiflexion and eversion and with squatting activities may suggest ankle instability. Pain after activity suggests an overuse or chronic injury. Pain during an activity suggests stress on the injured structure. ▶▶ Ascertain the area, nature, and behavior of the symptoms. Information about the time of injury, the time of the onset of swelling, and its location are important. The patient may report hearing a “snap,” “crack,” or “pop” at the time of injury, which could indicate a ligamentous injury or a fracture. The patient may report that their ankle felt weak and/or unstable at the time of the initial trauma or sometime thereafter. An inability to bear weight or the presence of severe pain and rapid swelling indicates a serious injury such as a capsular tear, fracture, or grade III ligament sprain. ▶▶ Help determine the specific structure at fault. ▶▶

Detect systemic conditions (e.g., collagen disease, neuropathy, radiculopathy, and vascular problems) or the presence of serious pathology.

In addition, questions regarding previous ankle injury, goals of the patient regarding function, level and intensity of sports involvement, and past medical history are important to help the clinician individualize the intervention to the patient.

SYSTEMS REVIEW As symptoms can be referred distally to the leg, foot, and ankle from a host of other joints and conditions, the clinician must be able to differentially diagnose from the presenting signs and symptoms (see Chapter 5). The cause of the referred symptoms may be neurologic or systemic in origin. If a disorder involving a specific nerve root (L4, L5, S1, or S2) is suspected, the necessary sensory, motor, and reflex testing should be performed. Peripheral nerve injuries may also occur in this region and often go unrecognized. These include Morton’s neuroma and entrapment of the tibial nerve or its branches, the deep fibular (peroneal) nerve, superficial fibular (peroneal) nerve, and sural and saphenous nerves. Systemic problems that may involve the leg, foot, and ankle include diabetes mellitus (peripheral neuropathy), osteomyelitis, gout and pseudogout, sickle cell disease, complex regional pain syndrome, peripheral vascular disease, and rheumatoid arthritis (refer to Chapter 5). A systemic problem such as rheumatoid arthritis may be associated with other signs and symptoms, including other joint pain, although the other joint pain may also be the result of overcompensation in the rest of the kinetic chain. Warning signs at the ankle and foot that should alert the clinician to a more insidious condition include:

immediate and continuous inability to bear weight, which may indicate a fracture; ▶▶ nocturnal pain, which may indicate malignancy, hemarthrosis, fracture, or infection; ▶▶ gross pain during ankle valgus and tenderness with pressure on the distal fibula, which may indicate a fractured fibula; ▶▶ pain and weakness during resisted eversion, which may indicate fracture of the fifth metatarsal bases; ▶▶ calf pain and/or tenderness, swelling with pitting edema, increased skin temperature, superficial venous dilatation, or cyanosis, which may indicate the presence of a deep vein thrombosis (DVT), requiring immediate medical attention (see Chapter 5); ▶▶ feelings of warmth or coldness in the foot. An abnormally warm foot can indicate local inflammation but can also originate from a tumor in the pelvic or lumbar region. An abnormally cold foot usually indicates a vascular problem. ▶▶

TESTS AND MEASURES Observation Observation of the lower extremity is extensive. It is extremely important to observe the entire kinetic chain when assessing the leg, foot, and ankle as foot and ankle posture has been implicated in foot and ankle pathology, as well as altered foot and ankle kinematics and kinetics.61 Weight-bearing and non–weight-bearing postures of the foot are compared. Observing the patient while they move from sitting to standing and walk to the treatment area gives the clinician a sense of the patient’s functional ability in weight-bearing and provides the first opportunity for gait analysis. An important part of the examination of the foot and ankle is the gait assessment (see Chapter 6). During gait, the transverse and longitudinal arches can be grossly assessed—the lateral longitudinal arch bears the body weight in the early stance, whereas the medial longitudinal arch provides support in the mid- and late-stance phase of gait.62 The foot should touch the ground, the heel first and the heel should begin to rise at approximately 35% of the gait cycle.62 Early heel rise may occur due to a tightness of the gastrocnemius–soleus complex whereas late heel rise may be secondary to a weakness of the calf musculature.62 Normally, the foot pronates during the early stance phase, but the foot should not remain pronated during heel rise and toe off.62 The following are assessed with the patient standing: Shoulder and pelvic heights (see Chapters 16 and 29).  ▶▶ Spinal curvature (see Chapter 27).  ▶▶ Pelvic rotation (see Chapter 29).  ▶▶ The degree of hip rotation.  In the femur, anteversion and retroversion angles should be noted (refer to Chapter 19). Excessive internal rotation of the hip toward the opposite hip (anteversion) may result in a flattening of the medial longitudinal arch and toeing-in/internal torsion of the ▶▶

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Rotational components of the tibia.  Tibial torsion is assessed with the patient in sitting, with their feet hanging over the end of the bed so that their knees are in approximately 90 degrees of flexion. The thumb of one hand is placed over the apex of one malleolus, and the index finger of the same hand is placed over the apex of the other malleolus. A qualitative estimate of the direction and magnitude of tibial torsion can be made by envisioning a line that passes through the malleoli and estimating its orientation to the frontal plane of the proximal tibia. Alternatively, tibial torsion can be measured with the patient in prone with the knee flexed to 90 degrees and the subtalar joint positioned and stabilized in subtalar neutral.*

▶▶

Hindfoot to leg orientation.  This can be an indicator of weight-bearing subtalar position. It is assessed by measuring the acute angle formed between a line representing the posterior aspect of the distal third of the leg, and a line approximately 1-cm distal to the first mark, representing the midline of the posterior aspect of the calcaneus (see Fig. 21-13). The angle is assessed as the patient shifts weight on the lower extremity to simulate single-limb support. If the lines are parallel or in slight varus (2–8 degrees), the leg–hindfoot orientation is considered normal. Movement of the hindfoot into eversion (hindfoot valgus) during this maneuver is indicative of subtalar pronation. Pronation of the foot is manifested by eversion of the heel, abduction of the forefoot, a decrease in the medial longitudinal arch, internal rotation of the leg in relation to the foot, and dorsiflexion of the subtalar and transverse tarsal joint complex. If the heel is in too much valgus, the forefoot is excessively abducted, or there is excessive external rotation of the tibia, more toes can be seen on the affected

Lower Leg, Ankle, and Foot

▶▶

Once the subtalar neutral position has been established, a line is drawn on the sole of the foot parallel to the length of the femur. A second line is drawn in line with the foot. The angle between these lines is the tibial torsion angle. There is normally an angle of 12–18 degrees to the frontal plane. Tibial torsion is generally less in children. A position of relative internal rotation of the tibia produces an increase in rigidity to the subtalar joint prior to midstance, due to premature stabilization of the longitudinal arch of the foot. Excessive external rotation of the tibia places an increased strain along the longitudinal arch, as well as the first MTP joint.

EXAMINATION

tibia (pigeon toes). Excessive external rotation of the hip away from the opposite hip (retroversion) may result in an elevation of the medial longitudinal arch. ▶▶ The degree of knee flexion or hyperextension.  A genu recurvatum (hyperextension) places the talocrural joint in more plantar flexion than normal and can often be a compensatory mechanism in the longer limb of individuals who have a leg-length inequality; see Chapter 29. An increase in knee flexion accomplishes the same compensation for a leg-length inequality. ▶▶ The degree of varus and valgus of the knee and tibia.  In the sagittal plane, a vertical tibia indicates normal ankle position. Tibia varum refers to the frontal plane position of the distal one-third of the leg, as it relates to the supporting surface. The midshaft of the distal one-third of the lower leg should be straight within the frontal plane. Excessive tibia varum, genu varus, or forefoot varus can increase the frontal angle of the talocrural joint, which promotes excessive weight-bearing on the lateral aspect of the foot unless compensatory pronation is available within the foot to bring the medial aspect of the foot to the support surface.

CLINICAL PEARL The neutral subtalar position is calculated based on a normal 2:1 ratio of inversion to eversion. To locate subtalar neutral, the patient is positioned in prone with the opposite hip flexed, abducted, and externally rotated. If evaluating the right ankle, the clinician uses the thumb and forefinger of the left hand to palpate the hollows over the neck of the talus on either side of the anterior portion of the ankle. Using the thumb and forefinger of the other hand, the clinician grasps the head of the fourth and fifth metatarsals and rocks the foot back and forth. As the foot is inverted, a bulge can be felt on the lateral aspect of the foot. With eversion, the bulge can be felt to bulge medially. The point at which the talar head is felt to bulge equally on the medial and lateral sides is the subtalar neutral position.

Tibia Fibula

Talus

Calcaneus

*

The subtalar neutral position refers to the position in which all bones of the subtalar joints and the talocrural joints line up optimally in their openpacked positions—a position of neither pronation nor supination.

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FIGURE 21-13  Hindfoot to leg orientation.

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side than the normal side when viewing the leg from behind (“too-many-toes sign”). If the patient is asked to raise up on the toes, the calcaneus should be observed to move into a position of inversion. An inability of the calcaneus to invert with this maneuver could indicate the presence of an abnormality in the subtalar joint mechanism, or a weakness of the posterior tibialis. The weight-bearing foot.  The following are major components of the normal weight-bearing foot: ▶▶ Both planar condyles of the calcaneus are on the floor surface when looking from the posterior, and there should be a slight calcaneal eversion with no more than one or two of the lateral toes visible.1 An imaginary plane representing the ground surface is applied to the anterior (plantar) surface of the calcaneus. The metatarsal heads should rest upon this plane. If the plane of the metatarsal heads is perpendicular to the bisection of the calcaneus, the forefoot-to-hindfoot relationship is normal, or neutral. ▶▶ The “normal” foot should demonstrate 6–8 degrees of calcaneal eversion during gait. The foot should pronate initially, just after initial contact (see Chapter 6). All of the metatarsal heads lie in one plane, which is in the same plane as the anterior (plantar) condyles of the calcaneus. ▶▶ The ball of the foot is level with the plantar surface of the heel. ▶▶ A normal forefoot-to-hindfoot relationship (see later). ▶▶ The orientation of the distal third of the lower leg should be vertical, to position the foot properly for the stance phase. ▶▶ The transverse tarsal joint complex is maximally pronated, while the subtalar joint, MTP, and IP joints are in neutral. ▶▶ The presence of a well-formed static medial arch should be noted, as well as its dynamic formation with heel raising. Specifically, there should be a distance between the navicular tuberosity and the floor that it easily noticeable but not excessive.1 The distance between the navicular tuberosity and floor can be measured with a ruler or digital calipers. The arch index, which is a measurement made from footprints, involves calculation of the ratio of the area of the middle third of the arch to the total area of the foot excluding the toes. It is important to note that a pilot study by Wearing et al.63 reported that body composition influences arch index values in overweight and obese subjects. ▶▶ Forefoot-to-hindfoot relationship.  Goniometric measurement of forefoot position relative to the hindfoot is a routine procedure used by rehabilitation specialists. This measurement is also frequently made by visual estimation. Neutral alignment of the forefoot relative to the hindfoot is present when a line representing the anterior (plantar) aspect of the metatarsal heads is perpendicular to the line bisecting the hindfoot. The forefoot-to-hindfoot angle is approximately 10–12 degrees.

Forefoot varus is the term used to describe inversion of the forefoot away from this neutral position, while forefoot valgus describes an everted forefoot position. The relationship can be assessed with the patient positioned in prone with their knee extended and their feet over the end of the table. The subtalar neutral position is located using the method described previously. Slight pressure is applied to the metatarsal heads while maintaining subtalar neutral. This will determine the relationship of the forefoot to hindfoot, and both of these to the bisection of the lower leg. A varus or valgus tilt of the forefoot in relation to the hindfoot becomes significant when the first metatarsal is in a plantar flexed position, as this positions the hindfoot into an inverted position during weight-bearing. ▶▶

Foot deviations in weight-bearing.  These include pes planus (low inclined subtalar joint axis that is characterized by a low arch and hindfoot valgus), pes cavus (high inclined subtalar joint axis that is characterized by a high arch and hindfoot varus), talipes equinus (plantar flexed foot), talipes equinovarus (supinated foot), and hallux valgus.

▶▶

The degree of foot pronation or supination in non–weightbearing.  The patient lies in the prone position, with the foot over the edge of the table. The clinician holds the foot over the fourth and fifth metatarsal heads with one hand. Both sides of the talus are palpated on the posterior aspect of the foot using the thumb and index finger of the other hand. The clinician then passively dorsiflexes the foot until a resistance is felt. At this point, and while maintaining the dorsiflexed position, the clinician moves the foot back and forth through the arc of supination and pronation. During supination, the talus should be felt to bulge laterally, while, during pronation, the talus should be felt to bulge medially. Supination at the subtalar joint occurs in association with 20 degrees of calcaneal inversion while pronation occurs in association with 10 degrees of calcaneal inversion.

▶▶

The degree of toe-out.  The normal foot in relaxed standing adopts a slight toe-out position of approximately 12–18 degrees from the sagittal axis of the body (Fick angle).

▶▶

Forefoot equinus.  To assess for forefoot equinus, the clinician stabilizes the hindfoot with one hand and applies pressure on the entire forefoot via pressure across the metatarsal heads, into dorsiflexion. If the plantar declination of the lateral structures cannot be reduced so that the plantar flexed attitude is no longer visible, a positive identification of forefoot equinus can be made.

▶▶

The presence of a talar bulge.  The patient is positioned in standing, and the clinician observes to see whether the talar head bulges excessively on the medial side of the midfoot, indicating excessive subtalar joint pronation in weight-bearing. Adaptive shortening of the gastrocnemius/soleus group is indicated with a prominence of the soleus, particularly on the medial side of the tendo calcaneus.

▶▶

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Modified Foot Posture Index Scoring

Talar head palpation –2

–1

0

1

2

Talar head palpable on lateral side/but not on medial side

Talar head palpable on lateral side/slightly palpable on medial side

Talar head equally Talar head slightly palpable on the lateral palpable on lateral and medial side side/palpable on medial side

Talar head not palpable on lateral side/but palpable on medial side

0

1

2

Curve below malleolus more concave than curve above malleolus

Curve below malleolus markedly more concave than curve above malleolus

EXAMINATION

TABLE 21-7

Supra and infra lateral malleollar curvature –1

Curve below the malleolus either straight or convex

Both infra and supra Curve below the malleolar curves malleolus concave, but roughly equal flatter/more shallow than the curve above the malleolus

Calcaneal frontal plane position –2

–1

0

1

2

More than an estimated 5 degrees inverted (varus)

Between vertical and an estimated 5 degrees inverted (varus)

Vertical

Between vertical and an estimated 5 degrees everted (valgus)

More than an estimated 5 degrees either (valgus)

0

1

2

Area of the talonavicular joint is flat

Area of the talonavicular joint is bulging slightly

Area of the talonavicular joint is bulging markedly

Prominence in the region of the talonavicular joint –2

–1

Area of the talonavicular Area of the talonavicular joint is markedly joint slightly, but concave definitely concave

Lower Leg, Ankle, and Foot

–2

Congruence of the medial longitudinal arch –2

–1

0

1

2

Arch high and acutely angled toward the posterior end of the medial arch

Arch moderately high and slightly acute posteriorly

Arch height normal and concentrically curved

Arch is lowered with some flattening in the central portion

Arch very low with severe flattening in the central portion—arch making ground contact

Abduction/adduction of the forefoot on the rear foot –2

–1

0

1

2

No lateral toes visible. Medial toes clearly visible

Medial toes clearly more visible than lateral

Medial and lateral toes equally visible

Lateral toes clearly more visible than medial

No medial toes visible. Lateral toes clearly visible

Data from: 1. Keenan AM, Redmond AC, Horton M, et al. The foot posture index: Rasch analysis of a novel, foot-specific outcome measure. Arch Phys Med Rehabil. 2007 Jan;88(1):88–93. 2. Redmond AC, Crane YZ, Menz HB. Normative values for the foot posture index. J Foot Ankle Res. 2008 Jul 31;1(1):6. 3. Redmond AC, Crosbie J, Ouvrier RA. Development and validation of a novel rating system for scoring standing foot posture: the foot posture index. Clin Biomech (Bristol, Avon). 2006 Jan;21(1):89–98.

The Modified Foot Posture Index (FPI)64–66 can be used to quantify the degree to which the foot is pronated, supinated, or in the neutral position. The user attaches a score based on a 5-point Likert scale to a series of six observations (Table 21-7). All observations are made with the subject standing at a relaxed angle and base of gait, double limb support, and static stance position. When the scores are combined, the aggregate value gives an estimate of the

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overall foot posture. The six clinical criteria employed are64,65: 1. Talar head palpation. The head of the talus is palpated on the medial and lateral side of the anterior aspect of the ankle and scored accordingly. 2. Supra- and infra-lateral malleolar curvature. In the neutral foot, the curves should be approximately equal.

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3. Calcaneal frontal plane position. With the patient standing in the relaxed stance position, the posterior aspect of the calcaneus is visualized with the observer in line with the long axis of the foot. 4. Prominence in the region of the talonavicular joint. In the foot, the area of the skin immediately superficial to the talonavicular joint is flat. However, the talonavicular joint becomes more prominent if the head of the talus is abducted in the rearfoot pronation, indicating a pronated foot. In the supinated foot, this area may be indented. 5. Congruence of the medial longitudinal arch. In a neutral foot, the curvature of the arch should be relatively uniform, similar to a segment of the circumference of a circle. When the foot is supinated, the curve becomes acuter at the posterior end of the arch. In an excessively pronated foot, the arch becomes flattened in the center. 6. Abduction/adduction of the forefoot on the rearfoot. In a supinated foot, the forefoot will adduct on the rearfoot resulting in more of the forefoot being visible on the medial side. Conversely, pronation of the foot causes the forefoot to abduct resulting in more of the forefoot been visible on the lateral side. The final FPI score will be a whole number between -12 and +12. High positive aggregate values indicate a pronated posture, whereas significantly negative aggregate values indicate a supinated foot posture. The score for a neutral foot should lie somewhere around zero. The Modified FPI demonstrates good intrarater reliability and moderate interrater reliability.67 Other areas that should be examined include the following: The condition of the nails.  When examining the nails a systematic approach is used, involving an inspection of the shape, contour, and color of the nails. The clinician should observe for the presence of subungual hematomas, subungual exostosis, onychocryptosis, onychia, onychauxis, onychomycosis, paronychia, tinea pedis, or blisters. ▶▶ Toe deformities.  Contractions of the capsule of the IP or MTP joints of the toes in association with tendon shortening may produce a series of deformities, ranging from hammer toe to mallet toe to claw toe. Hammer toe usually involves a flexion contracture of the anterior (plantar) surface of the PIP, with a mildly associated extension contracture of the MTP joint. Mallet toe results from a flexion deformity of the distal interphalangeal joint (DIP) with plantar contracture. Often a corn or callus is present on the posterior aspect of the affected joint. Corns are similar to calluses but have a central nidus. Claw toe deformity is a more advanced contracture of capsules and intrinsic musculature, which may also be associated with pes cavus and neurologic or primary muscle pathology to the lumbrical and interosseous muscles. The claw toe results in hyperextension of the MTP joints and flexion of the PIP and DIP joints. ▶▶ Functional hallux limitus.  Clinically, the presence of functional hallux limitus, an inability of the first MTP joint to extend without pain, can be determined by assessing the ROM available at the first MTP joint, while ▶▶

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the first ray is prevented from plantar flexing. The patient is positioned in standing, the feet shoulder-width apart. The patient is asked to actively raise the great toe off the floor while keeping the remaining toes and foot on the ground. The amount of hallux extension is measured; less than 10 degrees is considered limited.68 This test has been found to have a sensitivity of 0.72 and a specificity of 0.66.68 ▶▶ The leg, foot, and ankle are examined for the presence of bruising, swelling, or unusual angulation.  Ecchymosis may be present, but the blood usually settles along the medial or lateral aspects of the heel. The appearance of bluish-black plaques on the posterior and posterolateral aspect of one or both heels in a young distance runner is found in a condition called black-dot heel, which results from a shearing stress or a pinching of the heel between the counter and the sole of the shoe at initial contact during running. Extracellular fluid pools on the posterior aspect of the foot and around the malleoli after injury or surgery. Shortly after a lateral ligament sprain, the swelling is limited to the lateral ankle. Subsequently, the swelling is diffuse, and the localization of tenderness may be difficult. An objective measure of the amount of swelling present can be made using the figureof-eight method (see “Special Tests” section). Callus formation.  Calluses provide the clinician with an index as to the degree of shear stresses applied to the foot and clearly outline abnormal weight-bearing areas. In adequate amounts calluses provide protection, but in excess they may cause pain. Callus formation under the second and third metatarsal heads could indicate excessive pronation in a flexible foot, or Morton’s (interdigital) neuroma (see Chapter 5) if under the second through fourth. A callus under the fifth and sometimes the fourth metatarsal head may indicate an abnormally rigid foot. ▶▶ Any evidence of circulatory impairment or vasomotor changes.  Brick-red coloring or cyanosis, when the leg is dependent, is an indication of vascular impairment, especially if the color changes when the leg is elevated. Vasomotor changes include toenail changes, changes in skin texture, abnormal skin moisture or dryness, and loss of hair on the foot. Vasomotor changes may be associated with complex regional pain syndrome (see Chapter 5). ▶▶ The type of shoes.  High-heeled shoes have been associated with adaptive shortening of the gastrocnemius– soleus complex, knee pain, and low-back pain. They have also been associated with an increased potential for ankle sprains, hallux valgus, bunions, metatarsalgia, interdigital neuromas, peripheral nerve compression, and stress fractures. Shoes with a negative heel may result in hyperextension of the knees. ▶▶ The weight-bearing and wear patterns of the shoe.  The greatest amount of wear on the sole of the shoe should occur beneath the ball of the foot, in the area corresponding to the first, second, and third MTP joints and slight wear to the lateral side of the heel. Old running ▶▶

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Palpation Careful palpation should be performed on the leg, foot, and ankle to differentiate tenderness of specific ligaments and other structures. Areas of localized swelling and ecchymosis over the ligaments on the medial or lateral aspects of the foot and ankle should be noted (see Assessing Ankle Girth under Special Tests). The clinician should also make temperature comparisons and corroborate the findings with palpation of pedal pulses. For example, a cold foot may be indicative of limited circulation especially in the presence of a diminished pedal pulse (see Special Tests). Finally, the clinician should assess sensitivity to light touch (see Neurologic Tests) to help rule out the presence of sensory polyneuropathy in individuals with diabetes mellitus, peripheral nerve entrapment, or spinal nerve root impingement.

CLINICAL PEARL The Ottawa Ankle Rules69 (see Imaging Studies) are a set of clinical criteria based on palpation that can determine the need for foot and ankle radiographs.1

Posterior Aspect of Foot and Ankle Achilles Tendon.  The Achilles tendon is inspected for contour changes such as swelling, erythema, and thickening. Any gaps or nodules in the tendon and specific sites of pain

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Calcaneus.  At the distal end of the Achilles tendon is the calcaneal tuberosity. The posterior aspect of the calcaneus and surrounding soft tissue is palpated for evidence of exostosis (“pump bump” or Haglund’s deformity) and associated swelling (retrocalcaneal bursitis). The inferior medial process of the calcaneus, just distal to the weight-bearing portion of the calcaneus, serves as the attachment of the plantar fascia and is often tender with plantar heel pain.

Anterior and Anteromedial Aspects of the Foot and Ankle While reading the next section, the reader may find it helpful to remove a shoe and sock and self-palpate. Great Toe and the Phalanges.  Beginning medially, the clinician locates and palpates the great toe and its two phalanges. The first metatarsal bone is more proximal, the head of which should be palpated for tenderness on the lateral aspect (bunion) and inferior aspect (sesamoiditis). Moving laterally from the phalanges of the great toe, the clinician palpates the phalanges and metatarsal heads of the other four toes. Tenderness of the second metatarsal head could indicate the presence of Freiberg disease, an osteochondritis of the second metatarsal head (see Chapter 5). A callus under the second and the third metatarsal head may indicate a fallen metatarsal arch. Palpable tenderness in the region of the third and fourth metatarsal heads could indicate a Morton’s neuroma, especially if the characteristic sharp pain between the toes of this condition is relieved by walking barefoot. Tenderness on the lateral aspect of the fifth metatarsal head could indicate the presence of a tailor’s bunion.

Lower Leg, Ankle, and Foot

The non–weight-bearing component of the examination is initiated by having the patient seated on the edge of the bed, feet dangling. The feet should adopt an inverted and plantar flexed position. A mobile or nonstructural flatfoot will take on a more normal configuration in non–weight-bearing, whereas a fixed or structural flatfoot will maintain its planus state. By placing one hand on the patella and the other hand on the tips of the malleoli, the clinician should note approximately 20–30 degrees of external rotation of the ankle in relation to the knee.

should be carefully examined. Palpation of a tendon gap has been shown to demonstrate a moderate capacity (+LR 6.64) to confirm an Achilles tendon rupture but a moderate to low sensitivity, as well as a −LR (0.30), indicating that this test should not be used in isolation for screening purposes.70 For example, the presence of a palpable gap in the tendon accompanied by an inability to rise up on the toes would be a better indicator for a rupture of the tendon.

EXAMINATION

shoes belonging to patients who excessively pronate tend to display overcompression of the medial arch of the midsole and extensive wear of the lateral regions of the heel counter and medial forefoot. The upper portion of the shoe should demonstrate a transverse crease at the level of the MTP joints. A stiff first MTP joint can produce a crease line that runs obliquely, from forward and medial to backward and lateral. The cup at the rear of the shoe, which is formed by the heel counter, should be vertical and symmetrical with respect to the shoe and should be of a durable enough material to hold the heel in place. A medial inclination of the cup, with bulging of the lateral lip of the counter, indicates a pronated foot. A lateral bulge of the heel counter indicates a supinated foot. Scuffing of the shoe might indicate tibialis anterior weakness.38 The shape of the last influences the amount of motion that the shoe permits. As the degree of curvature in the last increases, more foot mobility is available.

Cuneiform.  The first cuneiform is located at the proximal end of the first metatarsal (see Fig. 21-1) and is palpated for tenderness. Navicular.  The navicular is the most prominent bone on the medial aspect of the foot. The navicular tuberosity can be located by moving proximally from the medial aspect of the first cuneiform (see Fig. 21-1). The talonavicular joint line lies directly proximal to the navicular tuberosity. In addition, the posterior tibialis, which can be made more prominent with resisted plantar flexion, adduction, and supination, can be used as a reference as it inserts on the plantar surface of the navicular (see later). Tenderness of the navicular could indicate the presence of a fracture or osteochondritis of the navicular (Köhler disease). Second and Third Cuneiforms.  These two bones can be palpated by moving laterally from the first cuneiform (see Fig. 21-1). Tenderness of these bones may indicate a cuneiform fracture.

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EXAMINATION

Anterior and Anterolateral Aspects of the Foot and Ankle Tibial Crest. The tibial crest is palpated for tenderness, which may indicate the presence of medial tibial stress syndrome (MTSS) (shin splints). Swelling in this area may indicate the presence of anterior compartment syndrome (see Chapter 5). The muscles of the lateral (peronei) and anterior compartments (tibialis anterior and the long extensors) are palpated here for swelling or tenderness. Swelling or tenderness of these structures usually indicates inflammation.

THE EXTREMITIES

FIGURE 21-14  Dorsal pedis pulse.

Posterior (Dorsal) Pedis Pulse.  The pulse of the posterior (dorsal) pedis artery, a branch of the anterior tibial artery, can be palpated over the talus, cuneiform bones (Fig. 21-14), between the first and second cuneiforms or between the first and second metatarsal bones. Medial Malleolus. The medial malleolus is palpated for swelling or tenderness. Moving proximally from the anterior aspect of the medial malleolus, the distal aspect of the tibia is palpated. Distal to that is the talus bone. Moving distal from the tibia, the clinician palpates the long extensor tendons, the tibialis anterior, and the superior and inferior extensor retinaculum. The tendon of the tibialis anterior is visible at the level of the medial cuneiform and the base of the first metatarsal bone, especially if the foot is positioned in dorsiflexion and supination. Talus.  The talus can be located by moving from the distal aspect of the medial malleolus along a line joining the navicular tuberosity. It can be more easily located by everting and inverting the foot. Eversion causes the talar head to become more prominent while inversion causes the head to be less visible. Sustentaculum Tali.  Distal and inferior to the medial malleolus, a shelf-like bony prominence of the calcaneus, the sustentaculum tali, can be palpated. At the posterior aspect of the sustentaculum tali, the talocalcaneal joint line can be palpated. Posterior Tibialis Tendon.  This tendon is palpable at the level of the medial malleolus, especially with the foot held in plantar flexion and supination. Distal and medial to this tendon, the crossing of the FDL and flexor hallucis tendons can be felt. Posterior Tibial Artery.  The posterior tibial artery (Fig. 21-9) can be located posterior to the medial malleolus and anterior to the Achilles tendon. Medial (Deltoid) Ligament of the Ankle. The medial (deltoid) ligaments of the ankle are very difficult to differentiate, so they are usually palpated as a group on the medial aspect of the ankle (see Fig. 21-4).

Lateral Malleolus.  The lateral malleolus is located at the distal aspect of the fibula. Distal to the lateral malleolus is the calcaneus. Fibularis (Peroneus) Longus.  The tendon of the fibularis (peroneus) longus runs superficially behind the lateral malleolus. Resisted pronation and plantar flexion of the foot make the tendon more prominent. Fibularis (Peroneus) Brevis.  The origin for the fibularis (peroneus) brevis is more distal to the fibularis (peroneus) longus and lies deeper. It becomes superficial on the lateral aspect of the foot, at its insertion on the tuberosity of the fifth metatarsal. Anterior Talofibular Ligament.  The ATFL can be palpated two to three finger-breadths anteroinferior to the lateral malleolus (see Fig. 21-5). This is usually the area of most extreme tenderness following an inversion sprain. The anterior aspect of the distal tibiofibular syndesmosis may also be tender following this type of sprain. Calcaneofibular Ligament.  The CFL can be palpated one to two finger-breadths inferior to the lateral malleolus (see Fig. 21-5). Posterior Talofibular Ligament.  The PTFL can be palpated posteroinferior to the posterior edge of the lateral malleolus (see Fig. 21-5). Sinus Tarsi.  The sinus tarsi is visible as a concave space between the lateral tendon of the EDL muscle and the anterior aspect of the lateral malleolus. The origin of the EDB is at the level of this tunnel. Tenderness with palpation of the sinus tarsi is considered one hallmark clinical sign of subtalar joint inflammation.1 Cuboid.  The cuboid bone can be palpated by moving distally approximately one finger-breadth from the sinus tarsi.

Active and Passive Range of Motion ROM testing is divided into an active range of motion (AROM) and a passive range of motion (PROM) examination, with overpressure being superimposed at the end of the available range to assess the end-feel. AROM tests are used to assess the patient’s willingness to move and the presence of movement restriction patterns such as a capsular or noncapsular pattern. The end-feel may provide the clinician with

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TABLE 21-8

 ormal Ranges of Motion and End-Feels N for the Lower Leg, Ankle, and Foot End-Feel

Talocrural plantar flexion

50

Tissue stretch

Talocrural dorsiflexion

20

Tissue stretch

Supination

45–60

 

Pronation

15–30

 

Hindfoot inversion

20

Tissue stretch

Hindfoot eversion

10

Tissue stretch

Toe flexion

Great toe: MTP, 45; IP, 90

Tissue stretch

   

Lateral four toes: MTP, 40; PIP, 35; DIP, 60 Great toe: MTP, 70; IP, 0 Lateral four toes: MTP, 40; PIP, 0; DIP, 30

 

Toe extension    

Tissue stretch    

Data from Rasmussen O. Stability of the ankle joint. Analysis of the function and traumatology of the ankle ligaments. Acta Orthop Scand Suppl. 1985;211:1–75; Seto JL, Brewster CE. Treatment approaches following foot and ankle injury. Clin Sports Med. 1994 Oct;13(4):695–718.

information as to the cause of a motion restriction. The normal ranges of motion and end-feels for the lower leg, ankle, and foot are outlined in Table 21-8. The open- and closepacked positions and capsular patterns for the ankle and foot are outlined in Table 21-1. General AROM of the foot and ankle in the non–weightbearing position is assessed first, with painful movements being performed last. The hip and knee joints may also be examined as appropriate. Weight-bearing tests are usually performed after the non–weight-bearing tests. If the symptoms are experienced during the general tests, then passive, active, and resisted tests of specific structures must be performed. If the general tests are negative, there is probably no immediate need to proceed with a more detailed examination, although this may have to be done if no other region appears to be the cause of the problem. Although specific motions at the distal tibiofibular joint cannot be produced voluntarily, the function of this joint can be assessed indirectly by asking the patient to twist around both feet in each direction while bearing weight. The reliability of foot and ankle measurements has been reported. The interrater reliability of non–weight-bearing measurements was as follows1: Ankle dorsiflexion ROM was between ICC = 0.00–0.87, Non–weight-bearing ankle plantar flexion was ICC = 0.74 ▶▶ Transverse tarsal inversion ranged between ICC = 0.302–0.88

The intrarater reliability of non–weight-bearing ankle dorsiflexion measurement was estimated to be good (ICC = 0.74).

Dorsiflexion The patient lies in the supine position, with the knee slightly flexed and supported by a pillow, while the clinician stands at the foot at the table, facing the patient VIDEO. Active dorsiflexion is initially performed with the knee flexed (Fig. 21-15). Care must be taken to prevent pronation at the subtalar and oblique transverse tarsal joint complex during dorsiflexion. The foot is slightly inverted to lock the longitudinal arch. Passive overpressure is applied. With the knee flexed to approximately 90 degrees, the length of the soleus muscle is examined. Passive overpressure into dorsiflexion, when the knee is flexed, assesses the joint motion, as well as the soleus length. The soleus is implicated if the pain is produced in this test, especially if resisted plantar flexion is painful or more painful with the knee flexed than with the knee extended. With the knee flexed, 20 degrees of dorsiflexion past the anatomic position (the foot at 90 degrees to the bones of the leg) is found in the normally flexible person. The flexibility of the soleus muscle may also be assessed in standing in able-bodied individuals by asking the patient to perform a deep squat or a lunge.

Lower Leg, Ankle, and Foot

Normal Range (Degrees)

Motion

Transverse tarsal eversion range was between ICC = 0.222–0.79 ▶▶ First MTP joint dorsiflexion was between ICC = 0.04–0.16 ▶▶ First MTP joint plantar flexion was between ICC = 0.07–0.21. ▶▶

EXAMINATION



Squat.  If the muscle length is normal, the patient should be able to place the whole foot on the floor, including the heel, while in the full squat position (Fig. 21-16). If the soleus is short, the heel will not touch the floor. ▶▶ Lunge.  A standard goniometer is aligned along the lateral aspect of the leg and the floor. The subject steadies themselves and then performs a weight-bearing lunge maneuver (Fig. 21-17). The angle recorded on the goniometer indicates the range of dorsiflexion under load. ▶▶

▶▶

FIGURE 21-15  Ankle dorsiflexion.

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EXAMINATION THE EXTREMITIES

FIGURE 21-16  Ankle dorsiflexion during a squat. FIGURE 21-18  Active ankle dorsiflexion (knee extended).

If the goniometer is set so that vertical is zero, the arm of the goniometer always aligns to the vertical and the scale rotates to indicate the inclination from the vertical. This angle is then recorded as the ankle dorsiflexion range. This method is considered the most appropriate method of measuring ankle dorsiflexion range, as it reflects the functionally available range for the individual. ▶▶

CLINICAL PEARL

Chronic adaptive shortening of the soleus muscle can be caused by excessive running, a weak posterior tibialis, or a weak quadriceps. Adaptive shortening of the soleus can result in forefoot pronation and a valgus stress at the knee.

To assess the length of the gastrocnemius, the patient is placed in the supine position with the knee extended, and the ankle positioned in subtalar neutral. The patient is then asked to dorsiflex the ankle (Fig. 21-18). Passive overpressure into dorsiflexion is applied. The normal range is 20 degrees. If the gastrocnemius is shortened, dorsiflexion of the ankle will be reduced as the knee is extended and increased as the knee is flexed. A muscular end-feel should be felt with the knee extended, and a capsular end-feel should be felt with the knee flexed.

CLINICAL PEARL Limited dorsiflexion with knee extension, combined with hindfoot valgus, is thought to be a sign of tight plantar flexors, particularly the gastrocnemius muscle.11 A decrease in the flexibility of the gastrocnemius can result from a number of dysfunctions, including dysfunction of the subtalar joint or transtarsal joint, an ankle sprain, high-heeled footwear, or poor gait/running mechanics.

Plantar Flexion The patient is placed in the supine position, while the clinician stands at the foot of the table, facing the patient VIDEO. The patient is asked to plantar flex the ankle (Fig. 21-19). Plantar

FIGURE 21-17  Ankle dorsiflexion during lunge with a goniometer.

FIGURE 21-19  Ankle plantar flexion.

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EXAMINATION

flexion of the ankle is approximately 30–50 degrees. When tested in weight-bearing with the unilateral heel raise, heel inversion should be seen to occur. Failure of the foot to invert may indicate instability of the foot/ankle, posterior tibialis dysfunction (see Strength Testing), or adaptive shortening.71 It is worth noting that both the forefoot and hindfoot work together to achieve heel height. Houck et al.72 reported that the hindfoot and first metatarsal both plantar flexed over 20 degrees to achieve a maximum heel height.

Lower Leg, Ankle, and Foot

CLINICAL PEARL The moment arms of the lateral and medial gastrocnemius muscles can vary depending on the degree of inversion or eversion. Studies have demonstrated that when the foot was positioned in 15 degrees of eversion, both the lateral and medial gastrocnemius muscles had moments toward eversion. However, when the foot was positioned in neutral or in inversion, the lateral and medial gastrocnemius muscles had moment arms toward inversion.73,74 This would tend to suggest that the gastrocnemius and soleus muscles may play a role in frontal plane actions at the subtalar joint when the foot is either supinated or pronated.11 For example, when the hindfoot is everted (as found in flatfoot deformity), the triceps surae may contribute to eversion, whereas when the hindfoot is in supination (as found in the late stance phase of gait), the triceps surae muscles may contribute to inversion.11

Hindfoot Inversion (Supination) and Hindfoot Eversion (Pronation) Both hindfoot inversion (Fig. 21-20) and hindfoot eversion (Fig.21-21) are tested by lining up the longitudinal axis of the leg and vertical axis of the calcaneus. Passive motion of hindfoot inversion (supination) is normally 20 degrees. The amount of hindfoot eversion (pronation) is normally 10 degrees.

FIGURE 21-20  Ankle inversion.

Strength Testing Ankle Gastrocnemius and Plantaris Muscles. Plantar flexion strength can be tested initially in non–weight-bearing (Fig. 21-22). However, unless there is significant weakness, clinician strength is usually insufficient to overcome ankle plantar flexor force, which necessitates a weight-bearing assessment of ankle plantar flexor strength. If no plantar flexion weakness is apparent in non–weight-bearing, a heel raise test is performed in the functional position, standing with the knee extended and the opposite foot off the floor VIDEO.

Great Toe Motion The patient is positioned in supine, with the leg being supported by a pillow, while the clinician stands at the foot at the table, facing the patient. Active extension of the great toe is performed and assisted passively without dorsiflexing the first ray. The amount of posterior (dorsal) mobility is usually classified as normal, hypomobile, or hypermobile. Although this method of assessment is common, its reliability and validity have been shown to be poor.59 Extension of the great toe occurs primarily at the MTP joint. Passive extension of the great toe at the MTP joint should demonstrate elevation of the medial longitudinal arch (windlass effect), and external rotation of the tibia. Passive MTP joint extension of between 55 and 90 degrees is necessary at the terminal stance, depending on length of stride, shoe flexibility, and toe-in/toe-out foot placement angle. Forty-five degrees of first MTP flexion and 90 degrees of IP joint flexion are considered normal.

FIGURE 21-21  Ankle eversion.

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FIGURE 21-22  Manual muscle testing of the plantar flexors.

Technically, one heel raise through full ROM, while standing with support on one leg, scores a 3/5 (fair) with manual muscle testing, with five single-limb heel raises scoring a 4/5 (good) and 10 single-limb heel raises scoring a 5/5 (normal). From a functional viewpoint, a wider range of scoring can sometimes prove more useful. Table 21-9 outlines an alternative scoring method. An alternative test, which is frequently used to assess talocrural and overall ankle function and is

TABLE 21-9

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often prescribed as an exercise, is the heel rise task. The task is performed using a block or a step, and the patient is positioned in standing with the balls of both feet on the block/step edge and the remaining parts of the feet over the edge. The patient may use a solid object for balance only. The patient is then asked to rise and lower his or herself on the balls of their feet as far as possible in each direction. The test can be also applied having the patient stand on only one leg. It is interesting to note that one study75 that measured both the ankle plantar flexion angle and the ankle dorsiflexion angle during this task found that the angles achieved were 23.7 degrees and 30.4 degrees respectively. The apparently large dorsiflexion angle compared to what is typically measured using a goniometer is likely the result that the motion combines both talocrural movement and forefoot movement.11 Although the task of raising up on the toes is generally thought to be predominantly performed by the triceps surae, a study by Kulig et al.76 reported significant contributions of the fibularis muscles and tibialis posterior during this task. Soleus Muscle.  The soleus muscle produces plantar flexion of the ankle joint, regardless of the position of the knee. To determine the individual functioning of the soleus as a plantar flexor, the knee is flexed to minimize the effect of the gastrocnemius muscle. The soleus is tested in a similar manner

Functional Testing of the Foot and Ankle

Starting Position

Action

Functional Test

Standing on one leg      

Lift toes and forefeet off ground (dorsiflexion)      

10–15 repetitions: functional 5–9 repetitions: functionally fair 1–4 repetitions: functionally poor 0 repetition: nonfunctional

Standing on one leg      

Lift heels off ground (plantar flexion)      

10–15 repetitions: functional 5–9 repetitions: functionally fair 1–4 repetitions: functionally poor 0 repetition: nonfunctional

Standing on one leg      

Lift lateral aspect of foot off ground (ankle eversion)      

5–6 repetitions: functional 3–4 repetitions: functionally fair 1–2 repetitions: functionally poor 0 repetition: nonfunctional

Standing on one leg      

Lift medial aspect of foot off ground (ankle inversion)      

5–6 repetitions: functional 3–4 repetitions: functionally fair 1–2 repetitions: functionally poor 0 repetitions: nonfunctional

Seated      

Pull small towel up under the toes or pick up and release small object (i.e., pencil, marble, cotton ball) (toe flexion)     

10–15 repetitions: functional 5–9 repetitions: functionally fair 1–4 repetitions: functionally poor 0 repetitions: nonfunctional

Seated      

Lift toes off ground (toe extension)      

10–15 repetitions: functional 5–9 repetitions: functionally fair 1–4 repetitions: functionally poor 0 repetitions: nonfunctional

Data from Palmer ML, Epler M. Clinical Assessment Procedures in Physical Therapy. Philadelphia, PA: JB Lippincott; 1990.

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EXAMINATION FIGURE 21-25  Manual muscle testing of the fibularis (peroneus) muscle group.

to that of the gastrocnemius, except that the patient performs the unilateral heel raise with some degree of knee flexion. Ability to perform 10–15 raises in this fashion is considered normal, 5-9 raises graded as fair, 1–4 raises graded as poor, and zero repetitions graded as nonfunctional. Alternatively, the strength of the soleus can be tested with the patient in prone VIDEO.

hindfoot position. Thus, when the hindfoot everts during the heel-rise task, this is seen as a clinical sign of tibialis posterior weakness. Fibularis (Peroneus) Longus, Fibularis (Peroneus) Brevis, and Fibularis (Peroneus) Tertius Muscles.  VIDEO The lateral compartment muscles and the fibularis (peroneus) tertius muscle VIDEO produce the motion of eversion. The patient is positioned in supine, with the foot over the edge of the table and the ankle in the anatomic position. Resistance is applied to the lateral border of the forefoot (Fig. 21-25). Digits.  Grades for the toes differ from the standard format because gravity is not considered a factor.   0: No contraction.  Trace or 1: Muscle contraction is palpated, but no movement occurs.   Poor or 2: Subject can partially complete the ROM.   Fair or 3: Subject can complete the test range.  Good or 4: Subject can complete the test range but is able to take less resistance on the test side than on the opposite side.  N or 5: Subject can complete the test range and take maximal resistance on the test side as compared with the normal side. Flexor Hallucis Brevis and Longus Muscles. The FHB VIDEO and FHL muscles VIDEO produce MTP joint flexion and IP joint flexion. The foot is maintained in midposition. The first metatarsal is stabilized, and resistance is applied beneath the proximal and distal phalanx of the great toe into toe extension. Flexor Digitorum Brevis and Longus Muscles.  The FDL and brevis muscles produce IP joint flexion. The motion is tested with the foot in the anatomic position. If the gastrocnemius muscle is shortened, preventing the ankle from assuming the anatomic position, the knee is flexed. The toes may be tested simultaneously. The foot is held in the midposition, and the metatarsals are stabilized. Resistance is applied beneath the distal and proximal phalanges VIDEO. Extensor Hallucis Longus and Brevis Muscles.  VIDEO The EHL and the EHB muscles produce the motion of extension

Tibialis Anterior Muscle.  The tibialis anterior muscle produces the motion of dorsiflexion and inversion. The knee must remain flexed during the test to allow complete dorsiflexion. The patient’s foot is positioned in dorsiflexion and inversion. The leg is stabilized, and resistance is applied to the medial posterior aspect of the forefoot into plantar flexion and eversion (Fig. 21-23) VIDEO. Tibialis Posterior Muscle. The tibialis posterior muscle produces the motion of inversion in a plantar flexed position. The leg is stabilized in the anatomic position, with the ankle in slight plantar flexion. The plantar flexion is important to minimize the influence of the tibialis anterior muscle.77 Resistance is applied to the medial border of the forefoot into eversion and dorsiflexion (Fig. 21-24) VIDEO. The standing heel raise test can also be used to detect tibialis posterior weakness. It is thought that during a standing heel rise that the tibialis posterior and fibularis muscles co-contract to control

FIGURE 21-24  Manual muscle testing of the tibialis posterior.

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Lower Leg, Ankle, and Foot

FIGURE 21-23  Manual muscle testing of the tibialis anterior.

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EXAMINATION THE EXTREMITIES

of the IP and MTP joints. The foot is maintained in midposition. Resistance is applied to the posterior aspect of both phalanges of the first digit into toe flexion. Extensor Digitorum Longus and Brevis Muscles. The EDL and the EDB muscles produce the motion of extension at the MTP and IP joints of the lateral four digits from a flexed position VIDEO. Resistance is applied to the posterior (dorsal) surface of the proximal and distal phalanges into toe flexion. Intrinsic Muscles of the Foot.  The intrinsic muscles of the foot are tested with the patient in either the supine or the sitting position. Most subjects are unable to voluntarily contract the intrinsic muscles of the foot individually. Abductor Hallucis Muscle.  The metatarsals are stabilized, and resistance is applied medially to the distal end of the first phalanx VIDEO. Adductor Hallucis Muscle.  The metatarsals are stabilized, and resistance is applied to the lateral side of the proximal phalanx of the first digit VIDEO. Lumbrical Muscles.  The lateral four metatarsals are stabilized, and resistance is applied to the middle and distal phalanges of the lateral four digits. Plantar Interossei Muscles.  The lateral three metatarsals are stabilized, and resistance is applied to the middle and distal phalanges. Posterior (Dorsal) Interossei and Abductor Digiti Minimi Muscles.  The metatarsals are stabilized, and resistance is applied: Posterior (Dorsal) interossei.  To the middle and distal phalanges. ▶▶ Abductor digiti minimi.  To the lateral side of the proximal phalanx of the fifth digit. ▶▶

Functional Tests Self-Report Measures

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The Ankle Joint Functional Assessment Tool.  The Ankle Joint Functional Assessment Tool (AJFAT) is composed of 12 questions rating the ankle’s functional ability (Table 21-10). The AJFAT questions are based on assessment tools previously used for evaluating the functional level of the knee. The Foot Function Index.  The Foot Function Index (FFI) is a functional outcome measure that consists of three subsections: pain, disability, and activity. Olerud-Molander Ankle Score.  Introduced in 1984, the Olerud-Molander Ankle Score continues to be widely used as a patient-reported outcome among people with ankle fractures. The assessment includes nine parameters: walking, stiffness, swelling, stair climbing, running, jumping, squatting, physical supports, and work capacity. Although this scale is quite practical, it has been criticized for lacking a methodologically robust content foundation and focusing solely on physical symptoms and performance.78 Ankle Fracture Outcome of Rehabilitation Measure (A-FORM).79  This measure, intended to address a notable gap in the patient-reported outcome measures currently

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available, was developed as a condition-specific, patientreported outcome measure that reported life impacts following ankle fractures. The framework assesses eight life impacts: physical, psychological, daily living, social, occupational or domestic, financial, anesthetic, and medication taking. Foot and Ankle Ability Measure. The Foot and Ankle Ability Measure (FAAM) is a region-specific instrument designed to assess activity limitations and participation restrictions for individuals with general musculoskeletal foot and ankle disorders, including those who have sustained an ankle sprain.80 The FAAM consists of the 21-item activities of daily living (ADL) subscale and separately scores the 8-item sports subscale. The FAAM has been found to have strong evidence for content validity, construct validity, test retestreliability, and responsiveness for general musculoskeletal foot and ankle disorders.81 Foot and Ankle Outcome Score (FAOS).82  The FAOS was developed to assess the patient’s opinion about a variety of foot and ankle related problems including lateral ankle instability, Achilles tendinosis, and plantar fasciitis. It consists of 5 subscales; pain, other symptoms, function in daily living, function in sport and recreation, and foot and ankle-related quality of life with each question getting a score from 0 to 4. Foot and Ankle Disability Index. This questionnaire, which is a former version of the FAAM, is identical to the FAAM with the exception of an additional five items, four of which assess pain, with the other questioning an individual’s ability to sleep. These five items were subsequently removed after factor analysis and item response theory analysis,81 and is now comprised of the 26-item ADL and 8-item sports subscales.1 The VISA-A Questionnaire.83  This questionnaire has been touted as a valid and reliable index of the clinical severity of Achilles tendinopathy. It has been found to have good testretest (r = 0.93), intrarater (three tests, r = 0.90), and interrater (r = 0.90) reliability as well as good stability when compared 1 week apart (r = 0.81).83 Cumberland Ankle Instability Tool (CAIT).84  The CAIT is a 9-item 30-point scale, for measuring severity of functional ankle instability (FAI). A score of ≤27/30 on the CAIT is interpreted as indicating presence of FAI. Identification of Functional Ankle Instability (IdFAI).85  The IdFAI is a questionnaire to detect whether individuals meet the minimum criteria necessary for inclusion in an FAI population. A score of ≥10 out of 37 for this test indicates the presence of FAI.

Physical Performance Tests Weight-Bearing Tests In weight-bearing, with the feet fixed, the patient should be asked to perform the following while the clinician notes any reproduction of pain or abnormal motion: ▶▶

Range-of-motion.  Ankle dorsiflexion is necessary for normal gait, climbing stairs and rising from a squatting position. The dorsiflexion lunge test can be used to assess functional dorsiflexion. This weight-bearing test

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Ankle Joint Functional Assessment Tool (AJFAT)   7.  How would you describe your ankle’s ability when you jog?   _______(0) Much less than the other ankle   _______(1) Slightly less than the other ankle   _______(2) Equal in amount to the other ankle   _______(3) Slightly more than the other ankle   _______(4) Much more than the other ankle   8. How would you describe your ankle’s ability to “cut,” or change direction, when running?   _______(0) Much less than the other ankle   _______(1) Slightly less than the other ankle   _______(2) Equal in amount to the other ankle   _______(3) Slightly more than the other ankle   _______(4) Much more than the other ankle   9.  How would you describe the overall activity level of your ankle?   _______(0) Much less than the other ankle   _______(1) Slightly less than the other ankle   _______(2) Equal in amount to the other ankle   _______(3) Slightly more than the other ankle   _______(4) Much more than the other ankle 10. Which statement best describes your ability to sense your ankle beginning to “roll over”?   _______(0) Much later than the other ankle   _______(1) Slightly later than the other ankle   _______(2) At the same time as the other ankle   _______(3) Slightly sooner than the other ankle   _______(4) Much sooner than the other ankle 11. Compared with the other ankle, which statement best describes your ability to respond to your ankle beginning to “roll over”?   _______(0) Much later than the other ankle   _______(1) Slightly later than the other ankle   _______(2) At the same time as the other ankle   _______(3) Slightly sooner than the other ankle   _______(4) Much sooner than the other ankle 12. Following a typical incident of your ankle “rolling,” which statement best describes the time required to return to activity?   _______(0) More than 2 days   _______(1) 1–2 days   _______(2) More than 1 hour and less than 1 day   _______(3) 15 minutes to 1 hour   _______(4) Almost immediately

Lower Leg, Ankle, and Foot

  1. How would you describe the level of pain you experience in your ankle?   _______(0) Much more than the other ankle   _______(1) Slightly more than the other ankle   _______(2) Equal in amount to the other ankle   _______(3) Slightly less than the other ankle   _______(4) Much less than the other ankle   2.  How would you describe any swelling of your ankle?   _______(0) Much more than the other ankle   _______(1) Slightly more than the other ankle   _______(2) Equal in amount to the other ankle   _______(3) Slightly less than the other ankle   _______(4) Much less than the other ankle   3. How would you describe the ability of your ankle when walking on uneven surfaces?   _______(0) Much less than the other ankle   _______(1) Slightly less than the other ankle   _______(2) Equal in ability to the other ankle   _______(3) Slightly more than the other ankle   _______(4) Much more than the other ankle   4. How would you describe the overall feeling of stability of your ankle?   _______(0) Much less stable than the other ankle   _______(1) Slightly less stable than the other ankle   _______(2) Equal in stability to the other ankle   _______(3) Slightly more stable than the other ankle   _______(4) Much more stable than the other ankle   5. How would you describe the overall feeling of strength of your ankle?   _______(0) Much less strong than the other ankle   _______(1) Slightly less strong than the other ankle   _______(2) Equal in strength to the other ankle   _______(3) Slightly stronger than the other ankle   _______(4) Much stronger than the other ankle   6. How would you describe your ankle’s ability when you descend stairs?   _______(0) Much less than the other ankle   _______(1) Slightly less than the other ankle   _______(2) Equal in amount to the other ankle   _______(3) Slightly more than the other ankle   _______(4) Much more than the other ankle

EXAMINATION

TABLE 21-10

Reproduced with permission from Rozzi SL, Lephart SM, Sterner R, et al. Balance training for persons with functionally unstable ankles. J Orthop Sports Phys Ther. 1999 Aug;29(8):478–486.

is performed by placing the foot perpendicular to a wall and lunging the knee toward the wall. The heel should not be lifted off from the floor, and the subtalar joint should be locked. The foot is sequentially moved further away from the wall until the maximum range of dorsiflexion is achieved. The distance from the foot to the wall is measured; less than 9–10 cm is considered restricted. The angle of the tibial shaft in reference to the wall is also measured; less than 35–38 degrees is restricted. ▶▶ Single leg stance.  Chronic ankle instability is a frequent consequence after lateral ankle sprain. The inability

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to maintain quiet stance during single standing has consistently been shown to be associated with ankle instability. ▶▶ Gait assessment.  An observational movement analysis of gait (see Chapter 6) can provide the clinician with information about the movement strategy used to complete a weight-bearing task. Typically, the gait analysis is first performed grossly before being followed by a joint by joint review during each phase of the gait cycle. ▶▶ Weight-bearing on the foot borders.  The patient is asked to bear weight on the medial borders of the feet while

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EXAMINATION THE EXTREMITIES

keeping the knees extended. The patient is then asked to bear weight on the lateral borders of the feet while maintaining the knee extension. ▶▶ Heel-raising.  In addition to being a general screening test, heel raising also assesses the ability of the medial arch to increase and produce a supinated/inverted arch. Under normal conditions, the tibialis posterior tendon inverts the hindfoot as the patient raises their heel. With poor or absent tibialis posterior function, the patient just rolls on the outside of the foot and demonstrates a decreased ability to unilaterally raise the heel. ▶▶ Twisting of the lower leg.  Twisting tests the ability of the foot to supinate on the ipsilateral side, and its ability to pronate on the contralateral side. The results of these tests may not be helpful in forming an actionable diagnosis, but they may be the only way to reproduce the patient’s symptoms and will, therefore, be of use in the formation of a diagnosis.

Running Tests Return to activity tests for the running athlete can include any of the following: 40 m run time. The patient is asked to run 40 m in a straight line, and the run is timed. ▶▶ Figure-8 run. Two or more cones are set out at about 10–15 feet apart. The patient stands beside one of the cones to begin so that the distant cone is to the side of the patient. The patient is instructed to face the same direction throughout the exercise while running sideways from the near side of one cone to the far side of the other, looping around the cones as a figure-8. The patient should keep the hips slightly flexed, and move on the balls of the feet, as quickly as possible. After running the figure-8 pattern in one direction for at least 30 seconds, the patient then reverses the direction whilst still facing in the same direction. ▶▶

▶▶

Square hop. A 2×2 foot square is marked out on the floor. Each of the four corners of the square is given a number from 1 to 4. The patient is asked to stand in the middle of the square on one leg and is then asked to jump to the corners of the square corresponding to the number sequence that the clinician calls out, returning to the center after each hop. For example, if the clinician calls out the sequence 1-3-2-4, the patient hops to corner number one, then hops back to the middle. The patient then hops to corner number three and back to the middle, and so on, ending with corner number four.

Star Excursion Balance Test The star excursion balance test (SEBT) is a clinical test purported to detect functional performance deficits in unilateral balance and dynamic neuromuscular control associated with lower extremity pathology in otherwise healthy individuals.86 The SEBT consists of a series of lower extremity reaching tasks in directions that challenge subjects’ postural control, strength, ROM, and proprioceptive abilities. The farther a subject can reach with one leg while balancing on the opposite leg, the better the functional performance they are deemed to have. The subject stands barefoot at the center of the grid with eight lines extending in a star pattern at 45-degree increments from the center of the grid.87 Subjects are asked to maintain a singleleg stance while reaching with the contralateral leg to touch as far as possible along the chosen line, and then to return to a bilateral stance while maintaining their equilibrium.87 The test is then repeated using the other leg.

Agility T-Test The qualities required for agility include physical demand, cognitive processing, and technical skill. The agility T-test measures movement in multiple directions as the individual navigates a T-shaped course, which consists of horizontal and longitudinal arms that are each 10 yards long (Fig. 21-26).

Hopping Tests

10 Yards

For those athletes returning to activities that require such factors as multiple changes in directions, cutting, and jumping/ landing, the following series of hopping tests can be used: Single-limb hop for distance (see Chapter 20). ▶▶ Triple hop (see Chapter 20). ▶▶ Crossover hop (see Chapter 20). ▶▶ Stair hop (see Chapter 20). ▶▶ Side to side hop (see Chapter 20). ▶▶ 6-m crossover hop. The test is performed as follows: the patient places his or her feet on one side of a white line or tape. A mark is made on the line/tape to indicate 6 m. The patient is asked to stand on one leg to the right of the line/ tape. The patient is then asked to jump, on one leg, to the left side of the line/tape, back to the right, and then back to the left, attempting to propel himself or herself as far forward as possible with each hop until they 6-m mark is reached. The performance is timed. ▶▶

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10 yards

Finish

Start

The Agility T-Test

FIGURE 21-26  Agility T-test.

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Sargent/Vertical Jump Test

TABLE 21-11

Efficiency index = weight (lb) × jump (in)/height (in).

Functional Examination Functional assessment of the ankle foot can be accomplished using gait analysis (see Chapter 6). Specifically related to the dysfunction of the ankle and foot are those listed in Table 21-11.

Passive Articular Mobility Passive articular mobility tests assess the accessory motions available between the joint surfaces. These same techniques

Potential Causes of Gait Dysfunction

Phase of gait

Observed Dysfunction

Probable Cause(s)

Initial contact

Low heel/flatfoot/forefoot

Limited ankle dorsiflexion Short step length

Loading response

Rapid ankle plantar flexion

 

Excessive foot pronation

 

Limited foot pronation

Limited ankle plantar flexion Ankle dorsiflexor muscle weakness Limited eccentric control of the knee extensors Excessive midfoot mobility Excessive hindfoot mobility Rigid pes planus deformity Limited eccentric control of the hip abductor and external rotator muscle groups Limited midfoot mobility Limited hindfoot mobility Rigid pes cavus deformity

Mid stance

Limited tibial progression

 

Limited foot pronation

 

Excessive foot pronation

Terminal stance

Limited trailing limb posture

Limited ankle dorsiflexion range of motion Limited eccentric control of the ankle plantar flexor muscles Limited knee extension range of motion Limited hip extension range of motion

Preswing

Limited ankle plantar flexion

Limited ankle plantar flexion range of motion Limited knee extension range of motion Limited knee flexion range of motion Limited hip extension range of motion

Initial swing

Limited foot clearance

Limited ankle dorsiflexion range of motion Concentric weakness of the ankle dorsiflexors Limited knee flexion range of motion

Limited ankle dorsiflexion range of motion Limited eccentric control of the ankle plantar flexor muscles Limited midfoot mobility Limited hindfoot mobility Rigid pes cavus deformity Excessive midfoot mobility Excessive hindfoot mobility Rigid pes planus deformity

Reproduced with permission from Davenport TE. Examination of the Foot and Ankle IN Hughes C: Independent Home Study Course 22.3.3: Foot and Ankle. La Crosse, WI: Orthopedic Section, APTA; 2014.

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Lower Leg, Ankle, and Foot

The Sargent jump test is designed to evaluate strength, speed, energy, and dexterity and to estimate power jumps. The individual squats and jumps upward into full extension; reaching

with one hand for a cardboard disk above.89 The distance jumped is calculated using the following equation:

EXAMINATION

The patient sprints from the base of the longitudinal arm to the center of the horizontal arm and then, facing forward, he or she sidesteps to one end of the horizontal arm without crossing feet, and then continues to the other end. To finish, he or she sidesteps back to the center of the horizontal arm and runs backward down the longitudinal limb to the starting point (Fig. 21-26). Typical times for athletic adults are between 8.92 and 13.5 seconds.88

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EXAMINATION

can be used to increase joint play using the varying grades of mobilization (see “Joint Mobilizations” in Techniques to Increase Joint Mobility). As with any other joint complex, the quality and quantity of joint motion must be assessed to determine the level of joint involvement. The joint play movement tests must be performed on both sides so that comparisons can be made. The patient is positioned in lying.

Distal Tibiofibular Joint THE EXTREMITIES

During ankle dorsiflexion, the fibula is thought to glide superiorly at the proximal tibiofibular joint and the tibia and fibula are thought to glide superiorly and separate slightly at the distal tibiofibular joint, while the talus is thought to glide posteriorly under the tibiofibular mortise.1 Although the glide at this joint would appear to be negligible, Mulligan has proposed that some ankle inversion injuries may be the result of a distal fibular positional fault. To perform the mobility tests of this joint, the patient is placed in supine, and the clinician grips the tibia and fibula using one hand for each (Fig. 21-27). While one hand prevents downward motion of the medial malleolus, the other hand glides the fibula anteriorly and posteriorly in relation to the tibia. To assess the motion of the tibial component, one hand stabilizes the fibula and lateral malleolus, while the other hand glides the tibia anteriorly and posteriorly in relation to the fibula. Theoretically, a superior and inferior glide can be assessed at this joint, but it is unclear whether the information provided by such testing would help the clinician in making a diagnosis or designing a plan of care.

Long-Axis Distraction of Ankle and Foot

of the talus assesses the joint’s ability to move into plantar flexion, whereas the posterior glide of the talus assesses the joint’s ability to move into dorsiflexion. The anterior–posterior glides can also be applied to the midtarsal (Fig. 21-34), intertarsal (Figs. 21-35 and 21-36), MTP (Fig. 21-37), and IP (Fig. 21-38) joints.

Calcaneal Inversion–Eversion (Subtalar)

To test the anterior glide of the talocrural joint, the clinician stabilizes the tibia and fibula and draws the talus and foot forward together (Fig. 21-32). Pushing the talus and foot together in a posterior direction on the tibia and fibula (Fig. 21-33) tests the posterior movement. The anterior glide

Subtalar joint motion is extremely important to normal foot function. A loss of eversion causes weight-bearing to occur along the lateral side of the ankle joint. The patient lies in the prone position with the knee slightly flexed and supported by a pillow, while the clinician stands at the foot of the table, facing the patient. The clinician grasps the calcaneus in one hand while the other hand locks the talus. The calcaneus is passively inverted (varus) and everted (valgus) on the talus (Fig. 21-39). The amount and quality of the motions as compared with the other foot are noted. Although some differences exist, generally calcaneal eversion will measure 5–10 degrees while calcaneal inversion will measure approximately

FIGURE 21-27  Mobility testing of the distal tibiofibular joint.

FIGURE 21-29  Long-axis distraction of subtalar joint.

The clinician stabilizes the proximal segment and applies traction to the distal segment. This test is performed at the talocrural joint (Fig. 21-28), the subtalar joint (Fig. 21-29), the MTP joints (Fig 21-30), and the IP joints (Fig 21-31).

Anterior–Posterior Glide

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FIGURE 21-28  Long-axis distraction of talocrural joint.

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EXAMINATION

FIGURE 21-33  Posterior glide of the talocrural joint.

FIGURE 21-31  Long-axis distraction of the IP joint.

FIGURE 21-34  A-P glide of mid-tarsal joints.

FIGURE 21-32  Anterior glide of the talocrural joint.

FIGURE 21-35  A-P glide of intertarsals.

Lower Leg, Ankle, and Foot

FIGURE 21-30  Long-axis distraction of the MTP joint.

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EXAMINATION THE EXTREMITIES

FIGURE 21-36  A-P glide of intertarsals.

FIGURE 21-38  A-P glide of IP joints.

20–30 degrees. A similar technique can be used to assess medial and lateral gapping at this joint. Medial gapping is associated with subtalar joint eversion, whereas lateral gapping is associated with subtalar joint inversion.

and locks the third to evaluate the second. The quantity and quality of motion are noted and compared with the other side.

Transverse Tarsal Joint Complex Motion

Special tests are merely confirmatory tests and should not be used alone to form a diagnosis. Selection for their use is at the discretion of the clinician and is based on a complete patient history. The results of these tests are used in conjunction with the other clinical findings. To assure accuracy with these tests, both sides should be tested for comparison.

The rotational movements of the transverse tarsal joint complex, which allow the forefoot to twist on the hindfoot, can be observed in the non–weight-bearing position. The clinician stabilizes the calcaneus with one hand while inverting and everting the foot at the transverse tarsal joint complex with the other hand (Fig. 21-40).39

First MTP Joint (First Ray) Motion The patient lies in the supine position, with the clinician at the foot of the table facing away from the patient. The clinician grasps and locks the first MTP joint, before grasping the great toe and moving it into extension and flexion (posteriorly [dorsally] and anteriorly [ventrally], respectively) (Fig. 21-41). Long-axis distraction and compression can also be applied (Fig. 21-42) to assess capsular and articular integrity, respectively. The limited range may result from a combination of biomechanical factors such as excessive pronation or joint glide restriction. To examine the conjunct rotation of the metatarsals, the clinician locks the second metatarsal to evaluate the first

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FIGURE 21-37  A-P glide of MTP.

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Special Tests

Assessing Ankle Girth As many foot and ankle pathologies are associated with quantifiable edema that may be associated with disablement, physical therapists need a reliable method by which

FIGURE 21-39  Calcaneal inversion and eversion.

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EXAMINATION to measure ankle girth following injury so that there can be clinical quantification of the volume of edema. Two methods are described: Figure-of-eight tape method.  The patient lies in the supine position or seated with the ankle to be measured in a neutral or comfortable position. The clinician places the zero endpoint of a tape measure midway between the tibialis anterior tendon and lateral malleolus. The tape is then drawn medially and is placed just distal to the navicular tuberosity. The tape is then pulled medially around the foot to then cross the plantar aspect (arch) toward the base of the fifth metatarsal. The tape is then pulled across the tibialis anterior tendon and around the ankle to a point just distal to the medial malleolus, before being finally pulled across the Achilles tendon and placed just distal to the lateral malleolus and across the start of the tape. It has been reported that the ankle figureof-eight method (Fig. 21-43) demonstrates very high inter- and intrarated reliability (ICC = 0.98–0.99).90–92 ▶▶ Volumetry method.  This is a direct measure of the volume of the foot and ankle through measurement of displaced water. A volumeter, which is a clear acrylic box measuring 32.5 cm × 12.5 cm × 22.5 cm is filled with a known volume of water, and the patient’s foot is placed into the volumeter with toe tips touching the front wall. As the patient’s foot enters the box, water flows from the spout in the box into a graduated cylinder. The amount of water displaced is measured. ▶▶

FIGURE 21-40  Mobility testing midtarsal inversion/eversion.

FIGURE 21-41  First MTP motion.

Lower Leg, Ankle, and Foot

FIGURE 21-43  Figure-of-eight tape method.

Ligamentous Stress Tests The examination of the ligamentous structures in the ankle and foot is essential, not only because of their vast array but also because of the amount of stability that they provide. Positive results for the ligamentous stability tests include excessive movement, as compared with the same test on the uninvolved extremity, pain (depending on the severity), or apprehension.

FIGURE 21-42 Long-axis distraction and compression at the first MTP joint.

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Mortise/Syndesmosis Cotton (Clunk) Test.  The patient lies in the supine position with their foot over the end of the bed. One hand is used to

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EXAMINATION THE EXTREMITIES

FIGURE 21-45  Kleiger (external rotation) test.

FIGURE 21-44  Cotton (Clunk) test.

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stabilize the distal leg on the bed while the clinician uses the other hand to grasp the heel and move the calcaneus laterally (see Fig. 21-44).93 A clunk can be felt as the talus hits the tibia and fibula if there has been significant mortise widening. Kleiger (External Rotation) Test. The Kleiger (external rotation) test is a general test to implicate the syndesmosis if pain is produced over the anterior or posterior tibiofibular ligaments and the interosseous membrane, but can also be used to assess the integrity of the medial (deltoid) ligament of the ankle complex. If this test is positive, further testing is necessary to determine the source of the symptoms. The patient sits with their legs dangling over the end of the bed; the knee flexed to approximately 90 degrees, and the foot relaxed. The clinician stabilizes the lower leg with one hand and, using the other hand, grasps the foot and externally rotates it (Fig. 21-45). Pain experienced at the anterolateral aspect of the distal tibiofibular syndesmosis is a positive sign for syndesmosis injury, whereas pain on the medial aspect of the ankle and/or displacement of the talus from the medial malleolus (depending on severity) with the ankle positioned in plantar flexion may indicate a tear of the medial (deltoid) ligament of the ankle. The Point Test.  The point test also referred to as the palpation test, is used to impose pressure on the anterior distal tibiofibular syndesmosis.94,95 The patient can be positioned in supine or sitting. The clinician applies pressure directly to the anterior aspect of the distal tibiofibular syndesmosis (Fig. 21-46). Pressure is applied gradually, and a positive test involves a report of pain by the patient.

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The Dorsiflexion Compression Maneuver. The dorsiflexion compression maneuver is performed to force the wider anterior portion of the talar dome into the ankle mortise, thereby inducing separation of the distal fibula and tibia. The patient sits at the edge of the examination table, and the clinician stabilizes the patient’s leg with one hand, while the clinician’s other hand passively moves the foot into dorsiflexion (Fig. 21-47). Pain experienced at the distal tibiofibular syndesmosis is a positive test result. A variation of the dorsiflexion maneuver exists, known as the dorsiflexion compression test, which involves patients moving their ankle joints into extreme dorsiflexion in bilateral weight-bearing. Patients are asked to note the pain they experience in this position and the position of the tibia is noted with an inclinometer. The patient then assumes an upright position and the clinician applies medial–lateral compression with two hands on the malleoli of the injured leg. The clinician maintains the medial–lateral compression, as the patient is asked to move the ankles into dorsiflexion again and to report if the endrange pain has changed compared with the previous movement. A positive test result is either a reported reduction in the end-range pain or an increase in dorsiflexion ROM. Fibula Translation Test.  The patient is placed in the side-lying position with the tested leg uppermost. The clinician applies an anterior and posterior force on the fibula at the level of the syndesmosis (Fig. 21-48). A positive test is a pain during translation and more displacement of the fibula than the compared side.

FIGURE 21-46  The point test.

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EXAMINATION

Although a cadaver study by Beumer et al.96 found this test to have a sensitivity of 82% and specificity of 88% (LR+ 6.8; LR− 0.2), the study only found increased translation when all ligaments were removed in the cadavers. The One-Legged Hop Test.  The one-legged hop test is performed by having the patient stand on the injured leg and hop continuously.95 Nussbaum et al.97 reported that patients with syndesmosis injuries could not complete 10 repetitions of unilateral hopping without significant pain. However, the one-legged hop test should be used with caution, and perhaps only if the other special tests are negative because performing this test may impose further separation of the distal tibiofibular syndesmosis.95 The Crossed-Leg Test.  The crossed-leg test mimics the squeeze test (see later) and attempts to induce separation of the distal

FIGURE 21-48  Fibula translation test.

FIGURE 21-49  The crossed-leg test.

syndesmosis.95,98 The patient sits in a chair, with the injured leg resting across the knee of the uninjured leg. The resting point should be at approximately mid-calf. The clinician then applies a gentle force on the medial aspect of the knee of the test leg (Fig. 21-49). Pain experienced in the area of the distal syndesmosis suggests the presence of injury. This test may not be useful for patients with knee or hip pathology because it may be difficult for them to assume the test position. Reliability and validity data for this test are not yet available. The Heel-Thump Test.  The heel-thump test is performed to force the talus into the mortise, in an attempt to impose a separation of the distal syndesmosis.95,99 The patient lies at the edge of the examination table, with the ankle resting in plantar flexion. The clinician holds the patient’s leg with one hand and with the other hand applies a gentle but firm thump on the heel with their fist (Fig. 21-50). This force is applied at the center of the heel and in line with the long axis of the tibia. Pain experienced at the distal tibiofibular syndesmosis

Lower Leg, Ankle, and Foot

FIGURE 21-47  The dorsiflexion compression maneuver.

FIGURE 21-50  The heel-thump test.

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EXAMINATION THE EXTREMITIES 1074

FIGURE 21-51  Posterior drawer test.

suggests the presence of injury. Although the heel thump test has been recommended to help differentiate between a syndesmotic sprain and a lateral ankle sprain, this test may not be specific for a syndesmotic sprain as the test has also been recommended to assess the possible presence of tibial stress fractures.100 Reliability and validity data for this test are not yet available. Posterior Drawer Test.  The posterior drawer test can also be used to test for the presence of instability at the distal tibiofibular joint. The patient is supine. The hip and knee are flexed to provide as much dorsiflexion of the ankle as possible. This drives the wide anterior part of the talus back into the mortise. An anterior stabilizing force is then applied to the cruris, and the foot and talus are translated posteriorly (Fig. 21-51). If the distal tibiofibular joint is stable, there will be no drawer available, but if there is instability, there will be a drawer. Squeeze Test.  In the squeeze test, the patient lies in supine or side-lying position and the clinician squeezes the lower third of the leg at a point just above the ankle (Fig. 21-52). Pain felt in the distal third of the leg may indicate a compromised syndesmosis (high ankle sprain), if the presence of a tibia and/ or fibula fracture, calf contusion, or compartment syndrome (see Chapter 5) has been ruled out.

FIGURE 21-52  Squeeze test.

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FIGURE 21-53  Calcaneus tilt.

Lateral Collaterals  The lateral collateral ligaments of the ankle resist inversion. An additional function is to prevent excessive varus movement, especially during plantar flexion. In extreme plantar flexion, the mortise no longer stabilizes the broader anterior part of the talus, and varus movement of the ankle is then possible. Calcaneus Tilt.  The patient lies in the supine position. The lower leg is stabilized using a lumbrical grip while the other hand grasps the foot and calcaneus. The clinician applies a medially directed force in an attempt to adduct the calcaneus, thereby gapping the lateral side of the ankle (Fig. 21-53). Pain on the lateral aspect of the ankle with this test, and/or displacement (depending on severity) may indicate a sprain of the ligament. Talar Tilt.  This test is used to determine whether the CFL is torn. The patient lies in a supine or side-lying position with the foot relaxed and the knee flexed. The clinician places the foot in the anatomical (90 degrees) position to bring the CFL perpendicular to the long axis of the talar. The talus is then tilted from side to side into adduction and abduction (Fig. 21-54). Adduction tests the CFL and, to some degree, the ATFL, whereas abduction stresses the deltoid ligament. No diagnostic accuracy studies have been performed to determine the sensitivity and specificity of this test. Anterior Drawer Test.  The anterior drawer stress test is performed to estimate the stability of the ATFL. The test is performed with the patient seated at the end of the bed or lying

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FIGURE 21-55  Anterior drawer test.

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Tendon Tests Thompson (Calf-Squeeze) Test for Achilles Tendon Rupture In this test, the patient lies in the prone position or in kneeling with the feet over the edge of the bed (Fig. 21-56). With the patient relaxed, the clinician gently squeezes the calf muscle and observes for the production of plantar flexion. An absence of plantar flexion indicates a complete rupture of the Achilles tendon. One study demonstrated that this test demonstrated the strongest sensitivity, specificity, positive likelihood ration, and negative likelihood ration, indicating that it is currently the best test to both screen for and confirm a diagnosis of Achilles tendon rupture.70

Lower Leg, Ankle, and Foot

supine with their knee flexed, to relax the gastrocnemius– soleus muscles, and the foot supported perpendicular to the leg. The clinician uses one hand to stabilize the distal aspect of the leg, while the other hand grasps the patient’s heel and positions the ankle in 10–20 degrees of plantar flexion (Fig. 21-55). Either the heel is very gently pulled forward, or the clinician can manually apply a posterior force on the tibia. The clinician attempts to visually and manually assess the quantity of talar movement and to determine if an asymmetry exists between the involved and the uninvolved ankle. If the test is positive, the talus, and with it the foot, rotates anteriorly out of the ankle mortise around the intact medial (deltoid) ligament of the ankle, which serves as the center of rotation. Variances in hand position, joint congruency, forces imparted, the perception of movement, scoring methods, and tissue variability are factors that may affect the reliability of this test.101 It has been reported that 4 mm of laxity in the ATFL, resulting from posttraumatic attenuation or fibrosis, will give a clinically apparent anterior drawer (2 mm is normal)— false-positive findings may be seen in up to 19% of uninjured ankles in those with ligamentous laxity.102,103 As is often the case, when combining the results from several tests, diagnostic accuracy can be enhanced. For example, a 2013 study by Croy et al.102 reported that when the combination of pain on lateral ligament palpation, hematoma formation of the lateral ankle, and a positive anterior drawer test were used a lateral ligament lesion was correctly diagnosed in 95% of cases.

EXAMINATION

FIGURE 21-54  Talar tilt.

The Dimple Sign.  Another positive sign for a rupture of the ATFL, if pain and spasm are minimal, is the presence of a dimple located just in front of the tip of the lateral malleolus during the anterior drawer test. This results from a negative pressure created by the forward movement of the talus, which draws the skin inwards at the site of the ligament rupture. This dimple is also seen with a combined rupture of the ATFL and CFLs. However, the dimple is only present within the first 48 hours after injury, due to organized hematoma and repair tissue blocking the communication between the joint and the subcutaneous tissues. Medial Collaterals (Deltoid Complex)  The medial collaterals function to resist eversion. Given their strength, these ligaments are usually only injured as the result of a major trauma.

Arc Test This test is used when there is a palpable swelling in the calf area to help determine the difference between a pure tendinopathy and swelling of the paratenon. The patient lies in the prone position or in kneeling with the feet over the edge of the bed (Fig. 21-56). While palpating the swelling, the clinician passively moves the foot/ankle into dorsiflexion and plantar

FIGURE 21-56  Patient position for the Thompson test.

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EXAMINATION THE EXTREMITIES

flexion. A swelling in the tendon due to pure tendonopathy moves with the tendon on movement of the ankle, while a swelling of the paratenon does not move.104

the test is positive for Achilles tendon rupture (in normal patients, the foot remains in plantar flexion).

Royal London Hospital Test

Articular Integrity Tests

The patient lies in the prone position with the foot over the end of the table, and the clinician stands at the end of the table. The clinician palpates the patient’s symptomatic calf while passively moving the patient’s foot/ankle. The test is positive when tenderness occurs 3 cm proximal to the calcaneus with the ankle in slight plantar flexion, that decreases as the ankle is dorsiflexed.104

Navicular Drop Test

CLINICAL PEARL A 2003 study104 that compared local palpation, the Royal London Hospital test and the arc test for the diagnosis of non-insertional Achilles tendonopathy, found there was no evidence of a difference of the three assessment methods (P > 0.05). However, when the three methods were combined, the overall sensitivity was 0.586 (confidence interval [CI], 0.469–0.741), and the overall specificity was 0.833 (CI, 0.758–0.889).104

Matles Test for Achilles Tendon Rupture The patient lies in the prone position with the foot over the end of the table, and the clinician stands at the end of the table. The patient is asked to actively flex the knee to 90 degrees while the position of the foot is observed throughout the motion (Fig. 21-57). If the foot falls into neutral or slight dorsiflexion,

The navicular drop test is a method to assess the degree to which the talus plantar flexes in space on a calcaneus that has been stabilized by the ground, during subtalar joint pronation. The clinician palpates the position of the navicular tubercle as the patient’s foot is non–weight-bearing but resting on the floor surface, with the subtalar joint maintained in neutral. The clinician then attempts to quantify the amount of inferior displacement of the navicular tubercle, as the patient assumes 50% weight-bearing on the tested foot (relaxed standing). A navicular drop that is greater than 10 mm from the neutral position to the relaxed standing position suggests an excessive medial longitudinal arch collapse of abnormal pronation.

Feiss Line The Feiss line test is used to assess the height of the medial arch, using the navicular position. With the patient non– weight-bearing, the clinician marks the apex of the medial malleolus and the plantar aspect of the first MTP joint, and a line is drawn between the two points (Fig. 21-58). The navicular is palpated on the medial aspect of the foot, and assessment is made of the position of the navicular relative to the imaginary line. The patient is then asked to stand with their feet approximately 3–6 inches apart. In weight-bearing, the navicular normally lies on or very close to the line. If the navicular falls one-third of the distance to the floor, it represents a first-degree flatfoot; if it falls two-thirds of the distance, it represents a second-degree flatfoot; and if it rests on the floor, it represents a third-degree flatfoot. No diagnostic accuracy studies have been performed to determine the sensitivity and specificity of this test.

Longitudinal Arch Angle The longitudinal arch angle (LAA) can be used to classify and measure foot arch posture. One study,105 using digital

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FIGURE 21-57  Matles test for Achilles tendon rupture.

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FIGURE 21-58  Feiss line.

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pedal pulses have been reported as specific but not sensitive for the early detection of peripheral arterial disease in individuals without diabetes mellitus.111 The interrater agreement of pedal pulse palpation has been found to range from fair to good, with reliability being enhanced by the use of standardized bony landmarks to locate the pulses.112

Jack’s Test

This test is used to detect the presence of fascial and ligamentous impairments of the foot. There are two parts to the test: Part 1: The patient is positioned in sitting. Using one hand just proximal to the 1st metatarsal head, the clinician stabilizes the ankle in the neutral position. The clinician then extends the first phalange while allowing the IP joint to flex. A positive test is considered if the passive extension is continued to the end range or until the patient’s pain is reproduced. Part 2: The patient stands on a step with the metatarsal heads just over the edge of the step. The patient is instructed to place equal weight on both feet. The clinician passively extends the first phalange while allowing the IP to flex. A positive test is considered if the passive extension is continued to end range or until the patient’s pain is reproduced.

Drawer Test The drawer test, used to detect second MTP joint pathology (sensitivity, 91.5%; specificity, 99.8%),107 is accomplished by displacing the proximal phalanx dorsally on a stabilized metatarsal head. A positive drawer sign is when there is a 2-mm or 50% dorsal displacement of the MTP joint.

Vascular Status Homans’ Sign This was the traditional test used to detect a deep vein thrombophlebitis (DVT). The patient lies in the supine position with their knee extended. The clinician stabilizes the thigh with one hand and passively dorsiflexes the patient’s ankle with the other. Pain in the calf with this maneuver was considered a positive sign for DVT. However, a positive Homan’s sign has been found to be insensitive, nonspecific, is present in fewer than 30% of documented cases of DVT,108,109 and the performance of the test may increase the risk of producing a pulmonary embolism (PE).

Buerger’s Test The patient is placed in the supine position with the knee extended. The clinician elevates the patient’s leg to approximately 45 degrees and maintains it there for at least 3 minutes. Blanching of the foot is positive for poor arterial circulation, especially if, when the patient sits with the legs over the end of the bed, it takes 1–2 minutes for the limb color to be restored.

Posterior (Dorsal) Pedis Pulse The posterior (dorsal) pedis pulse can be palpated just lateral to the tendon of the EHL over the posterior aspect of the foot (see Fig. 21-14). In individuals with diabetes mellitus, absent pedal pulses may indicate the onset of ischemic changes to the ankle and foot region.110 Diminished or absent

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Windlass Test Lower Leg, Ankle, and Foot

This test is used to assess for the presence of hallux limitus/ rigidus. The patient is positioned in sitting. While stabilizing the heel with one hand, the clinician dorsiflexes the hallux holding it at the IP joint. The clinician then measures the angle created between the hallux and the 1st metatarsal shaft on the medial aspect of the foot. Approximately 65 degrees of movement should be available. If the angle is between 15 and 40 degrees, hallux limitus is present. If the angle is less than 15 degrees, hallux rigidus should be suspected.

Plantar Fasciitis Test

EXAMINATION

imaging, found that static measurements of the LAA strongly predicted dynamic foot arch postures at mid support in running and mid stance in walking. When using a goniometer, measurement landmarks for the LAA include the medial malleolus, navicular tuberosity, and medial aspect of the first metatarsal head. Typical arch posture is defined as having an LAA between 130 and 150 degrees, pes planus as having an arch posture of less than 130 degrees, and pes cavus as having an arch posture of greater than 150 degrees.106

Neurologic Tests The applicable sensory, motor, and reflex tests should be performed if a disorder related to a spinal nerve root (L4–S2) or peripheral nerve is suspected. Although published descriptions of the sensory distributions of the spinal nerve root and peripheral nerves vary substantially, in general, the L4 dermatome involves the medial ankle and dorsum of the first toe, the L5 dermatome involves the lateral aspect of the dorsal surface of the foot and ankle, and the S1 dermatome involves the lateral border of the foot and heel.1 A neurogenic cause of foot pain must be considered in a patient, especially if the pain is refractory. The patient usually complains of pain that is poorly localized, which is aggravated by activity but may also occur at rest. Any difference in sensation between extremities should be noted and can be mapped out in more detail by testing pinprick sensation (Fig. 21-59). The segmental and peripheral nerve innervations are listed in Chapter 3. Common muscle stretch reflexes tested in this area are the Achilles reflex (S1–2) and the posterior tibialis reflex (L4–5). Specific pathologies associated with peripheral nerve entrapment are described in the intervention strategies section. The pathologic reflexes (Babinski and Oppenheim), tested when an upper motor neuron lesion is suspected, are described in Chapter 3.

Morton’s Test The patient is positioned in supine. The clinician grasps the foot around the metatarsal heads and squeezes the heads together. The reproduction of pain with this maneuver indicates the presence of a neuroma or a stress fracture. No diagnostic accuracy studies have been performed to determine the sensitivity and specificity of this test.

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EXAMINATION THE EXTREMITIES

of the ankle when there is bone tenderness in the posterior half of the lower 6 cm of the fibula or tibia and an inability to bear weight immediately after injury. Similarly, if there is bone tenderness over the navicular and/or fifth metatarsal, and an inability to bear weight immediately after injury, then radiographs of the foot are indicated (see Chapter 7). The Bernese ankle rules were developed to improve the identification of a fracture after low-level malleolus and/or midfoot trauma.116 This examination consists of three consecutive steps: indirect fibular stress applied 10 cm proximal to the fibular tip, direct medial malleolar stress, and simultaneous compression of the midfoot and hindfoot. In a prospective cohort of 364 patients who had sustained a low-energy supination-type injury, sensitivity and specificity were 1.0 and 0.91, respectively.116 Other imaging techniques include arthrography, fibular (peroneal) tenography, and magnetic resonance imaging (MRI). FIGURE 21-59  Sensory testing using pinprick.

Tinel’s Sign The posterior tibial nerve may be tapped behind the medial malleolus (Fig. 21-60). Tingling or paresthesia with this test is considered a positive finding.

Dorsiflexion-eversion Test The dorsiflexion eversion test113 can be used to help determine if the patient’s symptoms are the result of entrapment of the posterior tibial nerve (tarsal tunnel syndrome [TTS]). To perform the test, the clinician places the patient’s foot and ankle in maximal dorsiflexion and eversion with the MTP joints in extension. This position is held for 5–10 seconds, and any reproduction of symptoms indicates a positive test. A study by Alshami et al.114 reported that the dorsiflexioneversion test is more sensitive when performed in combination with hip flexion and knee extension.

Imaging Studies Radiography According to the Ottawa rules for ankle X-rays (with Buffalo modifications),115 X-rays are indicated to rule out fracture

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FIGURE 21-60  Tinel’s sign.

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Outcome Measures Outcome measures for this region include the FAAM,80 the Foot and Ankle Disability Index (FADI), the Lower Extremity Functional Scale (LEFS), the Sports Ankle Rating System,117 the AJFAT, the Chronic Ankle Instability Scale,118 and the FFI. FAAM. This is a region specific instrument designed to assess activity limitations and participation restrictions for individuals with general musculoskeletal foot and ankle disorders. It consists of the 21-item ADL and separately scored 8-item sports subscales. The FAAM has strong evidence for content validity, construct validity, test-retest reliability, and responsiveness with general musculoskeletal foot and ankle disorders.81 There is also evidence for validity in those with chronic ankle instability.119 ▶▶ FADI. This is a former version of the FAAM, and the two instruments are identical, with the exception of an additional five items found on the FADI. Four of these items assess pain, and the other item assesses an individual’s ability to sleep.16 ▶▶ LEFS. This is a broad region-specific measure appropriate for individuals with musculoskeletal disorders of the hip, knee, ankle, or foot. The LEFS consist of 20 items that assess activity limitations and participation restrictions. ▶▶ Sports Ankle Rating System. This was developed as a region specific measure consisting of both self-reported and clinician completed outcome measures. It consists of the quality-of-life measure, clinical rating score, and single assessment numeric evaluation. ▶▶ AJFAT. This is a region specific instrument that contain six items generally related to impairment and six generally related to activity.16 ▶▶ Chronic Ankle Instability Scale. This is designed to quantify the multidirectional profile of patients with chronic ankle instability. It contains four subscales with a total of 14 items. The subscales are defined as impairment, disability, participation, and emotion. ▶▶ Foot Health Status Questionnaire (FHSQ). ▶▶

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THE EVALUATION Following the examination, and once the clinical findings have been recorded, the clinician must determine a specific diagnosis or a working hypothesis, based on a summary of all of the findings. This diagnosis can be structure related (medical diagnosis) (Table 21-12) or a diagnosis based on the preferred practice patterns as described in the Guide to Physical Therapist Practice.

Due to the incorporated nature of the foot and ankle structures in functional activities, the rehabilitation of this region is best organized around a common framework. The techniques to increase joint mobility and the techniques to increase soft-tissue extensibility are described in the “Therapeutic Techniques” section.

Acute Phase The goals during the acute phase include: decreasing pain, inflammation, and swelling; ▶▶ protecting the healing area from reinjury; ▶▶ re-establishing pain-free ROM; ▶▶ preventing muscle atrophy; ▶▶ increasing weight-bearing tolerance; ▶▶ increasing neuromuscular control; ▶▶ maintaining fitness levels; ▶▶ attaining patient independence with a home-exercise program. ▶▶

The control of pain, inflammation, and swelling is accomplished by applying the principles of POLICE (protection, optimal loading, ice, compression, and elevation—see Chapter 8). Icing for 20–30 minutes several times a day, concurrent with nonsteroidal antiinflammatory drugs (NSAIDs) can aid in reducing pain and swelling. The injured ankle should be positioned and supported in the maximum amount of dorsiflexion allowed by pain and effusion. Maximal dorsiflexion places the joint in its closepacked position or position of greatest congruency. This allows for the least capsular distention and resultant joint effusion. With ankle sprains, this position produces an approximation of the torn ligament ends in grade III injuries to reduce the amount of gap scarring and reduces the tension in the grades I and II injured ligaments. The means by which to support or protect the joint during this phase will vary depending on the severity of the injury and the anticipated compliance of the patient to any restrictions placed on them by the physician. For example, mild-tomoderate ankle sprains (grade I and II sprains) can be readily supported by the use of an elastic bandage, open Gibney strapping (with or without felt-pad incorporation), taping,120 or the use of some type of thermoplastic stirrup such as an

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Lower Leg, Ankle, and Foot

INTERVENTION STRATEGIES

Air Cast (see next section). One of the main advantages of this type of immobilization is that pain-free protected plantar flexion and dorsiflexion are possible, whereas inversion and eversion are minimized. To increase ROM, the clinician can perform gentle capsular stretches and grades I–II joint mobilizations. Exercises in this phase include towel stretches VIDEO (Fig. 21-61), ankle circles VIDEO and pumps, VIDEO low-level biomechanical ankle platform system (BAPS) exercises (Fig. 21-62), and active and active assist exercises in straight planes (plantar flexion, dorsiflexion, inversion, and eversion) and proprioceptive neuromuscular facilitation (PNF) planes. Exercises for the foot intrinsics may include toe curl exercises with a towel VIDEO (Fig. 21-63) or having the patient pick up marbles from the floor with their toes and place the marbles in a small container or bowl VIDEO. Isometric exercises within the patient’s pain tolerance and pain-free ROM are initiated for all motions. These exercises are initially performed submaximally at multi-angles, progressing to maximal isometric contractions as tolerated. Mild manual resistive isometrics in all planes may also be started throughout the pain-free range. Active motion and exercise may also be used to effectively increase local circulation and further promote the resorption of any persistent edema. Exercises are progressed to include concentric exercises, once the isometric exercises are pain free. Seated lower extremity closed kinetic-chain exercises (Fig. 21-64) may also be performed during this phase. Each muscle or muscle group should be strengthened with a specific exercise that isolates the muscle or group. Resistance (rubber tubing/bands, weights, isokinetic devices, body weight exercises, etc.) is increased as tolerated. Emphasis should initially be at low resistance and endurance in all pain-free positions. As the program progresses, the joint range is increased from a stress-free position to a more stressful position. As with all exercises, the patient should become an active participant at the earliest opportunity. The exercises learned in the clinic need to be integrated appropriately into a home-exercise regimen. Pain-free weight-bearing, as tolerated, is encouraged with the use of any appropriate support or assistive device, such as taping, a brace, a cane or crutches VIDEO. The use of an assistive device is usually continued until the patient has a pain-free uncompensated gait. Even when using an assistive device, pain-free ankle motion during the normal gait cycle and as normal a gait as possible continues to be encouraged VIDEO. Specific joint mobilization techniques and muscle stretching are initiated to begin to increase ROM.

Bracing Braces can play an important role in both the initial intervention and prevention of ankle injuries. Acutely, their role is to compress, protect, and support the ankle. They also function to limit ROM of the injured ankle, most importantly plantar flexion, and inversion, which is a precarious position for the sprained ankle. Functional braces that provide medial–lateral stabilization such as the Air Cast (Air Cast, Inc., Summit, NJ) also

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THE EXTREMITIES

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TABLE 21-12

Differential Diagnosis of Common Causes of Leg, Foot, and Ankle Pain Patient Mechanism of Age Injury

Area of Symptoms

Symptoms Aggravated by

Observation

AROM

PROM

Pain with Pain on PF overpressure into DF Restricted range   of DF with knee extended

Gastrocnemius 20–40 strain

Sudden overload

Upper calf

Heel raise

Antalgic gait

Painful and limited DF

 

 

 

 

 

 

 

Plantar fascitis

20–60

Gradual with no known cause

Sole of foot Weight-bearing (under heel) especially first thing in the morning

Achilles tendinitis

20–40

Overuse

 

 

 

Posterior ankle Jumping, running Minor swelling of posterior ankle      

Posterior tibialis tendinitis  

20–40  

Overuse with a flat pronated foot  

Medial ankle, along the course of the tendon  

Activities involving Possible Pain on eversion Pain with weight-bearing peritendinous Pain on PF overpressure into eversion plantar flexion swelling over   medial ankle   Pain with   overpressure into PF

Morton’s neuroma  

40–60  

Gradual with no known cause  

Sole of foot  

Weight-bearing  

Retrocalcaneal bursitis

Varies

Direct irritation of Hindfoot bursa, usually from shoe

Friction

Unremark able Full and pain free Pain with Flattened overpressure arches into great toe Pronated foot extension

Painful and limited DF

Resisted

Weak foot intrinsics

Pain with Pain on PF overpressure into DF Restricted range   of DF with knee extended

Special Tests

Tenderness with Palpation

 

Mid to upper calf

 

 

Pressure Plantar aspect applied of heel over plantar fascial insertion site on the calcaneus  

Posterior ankle

 

 

Pain on resited inversion with the foot plantar flexed  

Rule out tear with heel raise symmetry  

Medial ankle  

Pronated foot Full and pain free Pain with overpressure Flattened arches   into toe extension 

Strong and painless  

   

Web spaces of toes  

Possible swelling, Usually Usually erythema of unremarkable unremarkable hindfoot

Usually Palpation unremarkable

 

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Just above the insertion site of the Achilles tendon on the calcaneus

Overuse

Anterior lower leg

Tarsal tunnel syndrome

25–50

Posttraumatic, neoplastic, inflammatory, rapid weight gain, fluid retention, abnormal foot/ ankle mechanics, or a valgus foot deformity

Excessive dynamic Pronated foot, Medial pes planus, pronation in malleolus, possible walking or distribution swelling running of posterior tibial nerve up the leg, or down into the medial arch, plantar surface of the foot and toes

Midfoot Sprain 15–40    

High impact landing sports Foot twisted when in fixed position

Midfoot  

Walking on toes  

Medial tibial stress syndrome  

15–30  

Overuse  

Anterior lower leg Posterior– medial lower leg

Exercise involving   involved lower   extremity  

Full and pain free Pain on PF Pain with combined PF   Pain on eversion and inversion  

Metatarsal stress fracture

15–45

Overuse

Forefoot

Weight-bearing activities

Usually Usually unremarkable unremarkable

Referred

Varies

May be Symptoms can be dermatomal referred from the if spinal lumbar spine, nerve hip, knee, or from involved; systemic diseases stockingsuch as diabetes like if DM, mellitus (DM), bilateral spondyloheels if arthropathy (Reiter’s Reiter’s syndrome)

Activities involving Unremarkable repetitive dorsiflexion

Pain with Pain with combined PF overpressure and inversion into PF

Weak toe flexion Full and pain free Pain with (late) extreme plantar flexion and eversion

Usually Usually Usually unremarkable unremarkable unremarkable      

Possible edema over fracture site

Pain on DF

Activities unrelated Varies, but may be Usually unremarkable unremarkable to foot and ankle; unrelated to activity

Usually unremarkable

 

Anterolateral lower leg

Positive Tinel’s No tenderness over tarsal usually tunnel

Generalized WeightUsually tenderness bearing unremarkable of midfoot lateral and   anterior–   posterior radiographs     

Posteromedial calf  

Maximal point Usually Palpation, tenderness unremarkable ultrasound, over the tuning fork, bone at the bone scan, fracture site MRI, CT scan Sensation, DTR, Tenderness Usually lab tests of joint if unremarkable, spondylobut weakness arthropathy may be present if spinal nerve root involved

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Lower Leg, Ankle, and Foot

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Anterior tibialis 15–45 tendinitis

THE EXTREMITIES

FIGURE 21-61  Towel stretch.

FIGURE 21-63  Towel toe curls.

provide a compressive force that assists in decreasing effusion. Patients who suffer a grade III ligament injury may require more protection and support than can be afforded by a thermoplastic device. In cases such as this, consideration should be given to using a functional walking orthosis, either with a fixed ankle or a hinged ankle (which can be motion restricted) that allows only plantar flexion and dorsiflexion. The advantage of the orthosis is that it is removable to allow the patient to continue to ice to minimize inflammation. Overall, braces have been demonstrated to be biomechanically effective in preventing, decreasing, or slowing motions that cause injury to the lateral ankle ligaments. Because of the deterioration of support, and the cost of tape (see “Taping” section), removable and reusable ankle braces were designed as an alternative to taping. In the presence of instability, the ankle joint is best supported by a commercial brace, with or without taping, depending on the stress of the sport.

PROM and strength rated at 4/5 to 5/5 with manual muscle testing as compared with the uninvolved side. A recurrence of symptoms should not be provoked. The goals of this phase are as follows: to restore normal joint kinematics;

to attain full range of pain-free motion; to improve neuromuscular control of the lower extremity in a full-weight-bearing posture on both level and uneven surfaces; ▶▶ to improve or regain lower extremity strength and endurance through the integration of local and kinetic chain exercises; ▶▶ to return to the previous level of function or recreation. ▶▶ ▶▶

For the patient to progress to the functional phase of the rehabilitation program, pain-free weight-bearing, and an uncompensated gait pattern must be present. However, pain may still be felt with activities more vigorous than walking. In addition, there should be minimal pain and tenderness, full

Exercises during this phase include manually resisted exercises, concentric exercises with tubing into dorsiflexion (Fig. 21-65), VIDEO plantar flexion VIDEO, inversion VIDEO, and eversion (Fig. 21-66) VIDEO. Exercise tubing can also be used for toe flexion VIDEO and extension VIDEO. Closed-chain exercises include, but are not limited to, seated marching on the floor VIDEO or pillow VIDEO, unilateral stance on the floor VIDEO, weight shifting VIDEO, standing bilateral or unilateral heel raises VIDEO, standing gastrocnemius stretch VIDEO, wall slide VIDEO, toe walking VIDEO, heel walking VIDEO, and supine leg press VIDEO. Emphasis should be placed on regaining any

FIGURE 21-62  BAPS exercise.

FIGURE 21-64  Seated heel raises.

Functional Phase

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▶▶

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Lower Leg, Ankle, and Foot

FIGURE 21-65  Dorsiflexion PRE with resistive tubing.

dorsiflexion that was lost. Regaining dorsiflexion can also be assisted by the use of a tilt board or heel cord stretching box. The gastrocnemius is stretched by keeping the knee straight (Fig. 21-67) and the soleus is stretched by flexing the knee (Fig. 21-68). Proprioceptive exercises are especially important for full functional return and injury prevention. Three factors are thought to cause functional instability of the ankle joint: Anatomic or mechanical instability. ▶▶ Muscle weakness. ▶▶ Deficits in joint proprioception.

FIGURE 21-67  Gastrocnemius stretch.

▶▶

One of the all-to-common consequences of an ankle injury is an alteration of the motor conduction velocity of the fibular (peroneal) nerve and the protective function of the fibularis (peroneal) muscles on the ankle joint. Examples of exercises to perform to enhance proprioception include unilateral stance on a pillow VIDEO, side (lateral) step up VIDEO, standing unilateral heel raise VIDEO, lunges onto VIDEO, or over VIDEO a pillow, backward step ups VIDEO, and crossover walking VIDEO. After isolated strength exercises are initiated in the early portion of this phase, multidirectional, multijoint exercises should begin. Ankle PNF exercises are started based on the patient’s tolerance.

FIGURE 21-66  Eversion PRE with resistive tubing.

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Multidirectional balance activities should progress from slight to partial weight-bearing exercises until the ROM is full and painless, at which time closed-chain exercises are carefully progressed to full-weight-bearing. The greater the severity of injury, the more significant the need for multidirectional balance and weight-bearing rehabilitation activities.

FIGURE 21-68  Soleus stretch.

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THE EXTREMITIES

These activities are effective in progressing the patient toward a progressive return to function. This progression involves beginning with a phase of walking or jogging on flat surfaces, ascending and descending stairs both forward and backward, with a progression to turning, changing directions and lateral movements while running, and eccentric loading with stair running. Further work is needed to fully determine the effect of training the responsiveness to ankle musculature to counteract potentially injurious stimuli. Until then, multidirectional balance activities and proprioceptive training should continue to be stressed as part of a clinical rehabilitation program. Tests found to correlate well with good recovery are descending stairs, walking on heels and toes, and balancing on a square beam. For some patients, the goal may be to return to sport. Progression to this level occurs when there is: full pain-free active and passive ROM; ▶▶ no complaints of pain or tenderness; ▶▶ 75–80% strength of the plantar flexors, dorsiflexors, invertors, and evertors compared to the uninvolved side; ▶▶ adequate unilateral stance balance (30 seconds with eyes closed). ▶▶

Before being allowed to return to full competition, the patient should be put through a functional test that simulates all requirements of his or her sport. Observational analysis should be made of the patient’s quality of movement and whether or not they are favoring the injured extremity in any way. Activities during this phase involve cutting drills, shuttle runs, carioca crossover drills, and sports-specific activities such as lay-ups and dribbling. Full-strength, fibular (peroneal) latency response time and proprioceptive sense about the ankle may not return for many weeks even though the patient has returned to activity. Running-related injuries are common, especially in novice runners.121 Providing advice on training progressions to runners following injury can be difficult. The so-called 10% rule is commonly used as a guideline for a maximum training progression. However, a well-designed randomized control trial (albeit with a small sample size, n = 60) failed to identify an increased risk of injury in novice runners progressing a weekly running distance by 24% over an 8-week period compared to those progressing their weekly running distance by the recommended 10% over a 12-week period.122 It is likely that a number of running injuries, including Achilles tendinopathy, hamstring strains, tibial stress fractures, and iliopsoas strains are linked to those who run further faster. In contrast, sudden increases in running distance may be linked to other types of running related injuries, such as iliotibial band syndrome, greater trochanteric bursitis, gluteus medius/ tensor fascia latae strain, patellofemoral pain, patellar tendinopathy, and MTSS.123 In all likelihood, most training injuries are the result of “too much, too soon, too fast, too quick”).124

CLINICAL PEARL

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During slow-speed running, the cumulative load at the knee joint is higher than the accumulative load during faster running.125

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Taping Historically, ankle taping has been the athletic trainer’s method of choice to attempt to prevent ankle sprains. Ankle taping is effective in restricting the motion of the ankle and has also been proved to decrease the incidence of ankle sprains by providing external stabilization. The material properties of athletic tape must be able to provide long-term support without interfering with athletic performance. However, although traditional taping has been shown to restrict motion, the tape loses 50% of its net support after as little as 10 minutes of exercise. Ideally, the material properties of athletic tape should mimic those of the ligaments and tendons and demonstrate low stiffness at lowest strain and high stiffness in regions of higher strain.126

CLINICAL PEARL A controlled laboratory testing using a single group, prospective, repeated-measures design demonstrated that use of a composite athletic tape with highly hyperelastic properties could be constructed and could maintain a larger portion of support during short duration exercises (83%). Interrater reliability was good (intraclass correlation coefficient >0.70) for the Kleiger, and fair to poor for the squeeze, dorsiflexion compression, cotton, and fibula translation test (intraclass correlation coefficient 6–9 months

Neoplasm

Persistent root pain 1 level involved

Neoplasm

Paralysis

Neoplasm or neurologic disease

Trunk and limb paresthesia

Neoplasm

Bilateral root signs and symptoms

Neoplasm

Nontraumatic strong spasm

Neoplasm

Nontraumatic strong pain in elderly patient

Neoplasm

Signs worse than symptoms

Neoplasm

Radial deviator weakness

Neoplasm

Thumb flexor weakness

Neoplasm

Hand intrinsic weakness or atrophy

Neoplasm, thoracic outlet syndrome, and carpal tunnel syndrome

Horner syndrome

Superior sulcus tumor, breast cancer, cervical ganglion damage, and brain stem damage

Empty end-feel

Neoplasm

Severe posttraumatic capsular pattern

Fracture

Severe posttraumatic spasm

Fracture

Loss of ROM posttrauma

Fracture

Posttraumatic painful weakness

Fracture

The Craniovertebral Region

Findings

EXAMINATION

TABLE 23-2

ROM, range of motion. Data from Meadows J. Orthopaedic Differential Diagnosis in Physical Therapy. New York, NY: McGraw-Hill Education; 1999.

between the upper and lower lids is noted. Pupillary size differences can occur in normal individuals but initially should arouse concern, because an abnormal unilateral change in size may be caused by an autonomic dysfunction or a central nervous system lesion.26 The superior lid should cover a portion of the iris but not the pupil itself unless ptosis or drooping of the eyelid is present26 (see Chapter 3). Missing teeth should be accounted for as a loss of teeth may be a result of trauma, avulsion, or loosening.

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Back View.  Alignment from the back is assessed by observing the patient from behind and noting the orientation of the head. The orientation of the head is best observed by noting any asymmetry in the position of the mastoids, which can indicate whether the head is more rotated or tilted to one side, both of which may indicate a positional fault of the craniovertebral joints. Bruising around the mastoids or around the crown of the head (Battle’s sign), with a history of trauma, may indicate the presence of a cranial vault injury, such as a

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EXAMINATION

basilar fracture. A low hairline may indicate a condition such as Klippel–Feil syndrome, a bone disorder characterized by the abnormal fusion of two or more spinal bones in the neck, and characterized by a short neck with decreased cervical movement, facial asymmetry, and a low posterior hairline.27 Radiologically, patients with Klippel–Feil syndrome show a failure of cervical segmentation.27

Active Range of Motion, Passive Overpressure, and Resistance THE SPINE AND TMJ

Short Neck Flexion.  The clinician instructs the patient to place his or her chin on the surface of the throat. This motion simulates flexion at the craniovertebral joints. If this maneuver produces tingling in the feet or electric shock sensations down the neck (Lhermitte’s sign), it is highly indicative of serious pathology. Although Lhermitte’s sign is not a specific symptom, it is commonly encountered in patients with meningitis and cervical spinal cord demyelination caused by multiple sclerosis (see Chapter 5). If the patient reports a pulling sensation during short neck flexion, the cervicothoracic junction may be at fault. Active short neck flexion tests cranial nerve XI and the C1 and C2 myotomes, as well as the patient’s willingness to move. Placing the neck in short neck flexion places the short neck extensors (C1), which are innervated by the spinal accessory nerve, on a stretch. The clinician applies overpressure and tests the short neck extensors by asking the patient to resist (Fig. 23-5). Positive findings with this test are severe pain, nausea, muscle spasm, or cord signs. Short Neck Extension.  The clinician instructs the patient to look upward by only lifting the chin. The patient extends the head on the neck, and the clinician attempts to lift the

FIGURE 23-6 Short neck extension with overpressure and resistance.

occiput in the direction of the ceiling (Fig. 23-6). An inability to perform, or pain during, this motion (in the presence of normal motion in the other planes) may indicate significant tearing of the anterior cervical structures. If this test produces tingling in the feet, it is highly suggestive of compression to the spinal cord. This compression may occur because of “buckling” or ossification of the ligamentum flavum, with resultant loss of its elasticity. A loss of balance or a drop attack with this maneuver would strongly suggest a compromise of the vertebrobasilar system. A drop attack is defined as a loss of balance without a loss of consciousness (see Chapter 24). The short neck flexors (C1), which are innervated by the spinal accessory nerve, can be tested in this position by applying overpressure as though lifting the patient’s chin toward the ceiling while the patient resists (see Fig. 23-6).

CLINICAL PEARL If the neck is unstable secondary to a dens fracture or a transverse ligament tear, the patient will be unable or unwilling to flex or extend the neck in the traditional manner, often because of severe muscle spasm.

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FIGURE 23-5  Short neck flexion with overpressure and resistance.

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Side Bending.  The patient is asked to side bend their head around the appropriate axis (through the patient’s nose). Side bending is included here for completeness. Much more a function of the lower cervical spine, side bending of the neck is nonetheless significantly decreased in cases of craniovertebral instability or articular fixation. It could be argued that, in the presence of serious ligamentous disruption due to a subluxation of the atlas under the occiput, this motion

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Palpation Objective palpation of this area is guided by a sound anatomic knowledge. Palpation usually proceeds layer by layer. It should be noted that asymmetric joint geometry is common

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Atlas.  By placing the palpating fingers between the mastoid process and the descending ramus of the mandible, the clinician can locate the transverse process of the atlas. The inferior oblique and the superior oblique both have attachments to this site. Axis.  The spinous process of C2 is the first prominent bony landmark that is accessible to palpation below the external occipital protuberance of the occiput. The spinous process of C2 serves as the origin of the inferior oblique muscle and the rectus capitis posterior major muscle.

The Craniovertebral Region

A loss of rotation associated with pain and a history of recent trauma. This could indicate the presence of an acute/subacute, posttraumatic arthritis of the craniovertebral joints. Since it may also indicate a softtissue injury, further testing would be required. ▶▶ A loss of rotation associated with pain and a history of chronic trauma. This finding could indicate a chronic painless hypomobility with an adaptive but painful ipsilateral hypermobility involving the craniovertebral joints (e.g., pain with right rotation could occur if the right O-A joint cannot flex, and there is a hypermobility of the right A-A joint). It may also occur if the left O-A joint cannot extend. Again, further testing is needed to confirm this hypothesis. ▶▶ A loss of rotation ROM associated with no pain, but with a history of chronic trauma. This finding, which could indicate a chronic, posttraumatic arthritis, is likely to be an incidental finding since most patients seek help because of pain. However, depending on the extent of the loss of rotation, the patient may have become aware of a loss of function. ▶▶ Full rotation ROM associated with pain and a history of chronic trauma. This could indicate a chronic fibrotic (painless) hypomobility with an adaptive but painful contralateral hypermobility (e.g., pain with right rotation could occur if the left O-A joint cannot flex and the right O-A joint develops a compensatory hypermobility). ▶▶

in this region. The skin is assessed for its thickness, moisture, and ease of displacement in all directions. Abnormal autonomic skin reactions, such as erythematous changes, increased sweat production, and pain that can be induced with minimal palpatory pressure, may indicate a segmental dysfunction. Palpation may be started in the area indicated by the patient as painful. These painful sites must be correctly localized. The bony landmarks of this region that should be routinely palpated include the occiput, mastoid, atlas, and axis. Occiput.  The clinician locates the external occipital protuberance, which is the most prominent bony structure at the occiput in the midline. By following the external occipital protuberance laterally, the clinician can locate the superior nuchal line. The semispinalis capitis muscle is located about 1½ fingerbreadths below the superior nuchal line. Mastoid.  The mastoid processes are located behind each ear. Once this structure is located, the clinician moves the fingers inferiorly toward the tip of the mastoid process. Starting from the medial tip of the mastoid process, the palpating finger is moved superiorly to the upper pole of the mastoid sulcus, an important area in the examination of the irritation zones of the occiput and C1.

EXAMINATION

may provoke symptoms, but it is likely that such a significant incidence of instability would be detected earlier in the examination. The side-bending motions that do occur in the craniovertebral joints are essentially conjunct motions, so the results from this test are unlikely to provide much in the way of additional information. Rotation.  Neck and head rotation could be considered as the functional motion of the craniovertebral joints. Thus, if the patient’s symptoms and loss of motion are not reproduced with active rotation, it is doubtful that damage to tissues making up the craniovertebral joints is significant or even present. The patient is asked to perform active neck rotation. An inability to move any amount in either direction is potentially a very serious sign, as it could indicate the presence of a dens fracture or a C1–2 dislocation–fracture. Every measure must be taken to determine the cause of this inability to move. In cases of a suspected fracture or severe instability, the patient should be placed in a cervical collar and the physician immediately notified. In addition to the presence of a fracture, some of the other serious conditions that can be provoked by cervical rotation include vertebral artery compromise—cervical rotation is the most likely (single) motion to reproduce signs or symptoms of vertebral artery compromise (see Chapter 24). The findings from the cervical rotation tests may also afford the clinician some information with regard to a biomechanical lesion of the craniovertebral joints:

Passive Physiologic Mobility Testing of the Occiput, Atlas, and Axis O-A Joint.  When mobility testing this joint, the first point to remember is that the joint is capable of both flexion and extension, and that side bending and rotation also can occur, albeit slight. The second point to keep in mind is that the arthrokinematics of this joint are the reverse of those occurring in the other zygapophyseal joints and that they occur in a different plane (horizontal). The joint mobility of the O-A joint can be assessed in sitting VIDEO or in supine. With the patient supine, the head is extended around the axis for the O-A joint VIDEO. The head is then side bent left and right. As the side bending is performed, a gradual translational force is applied in the direction opposite to the side bending. The range of movement of the side bending is assessed from side to side as is the end-feel of the translation. This procedure is then repeated for flexion. During extension of the O-A joint (Fig. 23-7), the occipital condyles glide anteriorly to the limit of their symmetric extension range. During left side bending and right translation in extension, the coupled right rotation is produced. This rotation causes the right occipital condyle to return toward a neutral position while the left condyle advances toward the extension barrier. If left side bending in extension is limited,

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EXAMINATION THE SPINE AND TMJ

FIGURE 23-7  Passive mobility testing of O-A in extension.

then the limiting factor is on the left joint of the segment (ipsilateral to the side bending), which is preventing the advance of the condyle into its normal position. Thus, extension and right translation test the anterior glide of the left O-A joint, whereas extension and left translation stress the anterior glide of the right O-A joint (Table 23-3). During flexion of the O-A joint, the occipital condyles glide posteriorly (Fig. 23-8). The right rotation associated with left side bending causes the left condyle to move away from the flexion barrier toward the neutral position while the right condyle is moved posteriorly further into the flexion barrier. Thus, flexion and translation to the right test the posterior glide of the right O-A joint, whereas flexion and left rotation test the posterior glide of the left O-A joint (see Table 23-3). It is apparent that during these tests, the arthrokinematic and osteokinematic movements are tested simultaneously; thus, the end-feel must be used to determine the cause of the restriction.

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TABLE 23-3

 ovement Restrictions of the M Craniovertebral Joints and Their Probable Causes

Movement Restriction

Probable Causes

Flexion and right side bending      

Left flexion hypomobility Extensor muscle tightness Posterior capsular adhesions Left subluxation (into extension)

Extension and right side bending 

Right extension hypomobility Left flexor muscle tightness Anterior capsular adhesions Right subluxation (into flexion)

Flexion and right side-bending motion greater than extension and left side bending

Left capsular pattern (arthritis and arthrosis)

Flexion and right side bending equal to extension and left side bending

Left arthrofibrosis (very hard capsular end-feel)

Right side flexion in flexion and extension

Probably an anomaly

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FIGURE 23-8  Passive mobility testing of O-A in flexion.

A-A Joint.  There are a number of methods to assess the passive physiologic mobility of the A-A joint VIDEO. The most common method described in many texts involves the patient lying supine and the clinician passively applying full cervical flexion and then introducing cervical rotation. The problem with this technique is that it relies on the fact that the mid-tolower cervical spine will be locked with the flexion. Because the neck is often prevented from further flexion when the chin meets the sternum, the clinician has no way of knowing whether full cervical flexion has occurred. Thus, some of the subsequent rotation may be attributed to a combination of cervical spine and A-A motion. This assumption may not be important with asymmetric lesions but can result in falsenegative findings with symmetric lesions. A better method of assessment involves the use of cervical side bending. With the patient positioned in supine, the clinician side bends the head and neck around the craniovertebral axis and then rotates the head in the direction opposite to the side bending (Fig. 23-9). The clinician assesses the amount of range available and then assesses the other side.

CLINICAL PEARL In a study by Smedmark and colleagues,28 passive intervertebral motion of the cervical spine was assessed independently by two physical therapists. The therapists had equal backgrounds concerning education and clinical experience. Sixty-one patients seeking care for cervical problems at a private clinic were included in the study where three segments of the cervical spine and the mobility of the first

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rib were graded as stiff or not stiff. Data were analyzed by percentage agreement and κ coefficient. Results demonstrated interexaminer reliability of between 70% and 87% and κ coefficients ranging between 0.28 and 0.43 were considered to be only “fair to moderate.”   In a similar study by Pool and colleagues,29 which assessed the interexaminer reproducibility of physical examination of the cervical spine, two physiotherapists independently judged the general mobility and intersegmental mobility (segments C0–T2) of the neck and the pain that was provoked. Agreement for general mobility showed κ between 0.05 and 0.61, and for the intersegmental mobility, it showed κ values between −0.09 and 0.63. Agreement for provoked neck pain within one point of an 11-point numerical rating scale varied between 46.9% and 65.7% for general mobility and between 40.7% and 75.0% for intersegmental mobility. The intraclass correlation coefficients (ICCs) varied between 0.36 and 0.71 for general mobility and between 0.22 and 0.80 for intersegmental mobility. The study concluded that despite the use of a standardized protocol to assess general mobility and intersegmental mobility of the cervical spine, it is difficult to achieve reasonable agreement and reliability between two examiners. Likewise, the patients were not able to score the same level of provoked pain in two assessments with an interval of 15 minutes.

Combined Motion Testing Flexion and extension at the O-A joints involve a posterior and anterior gliding of the occipital condyles, respectively.

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Linear Segmental Stress Testing

The Craniovertebral Region

FIGURE 23-9  Passive mobility testing of A-A rotation in supine.

EXAMINATION

The same gliding (although reciprocal in opposing facets) is utilized in the rotation. At the A-A joint, flexion and extension primarily involve a “rolling” action of the condyles, with an insignificant amount of gliding. Therefore, craniovertebral flexion and extension will have a minimal effect on A-A rotation.30 Thus, if a symptom or ROM is drastically altered by craniovertebral flexion or extension, an assumption could be made that the dysfunction is at the O-A joint.30 For example, if the right occipital condyle cannot glide posteriorly, the right joint will be unable to flex or to permit rotation to the right, as both of these motions involve a posterior glide at the right O-A joint. In the combined motion tests, the right rotation restriction will be more evident when combined with craniovertebral flexion but will be less evident when combined with craniovertebral extension. The findings from the combined motion tests can be used to determine which joint glide is to be assessed. For example, if it was determined in the combined motion testing that the right O-A joint is restricted or painful with flexion (implicating the posterior glide), the O-A joint is positioned and assessed in its extreme of flexion and right rotation (the two motions associated with a posterior glide of the right O-A joint).

The craniovertebral region demonstrates a high degree of mobility, but little stability, with the ligaments affording little protection during a high-velocity injury. Instability of this region can result from a number of causes: Trauma (especially a hyperflexion injury to the neck). ▶▶ RA, psoriatic arthritis, or ankylosing spondylitis. Nontraumatic hypermobility or frank instability of the O-A joint has been reported in association with RA. ▶▶ Corticosteroid use. Prolonged exposure to this class of drug can produce a softening of the dens and transverse ligament by deteriorating the Sharpey fibers, which attach the ligament to the bone. Steroid use also promotes osteoporosis, predisposing bones to fracture. ▶▶ Recurrent upper respiratory tract infections or chronic sore throats in children. Grisel syndrome is a spontaneous A-A dislocation, affecting children between the ages of 6 and 12 years.31 The outstanding symptom is a spontaneously arising torticollis. The most likely etiology seems to be an inflammation of the retropharyngeal space caused by upper respiratory tract infections or by a adenotonsillectomy producing pharyngeal hyperemia and bone absorption. ▶▶ Down syndrome. Nontraumatic hypermobility or frank instability of the O-A joint has been reported in children and adolescents with Down syndrome. ▶▶ Immature development. Patients younger than 12 years of age often have an immature or absent dens (see later). ▶▶ Osteoporosis. ▶▶

It must be remembered that the A-A joint complex consists of three joints. The median joint, although it has no weightbearing function, is extremely important in maintaining stability, while at the same time facilitating motion within this

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EXAMINATION THE SPINE AND TMJ

joint complex. The stability of the A-A joint depends greatly on the ligamentous structures and on a normal and intact dens. Occasionally, the integrity of the dens can be compromised because of the following reasons: 1. Anomalies of the dens, including the following: a. Os odontoideum. This is a condition in which the IVD between the developing bodies of axis and atlas does not ossify. b.  Congenital absence of the dens. c. An underdeveloped dens whose lack of height renders it unchecked by the transverse ligament. The body of the dens is not of sufficient size to be retained in the osseoligamentous ring of the atlas until a child is approximately 12 years old. Great care and justification are needed with any craniovertebral mobilization or manipulative technique with this age group. 2. Pathologies affecting the dens, including the following: a. Demineralization or resorption of the dens, such as that occurring in patients with Grisel syndrome or RA. b. An old, undisplaced fracture (especially of the dens), which originally escaped diagnosis and subsequently formed a pseudoarthrosis. Indications for Stability Testing.  Clinical cervical spine instability may demonstrate only subtle symptoms and clinical examination features, and frequently normal radiographic findings.32 The following findings are considered to be indications to perform stability or stress tests of the craniovertebral region33: History of neck trauma or any of the causes of instability listed previously. ▶▶ Patient report of neck instability usually described as the head feeling heavy. ▶▶ Presence of the following signs and symptoms: ■■ A lump in the throat ■■ Lip paresthesia ■■ Nausea or vomiting ■■ A severe headache and muscle spasm ■■ Dizziness The patient is positioned in supine to remove any muscular influences. If the patient is unable to lie down, the clinician may need to reconsider the appropriateness of performing these tests. ▶▶

FIGURE 23-10  Longitudinal stability testing.

the thumbs. Once the arches are located, the clinician pushes down on the anterior arches of C2 with the thumbs toward the table, while the patient’s occiput and C1, cupped in the clinician’s hands, is lifted, keeping the head parallel to the ceiling but in slight flexion35 (Fig. 23-11) VIDEO. The patient is instructed to count backward aloud. The position is held for approximately 15 seconds or until an end-feel is perceived. This test has been found to have a specificity of 95% and a sensitivity of 95%.34 Sharp–Purser Test.  This test was designed originally to test the sagittal stability of the A-A segment in patients with RA, because a number of pathologic conditions can affect the stability of the osseoligamentous ring of the median joints of this segment in this patient population. These changes result in degeneration and thinning of the articular cartilage between

Longitudinal Stability. General traction is applied to the entire cervical region. If this maneuver does not reproduce the signs or symptoms, C2 is stabilized so that the traction force may be directed at the craniovertebral region (A-A membrane) (Fig. 23-10). The diagnostic value of longitudinal stability testing to the entire cervical region is as yet unknown. When localized to the A-A membrane, the test has been found to have a sensitivity of 95% and a specificity of 95%.34

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Anterior Shear: Transverse Ligament. The patient is positioned in supine, with his or her head cradled in the clinician’s hands. The clinician locates the anterior arches of C2 by moving around the vertebra from the back to the front using

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FIGURE 23-11  Transverse ligament test.

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EXAMINATION

FIGURE 23-13  Alar ligament test in sitting.

the odontoid process and the anterior arch of the atlas, or, occasionally, in a softening of the dens. The aim of the test was to determine whether the instability was significant enough to provoke central nervous system’s signs or symptoms. However, the original test was poorly defined and only involved upper cervical flexion. Hence, a modified version was introduced which is described. The patient is positioned in sitting. The patient is asked to segmentally flex the head around a craniovertebral axis (short neck flexion) and relate any signs or symptoms that this might evoke to the clinician. In addition, a positive test may be indicated by the patient hearing or feeling a clunk. Local symptoms, such as soreness, are ignored for the purposes of evaluating the test. If no serious signs or symptoms are provoked, the clinician stabilizes C2 posteriorly with one hand and applies a posteriorly oriented force to the forehead of the patient (Fig. 23-12) VIDEO. In the presence of a positive test, a provisional assumption is made that the symptoms are caused by excessive translation of the atlas, compromising one or more of the sensitive structures listed previously, and the physical examination is terminated. No intervention should be attempted other than the issuing of a cervical collar to prevent craniovertebral flexion and an immediate referral to the patient’s physician.

(Fig. 23-14), and while monitoring the motion at the C2 segment, the clinician introduces slight compression to the crown of the head, to facilitate atlantooccipital side bending through the craniovertebral joints, to slacken the alar ligament. Further rotation should now be possible. Testing is recommended to be performed in three planes (neutral, flexion, and extension) to account for variation in alar ligament orientation. Osmotherly et al.36 examined the direct effect of the side bending and rotation stress tests on the alar ligaments using magnetic resonance imaging (MRI) and concluded that both side bending and rotation stress testing result in a measurable increase in length of the contralateral alar ligament, which is consistent with the mechanisms that have been described to support their clinical use. Transverse Shear33.  Transverse shearing of the craniovertebral joints is performed with the patient supine. The clinician stabilizes the mastoid, and C1 is moved in a transverse direction, using the soft part of the metacarpophalangeal joint of the index finger (Fig. 23-15). The test is repeated by stabilizing C1 and translating the mastoid. C1 and C2 can be tested similarly. The soft aspect of each second metacarpal head is placed on the opposite transverse processes and laminae of C1 and C2, with the palms facing each other. The clinician stabilizes C1 and then attempts to move C2 transversely using the soft part of metacarpals (Fig. 23-16). No movement should be felt. The diagnostic value of this test is as yet unknown.

Coronal Stability: Alar Ligament.  The alar ligaments have been described primarily as limiting occipitoatlantoaxial rotation and side bending (e.g., rotation or side bending to the right tightens the left alar), whereas flexion typically tightens both alar ligaments. Both the side bending and rotation stress test for the alar ligaments are based on preventing the inherent coupling of rotation and side bending in the occipitoatlantoaxial complex, that is, side bending of the occiput on the atlas is accompanied by immediate ipsilateral rotation of the axis beneath the atlas.36 The patient can be positioned in sitting or supine. The posterior aspect of the spinous process and lamina of the axis (C2) is palpated/stabilized with one hand while the patient’s head is side bent or rotated (Fig. 23-13) VIDEO VIDEO (2x videos). This is a test of immediacy—if the C2 transverse process does not move as soon as the head begins to side bend or rotate, laxity of the alar ligament should be suspected. To confirm the findings in this test, the point of rotation is maintained, as the patient’s head is cradled by the clinician

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FIGURE 23-14  Confirmatory test for alar ligament in sitting.

The Craniovertebral Region

FIGURE 23-12  Modified Sharp–Purser test.

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THE SPINE AND TMJ

FIGURE 23-15  Transverse shear of O-A joint.

Neurologic Examination The neurologic examination is performed to assess the normal conduction of the central and peripheral nervous systems. The presence of neurologic symptoms deserves special attention. Many of the symptoms that occur in the upper limb have their origins in the neck. The patient with neck trauma can report seemingly bizarre symptoms, but these need to be heeded until the clinician can rule out serious pathology. Cervical myelopathy, involving an injury to the spinal cord itself, is associated with multisegmental paresthesias, UMN signs and symptoms such as spasticity, hyperreflexia, visual and balance disturbances, ataxia, and sudden changes in bowel and bladder function. The presence of any UMN sign or symptom requires immediate medical referral. In addition to the muscle stretch (deep tendon), reflexes and sensory tests outlined in Chapter 25, the clinician should perform the spinal cord reflexes of Babinski and Hoffman (see Chapter 3). A study by Sung and Wang demonstrated that the Hoffman test is the most sensitive reflex test in the detection of cervical myelopathy.37

Imaging Studies The standard, initial cervical spine radiographic series in trauma patients includes a cross-table lateral view, an

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FIGURE 23-16  Transverse shear of A-A joint.

Dutton_Ch23_p1141-p1174.indd 1156

anteroposterior view, and an open-mouth view, the latter of which is used to help rule out a fracture of the dens (see Chapter 7).3 The usefulness of the anteroposterior view has been questioned because it provides little additional information. Although this three-view screening series can detect the majority of axis injuries, the C2 vertebra often is obscured by overlying bony maxillary, mandibular, and dental structures; therefore, C2 fractures may be missed.3 The clinician needs to be aware of the limitations of plain radiographs, as problems exist with both specificity and sensitivity. However, radiographs can provide a gross assessment of the severity of the degenerative changes of the spine. Sagittal reconstruction of CT images is important because axial images may not detect a transverse odontoid fracture.3 Although CT is excellent in evaluating bony injuries, it can miss soft tissue and significant ligamentous injuries.3 Recently, therefore, dynamic flexion/extension lateral fluoroscopic evaluation has been advocated in polytrauma patients to identify occult ligamentous instabilities and confirm that the cervical spine is uninjured. As with any diagnostic study, the findings must be correlated with the history and physical examination.

INTERVENTION STRATEGIES The intervention for the craniovertebral region may commence when the possibility of serious injury including fracture, dislocation, or injury to the spinal cord and vertebral artery has been ruled out. The gamut of musculoskeletal injury to the craniovertebral region of the spine ranges from a simple strain (muscle) or sprain (ligament) to injuries of the bone and neurovascular injuries. The most common injuries seen clinically are muscle strains and postural dysfunctions. A correct diagnosis can usually be accomplished through a detailed history and a comprehensive examination. Confirmation of the correct diagnosis can be made with an assessment of the response of the patient to the initial rehabilitation program. Muscle strains are common in the cervical spine because most of the cervical muscles attach via myofascial tissue inserting into the periosteum rather than by the more resilient tendon.2 The severity of the strain is dependent on the magnitude of forces involved. If the force is sufficient, both the muscle and the associated joint become involved. In an abnormal spine, the forces needed to cause injury are reduced. Repetitive microtrauma is a common cause of craniovertebral dysfunction. Postural dysfunctions of this region, particularly the forward head posture (see Chapter 25), usually manifest themselves at the O-A joint, resulting in fixed capital extension and a loss of O-A flexion. Patients with postural dysfunctions may develop secondary myofascial trigger points (MTrPs) and myofascial pain syndromes. In postural dysfunctions and trauma-related injuries, other joints and regions may be involved and require further investigation. Pain, tenderness, active ROM restrictions, muscle imbalances, and segmental motion restrictions are common findings with craniovertebral dysfunction.

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The techniques to increase joint mobility and soft tissue extensibility are described later, under “Therapeutic Techniques” section.

Acute Phase The goals of this phase include ▶▶

Various electrotherapeutic modalities and physical agents may be used during the acute phase to modulate pain and to decrease inflammation and muscle spasm (see Chapter 8). Therapeutic cold and electrical stimulation may be used for 48–72 hours. The cryotherapy is continued at home. A transcutaneous electrical nerve stimulation (TENS) unit may be prescribed to help control pain and encourage ROM exercises. Joint protection may be appropriate. In such cases, a soft or semirigid cervical collar may be prescribed for 7–10 days to reduce muscle guarding (see Chapter 25). Nonsteroidal antiinflammatory drugs (NSAIDs) are often prescribed for 2–3 weeks to help decrease inflammation and to control pain, thereby increasing the potential for an early return to function. Bed rest, along with analgesics and muscle relaxants for no more than 2–3 days, is prescribed for patients with a severe injury. However, in less severe cases, bed rest has not been shown to improve recovery and, compared with mobilization or patient education, the rest tends to prolong symptoms. The patient is also taught how to find the neutral position for the upper cervical spine. The neutral position is defined as the least painful position that minimizes mechanical stresses. The ROM exercises are initiated as early as possible, based on patient tolerance, to prevent hypomobility. Neck flexion and rotation exercises are usually performed first. Extension and side-bending exercises are introduced based on the response of the patient to the flexion and rotation exercises. The rotation and side-bending exercises are performed in the supine position and then progressed to weight bearing. All of the exercises should be performed in the pain-free range. Upper extremity ROM and strengthening exercises should also be introduced to promote the early integration of the entire upper kinetic chain. Important muscles to include are the rhomboids, middle and lower trapezius, latissimus dorsi, serratus anterior, and deltoid. In addition, the muscles of the rotator cuff should be strengthened. Gentle manual techniques (see “Therapeutic Techniques” section later), such as sustained or rhythmic specific traction (grade I or II) mobilizations and massage, may also be used. As the patient progresses, muscle stretching may be introduced. Manual techniques can have a mechanical effect on joint mobility and soft tissue extensibility. In addition, these techniques can have beneficial neurophysiologic effects, which can help alleviate pain and muscle spasm. Self-stretching and self-mobilization techniques are taught to the patient at the earliest and appropriate opportunity (see “Therapeutic Techniques” section later).

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the pain has significantly decreased so that there is minimal pain with activities of daily living; and ▶▶ there is a significant improvement in the pain-free ranges of motion. ▶▶

Functional Phase The duration of this phase can vary tremendously and depends on several factors: The severity of the injury. Healing capacity of the patient. ▶▶ How the condition was managed during the acute phase. ▶▶ The level of patient involvement in the rehabilitation program. ▶▶

The Craniovertebral Region

reducing pain, inflammation, and muscle spasm; reestablishing a nonpainful ROM; ▶▶ improving neuromuscular postural control; ▶▶ retarding muscle atrophy; and ▶▶ promotion of healing. ▶▶

Active joint protection techniques may be part of the acute phase. Joint protection exercises work by supporting the joint and reducing the applied stresses. Joint protection exercises include cervical stabilization exercises. These exercises initially are performed in single planes and in the neutral position, using submaximal isometric contractions. As with the ROM exercises, it is recommended that these exercises be performed initially in the supine position, and later, in sitting, as tolerance increases. As the pain-free ranges increase, the exercises are performed throughout the newly attained pain-free ranges. Aerobic conditioning must also be included as part of the comprehensive rehabilitation program. A stationary bike, tread-mill, or a stair-stepping machine can be used. The patient is advanced to the functional phase when

▶▶

The goals of this phase are to significantly reduce or completely resolve the patient’s pain; ▶▶ restore full and pain-free ROM; ▶▶ fully integrate the entire upper kinetic chain; and ▶▶ restore full cervical and upper quadrant strength and neuromuscular control. ▶▶

During this phase, the ROM exercises are continued until maximum range of motion is attained. The strengthening program is progressed from submaximal isometrics in single planes to maximal isometrics in single planes. Then the patient is progressed to isometrics in combined motions (flexion and side bending and extension and side bending). The strength training is then progressed to concentric and eccentric exercises in single planes, using elastic tubing, pulleys, or isolation exercises. Proprioceptive neuromuscular facilitation patterns are introduced when appropriate. Elastic tubing is issued to the patient to allow training at home. For progression to return to play, the athlete should demonstrate normal and pain-free single-plane and multiplane ROM; ▶▶ normal cervical, cervicothoracic, glenohumeral, and scapulothoracic strength; and ▶▶ the normal flexibility of cervical, cervicoscapular, and cervicothoracic musculature. ▶▶

Return to sports activities should be designed to mimic the sport as closely as possible. The goal should be to improve

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the balance, power, and endurance of the cervical, cervicothoracic, glenohumeral, and scapulothoracic muscle groups and force couples.

THE SPINE AND TMJ

INTEGRATION OF PATTERNS 4B AND 4D: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, AND RANGE OF MOTION SECONDARY TO IMPAIRED POSTURE AND CONNECTIVE TISSUE DYSFUNCTION Myofascial Pain Patterns Myofascial pain syndromes are closely associated with tender areas that have come to be known as MTrPs (see Chapter 10). The term myofascial trigger point is a bit of a misnomer because trigger points may also be cutaneous, ligamentous, periosteal, and fascial. Dysfunctional joints also are associated with trigger points and tender attachment points. The interventions for MTrPs are outlined in Chapter 10. These include stretch and spray, muscle stripping, massage therapy, myofascial release, ischemic compression, stretching, postural correction and education to eliminate any causative or perpetuating factors, electrotherapeutic and thermal modalities, cryotherapy, injections, and joint mobilizations.

INTEGRATION OF PATTERNS 4D AND 4E: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, AND RANGE OF MOTION SECONDARY TO CONNECTIVE TISSUE DYSFUNCTION AND LOCALIZED INFLAMMATION Osteoarthritis Osteoarthrosis of the A-A joints, unrelated to trauma, is a rare cause of pain in the craniovertebral region and an even more uncommon cause of A-A instability. It could be argued that if osteoarthrosis of the lateral mass articulations progresses, the synovitis may gradually involve the ligamentous structures, thereby weakening them and rendering them prone to rupture.

Inflammatory Arthritis

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The greatest risk for complications with the spondyloarthropathies in the craniovertebral region occurs at the A-A joint, where there are two different synovial articulations: the two lateral facet joints and the articulation between the odontoid process of C2 and the anterior part of C1.38 The transverse ligament is typically the weakest part of the complex in the presence of spondyloarthropathy. Rheumatoid Arthritis.  The most common inflammatory lesion found in the retro-odontoid space is RA, which induces abnormal proliferation of the synovial soft tissue (pannus) and frequently causes the destruction of the bony structure (see Chapter 5).

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Ankylosing Spondylitis.  See Chapter 5. Gout.  See Chapter 5.

Craniovertebral Instability There has been much controversy about defining and diagnosing spinal instability. Segmental spinal instability generally is defined as a greater displacement between vertebrae than that which occurs under physiologic load. Therefore, maximum flexion and extension radiographs usually are used to determine hypermobility between vertebrae. Craniovertebral instability frequently is encountered in inflammatory, neoplastic, degenerative, and traumatic disorders, in addition to congenital and developmental abnormalities. Clinically, instability appears as a subluxation or spinal deformity accompanied by severe pain or neurologic deficits. Several types of craniovertebral instability are recognized; among them are the following: Translational or rotary instability of C1.  Translational anterior A-A instability is detected on lateral cervical radiographs as a widened, mobile ADI as described earlier. Patients with congenital abnormalities of the odontoid process may develop chronic A-A subluxation. Posterior translation of C1 is also possible, but for this to occur, the dens or anterior arch of the atlas must be fractured or incompetent. Rotational A-A instability appears as asymmetric rotation of the C1 lateral masses on plain radiographs. Rotational subluxations that are irreducible, recurrent, or associated with transverse ligament disruption require surgery. ▶▶ O-A instability.  O-A instability is demonstrated radiographically by movement between the dens and basion (the middle point on the anterior margin of the foramen magnum), by distraction or translation of the occipital condyles, or by vertical migration. ▶▶

Surgical stabilization is required to correct instability when conservative intervention has failed or when spontaneous healing with an orthosis, such as a halo brace, is unlikely.

PATTERN 4F: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, AND RANGE OF MOTION, OR REFLEX INTEGRITY, SECONDARY TO SPINAL DISORDERS Peripheral Vertigo Dizziness is the third most common complaint among outpatients, after chest pain and fatigue.23 There are several types of dizziness, some benign and some serious, and it is important that the clinician be able to make the distinction. Among the causes of dizziness that must be carefully considered by the clinician examining the cervical spine are the central and peripheral (Table 23-4) causes of vertigo or dizziness (see Chapter 3). The following are some of the potential causes of peripheral vestibular dysfunction. Vestibular Neuritis.  Vestibular neuritis is thought to represent a reactivated dormant herpes infection in Scarpa’s

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TABLE 23-4

Peripheral Vestibular Disorders

Data from Huijbregts P, Vidal P. Dizziness in orthopaedic physical therapy practice: classification and pathophysiology. J Man Manip Ther. 2004;12(4):199–214.

ganglion, within the superior division of the vestibular nerve, which innervates the anterior and horizontal semicircular canals (SCCs) (see Chapter 3). Ramsay Hunt Syndrome. Ramsay Hunt syndrome is caused by varicella zoster and is a variant of vestibular neuritis, with multiple cranial nerves involved. This involvement results in facial paresis, tinnitus, hearing loss, and a vestibular defect.39,40 It may also involve cranial nerves V, IX, and X. Labyrinthitis.  Infection of the labyrinth can be viral or bacterial. Acute labyrinthitis usually presents with severe vertigo, sudden or progressive hearing loss, nausea, vomiting, and fever. The condition lasts for 1–5 days, with subsequent resolution of complaints over a 2–3-week period. Benign Paroxysmal Positional Vertigo (BPPV). BPPV, a mechanical disorder of the inner ear, is the most common peripheral vestibular disorder and the most common cause of dizziness in the elderly, with the incidence increasing with age.39 BPPV presents as brief periods of vertigo experienced with a change in the position of the person’s head relative to gravity.41 BPPV is typically caused by the otoconia being dislodged from the utricle and settling within one or more of the three SCCs creating abnormal stimulation of the fluid-filled canal dynamics. The more serious causes of BPPV (see also Chapter 3) include head trauma, vestibular neuritis, an insult to the labyrinth, surgical stapedectomy, degeneration of the inner ear, and vestibular artery compromise. Two pathophysiological theories have been proposed to explain the etiology of BPPV, cupulolithiasis and canalithiasis42: ▶▶

Cupulolithiasis.  The sedimentous material, possibly macular otoconia, is released into the endolymphatic fluid in the SCC within the short arm of the canal. This release of the sedimentous material is hypothesized to result from trauma or degenerative changes. The canal most commonly involved is the posterior SCC. When the head is upright, this material will settle on the SCC cupula. Fixed deposits on the cupula increase the density of the structure, making the cupula, which previously had the same density as the surrounding endolymphatic fluid, more sensitive to gravity and, therefore, the head position.

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Canalithiasis.  An accumulation of utricle debris (otoconia) within the long arm of the canal, which can move within the posterior SCC and stimulate the vestibular sense organ (cupula), causing vertigo and nystagmus.39

The name BPPV implies that this type of vertigo is positional in nature. However, it may be more correct to call BPPV a positioning-type vertigo.42 Symptom duration is brief: 30–60 seconds; hence, it is a positioning-type vertigo rather than a positional-type vertigo, as occurs in vertebrobasilar insufficiency.42 The diagnosis usually is made solely on the basis of the history and findings on positional testing, although it is possible to confuse BPPV with orthostatic hypotension, another common cause of dizziness in the elderly. Whereas orthostatic hypotension causes dizziness when the patient sits up or stands, BPPV can occur in all positions, especially with changes in head position. For example, patients who complain of vertigo with rolling on a bed of getting out of bed are 4.3 times more likely to have BPPV.43 The two tests commonly used to diagnose BPPV are the Dix–Hallpike test or the side-lying test.44 The diagnostic criteria for posterior canal BPPV are vertigo associated with the characteristic nystagmus—torsional (superior pole of the eye directly toward the lowermost ear [i.e., the involved ear])41 and upbeating,45 with a latency of 1–45 seconds before onset, and the duration of less than 60 seconds—and fatigue with repeated positioning. The side of the lesion is diagnosed with a maneuver similar to the Dix–Hallpike test (see Fig. 3-26 in Chapter 3). Once diagnosed, one of two procedures can be used to treat BPPV: Epley Canalith-Repositioning Procedure.  The Epley canalith repositioning maneuver is designed to return the otoconia from the SCC back to the macule of the utricle, from whence it can be reabsorbed. The maneuver uses a series of head positions. With each head position, the debris settles to the lowest portion of the canal, moving the debris away from the ampulla into the common crus and then into the utricle.41 In addition to the head position changes, there are a number of body position changes. With each change in position, the movement of debris through the canal and away from the ampulla may create changes in pressure across the cupula, resulting in the generation of the typical torsional and upbeating nystagmus, which is predictive of a successful outcome of the maneuver.41 The procedure for treatment of the right posterior SCC is performed as follows. The patient is seated on the bed with the legs extended, with the clinician standing to the side of the patient (Fig. 23-17). The patient’s head is rotated 45 degrees toward the right, and the patient is then lowered into the supine position, toward the side of the involved ear with the neck extended 30 degrees over the edge of the treatment table (Fig. 23-18). This is the headhanging position. While maintaining the cervical extension, the head is slowly rotated through 90 degrees of motion ending in 45 degrees of neck rotation toward the uninvolved side (Fig. 23-19). The patient is then asked to roll onto the uninvolved side (left) while maintaining the position of the head in relation to the trunk (Fig. 23-20). The patient then sits up (Fig. 23-21). Each position is maintained for a minimum of 45 seconds or as long as the nystagmus lasts plus an additional 20 seconds, and the procedure is repeated three times.

The Craniovertebral Region

Vestibular neuritis Ramsay Hunt syndrome Labyrinthitis Benign proximal positional vertigo Ménière disease Acute peripheral vestibulopathy Otosclerosis Head trauma Cerebellopontine angle tumor Toxic vestibulopathies Acoustic neuropathy Perilymphatic fistula Autoimmune disease of the inner ear

▶▶

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FIGURE 23-17  Patient seated on the bed with the legs extended and with the clinician standing to the side of the patient.

FIGURE 23-19  While maintaining the cervical extension, the head is slowly rotated through 90 degrees of motion.

Liberatory (Semont) Canalith-Repositioning Maneuver.  The patient is positioned upright on a bed (Fig. 23-17). The procedure for treatment of the right posterior SCC is performed as follows. The clinician turns the patient’s head

45 degrees toward the left ear (Fig. 23-22). The patient is then asked to drop quickly onto his or her right side so that the head touches the bed behind the right ear (Fig. 23-23). The position is maintained for 90 seconds and then the patient is asked to move the head and trunk in a swift movement toward the other side without stopping in the upright position, so that the head comes to rest on the left side of his or her forehead (Fig. 23-24). The head is then gently tapped on the treatment table, and the position is maintained for 1.5 minutes. The patient is then asked to sit up (Fig. 23-21). This maneuver should be repeated three times. To maintain the otoconia in the utricle following either of these maneuvers, the patient is fitted with a soft collar and is instructed not to bend over, lie back, move the head up

FIGURE 23-18  The patient’s head is rotated 45 degrees toward the right, and then lowered into the supine position.

FIGURE 23-20  The patient rolls onto the uninvolved side (right side in picture, but left side in text) while maintaining the position of the head.

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fullness in the ear.42,46 Attacks are often associated with nausea and vomiting. Age at onset is usually between the ages of 20 and 50 years, and men are more often affected than women.47,48 The underlying cause is thought to be an increase in the volume of the endolymphatic fluid in the membranous labyrinth, which displaces the inner ear structures with resultant signs and symptoms of horizontal or rotary nystagmus.47,48 FIGURE 23-21  The patient sits up.

or down, or tilt the head to either side for the remainder of the day. Ménière Disease.  This condition is characterized by paroxysmal vertigo, lasting minutes to days, accompanied by tinnitus, fluctuating low-frequency hearing loss, and a sensation of

FIGURE 23-22  The clinician rotates the patient’s head to the left.

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Acute Peripheral Vestibulopathy. This condition is characterized by a sudden onset of vertigo, nausea, and vomiting, which last for up to 2 weeks and is not associated with hearing loss. Otosclerosis.  The pathophysiologic mechanism behind otosclerosis is immobility of the stapes and resultant conductive hearing loss. Associated signs and symptoms include vertigo and nystagmus. Vestibular Rehabilitation.  The use of a custom-designed physical therapy program in the rehabilitation of patients with unilateral peripheral vestibular hypofunction is aimed at promoting vestibular compensation, promoting central habituation and adaptation, and readjusting the vestibulo-ocular reflexes (VORs) and vestibulospinal reflexes (see Chapter 3). Repetition of head movements and positions that provoke dizziness and vertigo form the basic premise of habituation training, even though many of the exercises may initially increase the patient’s symptoms. Adaptation exercises consist

FIGURE 23-24  The patient moves the head and trunk in a swift movement toward the other side.

The Craniovertebral Region

FIGURE 23-23  The patient drops quickly onto her right side.

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TABLE 23-5

Cawthorne–Cooksey Exercises for Patients with Vestibular Hypofunction

THE SPINE AND TMJ

A.  In bed   1.  Eye movements—at first slow, then quick    a.  Up and down    b.  From side to side    c.  Focusing on a finger moving from 3 to 1 ft away from face   2.  Head movements—at first slow, then quick; later with eyes closed    a.  Bending forward and backward    b.  Turning from side to side B. Sitting   1.  Same as A1 and A2, above   2.  Shoulder shrugging and circling   3.  Bending forward and picking up objects from ground C. Standing   1.  Same as A1 and A2 and B3, above   2.  Changing from sitting to standing position with eyes open and shut   3.  Throwing a small ball from hand to hand (above eye level).   4.  Throwing ball from hand to hand under knee   5.  Changing from sitting to standing and turning round in between D.  Moving about (in class)   1.  Circle around center person who will throw a large ball and to whom it will be returned   2.  Walk across room with eyes open and then closed   3.  Walk up and down slope with eyes open and then closed   4.  Walk up and down steps with eyes open and then closed   5.  Any game involving stooping and stretching and aiming, such as skittles, bowls, or basketball Diligence and perseverance are required, but the earlier and more regularly the exercise regimen is carried out, the faster and more complete will be the return to normal activity. Data from Dix MR. The rationale and technique of head exercises in the treatment of vertigo. Acta Otorhinolaryngol Belg. 1979;33(3):370–384.

of repeated head movements while focusing on a target and are designed to improve gaze stability through adaptation of the VOR and development of compensatory saccadic eye movements (see Chapter 3). Several progressions have been devised (Table 23-5 and Box 23-1). Brown and colleagues, in a retrospective case series of 48 patients with central vestibular dysfunction, noted improvement in both subjective and objective measures of balance after physical therapy intervention.49 The treatment consisted of one or more of the following: balance and gait training, general strengthening and flexibility exercises, vestibular adaptation exercises, education in the use of assistive devices and safety awareness techniques to avoid falls, and utilization of varied senses, particularly somatosensation and vision, to aid in maintaining balance.49

Cervicogenic Dizziness Cervicogenic dizziness (CGD) is also known as proprioceptive vertigo, cervicogenic vertigo, and cervical dizziness. CGD, a diagnosis of exclusion, is a clinical syndrome characterized by the presence of dizziness and associated neck pain.23 It is a diagnosis and disorder that seems to be poorly understood, making it difficult for a clinician to differentiate CGD from other disorders that cause dizziness including vestibular, cardiovascular, metabolic, neurological, psychological, and vision problems.22,50

CGD is characterized by the presence of imbalance, unsteadiness, disorientation, neck pain, limited cervical ROM, and may be accompanied by a headache.50 The neuromusculoskeletal causes of CGD appear to result from an alteration to proprioceptive spinal afferents from the mechanoreceptors of the neck. When considering other causes, it would seem likely that direct damage to the vestibular apparatus, or severe damage to the vertebral artery, will produce immediate dizziness, whereas dizziness arising from the cervical joints or a less severely injured vertebral artery may not occur until the joints themselves became abnormal, or until the ischemia has had time to make itself felt (Table 23-6). Malmstrom et al.51 found posterior neck and zygapophyseal joint tenderness and excessive cervical ROM to be characteristic of CGD. Others have found reduced performance in the craniocervical flexion test in patients with chronic neck pain.23,52

CLINICAL PEARL CGD should not be considered if the patient does not have neck pain, either at rest, with movement, or with palpation.50   CGD typically does not include aural fullness, tinnitus, or hearing loss.50

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Box 23-1  Exercises to Improve Postural Stability

The Craniovertebral Region

These exercises are devised to incorporate head movement (vestibular stimulation) or to foster use of different sensory cues for balance.   1. The patient stands with his or her feet as close together as possible, with both or one hand helping maintain balance by touching a wall if needed. The patient then turns his or her head to the right and to the left horizontally, while looking straight ahead at the wall for 1 minute without stopping. The patient takes his or her hand or hands off the wall for longer and longer periods of the time while maintaining balance. The patient then tries moving his or her feet even closer together.   2.  The patient walks, with someone for assistance if needed, as often as possible (acute disorders).   3. The patient begins to practice turning his or her head while walking. This will make the patient less stable, so the patient should stay near a wall as he or she walks.   4. The patient stands with his or her feet shoulder-width apart with eyes open, looking straight ahead at a target on the wall. He or she progressively narrows the base of support from feet apart to feet together to a semi-heel-to-toe position. The exercise is performed first with arms outstretched, then with arms close to the body, and then with arms folded across the chest. Each position is held for 15 seconds, before the patient does the next-most-difficult exercise. The patient practices for a total of 5–15 minutes.   5. The patent stands with his or her feet shoulder-width apart with eyes open, looking straight ahead at a target on the wall. The patient progressively narrows his or her base of support from feet apart to feet together to a semi-heel-to-toe position. The exercise is performed with eyes closed, at first intermittently and then for longer and longer periods of time. The exercise is performed first with arms outstretched, then with arms close to the body, and then with arms folded across the chest. Each position is held for 15 seconds, and then the patient tries the next position. The patient practices for a total of 5–15 minutes.   6. A headlamp can be attached to the patient’s waist or shoulders, and the patient can practice shifting weight to place the light into targets marked on the wall. This home “biofeedback” exercise can be used, with the feet in different positions and the patient standing on surfaces of different densities.   7. The patient practices standing on a cushioned surface. Progressively more difficult tasks might be standing on hard floor (linoleum, wood), thin carpet, shag carpet, thin pillow, and sofa cushion. Graded-density foam can also be purchased.   8. The patient practices walking with a more narrow base of support. The patient can do this first, touching the wall for support or for tactile cues and then gradually touching only intermittently and then not at all.   9. The patient practices turning around while walking, at first making a large circle but gradually making smaller and smaller turns. The patient must be sure to practice turning in both directions. 10.  The patient can practice standing and then walking on ramps, either with a firm surface or with more cushioned surface. 11. The patient can practice maintaining balance while sitting and bouncing on a Swiss ball or while bouncing on a trampoline. This exercise can be incorporated with attempting to maintain visual fixation of a stationary target, thus facilitating adaptation of the otolith-ocular reflexes. 12. Out in the community, the patient can practice walking in a mall before it is open and, therefore, while it is quiet; can practice walking in the mall while walking in the same direction as the flow of traffic; and can then walk against the flow of traffic. Data from Rothman RH, Simeoni FA. The Spine. Philadelphia, PA: WB Saunders; 1982.

Once competing pathologies have been ruled out (cervical instability, vertebral artery occlusion, Ménière disease, central or peripheral vestibular disorders, BPPV, vestibular migraine, whiplash associated disorder, etc.) in order to determine whether a patient potentially has CGD, it is essential to clarify the symptoms and nature of onset—the patient should have a history of neck pathology and also experience dizziness that has a close temporal relationship with the onset of cervical spine symptoms.50 A neurological screen should include an assessment of radicular symptoms, myotomes, dermatomes, deep-tendon reflexes, UMN signs, and

cranial nerve function.50 The patient’s vestibular function can be tested using such tests as an oculomotor evaluation (nystagmus, smooth pursuit, and saccades), Dix–Hallpike test, and the VOR. CGD and dizziness from vestibular disorders can be differentiated using the head–neck differentiation test with the patient seated on a swivel chair. Provocation of dizziness with trunk rotation under a head stabilized in space implicates the cervical spine, whereas dizziness with head and trunk rotation together (en bloc rotation) indicates a vestibular component to the patient’s symptoms.50 1163

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TABLE 23-6

Differential Diagnostic Characteristics of Cervicogenic Dizziness, BPPV, and VBI

THE SPINE AND TMJ

 

Vertigo Type

Nystagmus Characteristics

Associated Signs and Symptoms

Cervicogenic dizziness      

Positioning type

No latency period

Nystagmus

     

Brief duration Fatigable with repeated motion  

Neck pain Suboccipital headaches Cervical motion abnormality

BPPV    

Positioning type    

Short latency: 1–5 seconds Brief duration: 90 degrees Elbow flexion 6/10) is the most consistent predictor of a poor outcome.119 Financial compensation, which is determined by the continued presence of pain and suffering, appears to provide a barrier to recovery and may promote persistent illness and disability.119 In one study, the incidence of insurance claims for whiplash was found to be 417 per 100,000 persons under a fault-based motor insurance system but decreased to 300 per 100,000 persons under a no-fault system.128 Yet not all persons involved in motor vehicle crashes develop symptoms, and not all symptomatic patients experience chronic injury. The differences in the rating of prolonged symptoms between systems with and without compensation raise questions about the real incidence of chronic WADs.

INTEGRATION OF PATTERNS 4B, 4F, AND 5F: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, RANGE OF MOTION SECONDARY TO IMPAIRED POSTURE, SYSTEMIC DYSFUNCTION (REFERRED PAIN SYNDROMES), SPINAL DISORDERS, MYOFASCIAL PAIN DYSFUNCTION, AND PERIPHERAL NERVE ENTRAPMENT Thoracic Outlet Syndrome 1246

The thoracic outlet is the anatomic space bordered by the first thoracic rib, the clavicle, and the superior border of

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the scapula, through which the great vessels and nerves of the upper extremity pass (Fig. 25-4). The bony boundaries of the outlet include the clavicle, first rib, and scapula, and the outlet passage is further defined by the interscalene interval, a triangle with its apex directed superiorly. This triangle is bordered anteriorly by the anterior scalene muscle, posteriorly by the middle scalene muscle, and inferiorly by the first rib (see Fig. 25-4). TOS is a syndrome characterized by symptoms attributable to compression of the neural or vascular structures that pass through the thoracic outlet. The other names used for TOS are based on descriptions of the potential sources of its compression. These names include cervical rib syndrome, scalenus anticus syndrome, hyperabduction syndrome, costoclavicular syndrome, pectoralis minor syndrome, and first thoracic rib syndrome. The lowest trunk of the brachial plexus, which is made up of rami from the C8 and T1 nerve roots, is the most commonly compressed neural structure in TOS. These nerve roots provide sensation to the fourth and fifth fingers of the hand and motor innervation to the intrinsic hand muscles. The subclavian artery and the lower trunk of the plexus pass behind the clavicle, and into the costoclavicular space (see Fig. 25-4). From there they pass over the first rib, between the insertions of the anterior and middle scalene muscles and are joined by the subclavian vein. Thus, the course of the neurovascular bundle can be subdivided into three different sections, based on the areas of potential entrapment: 1. As the brachial plexus and subclavian artery pass through the interscalene triangle (see Fig. 25-4), interscalene triangle compression can result from injury of the scalene or scapular suspensory muscles. In some cases, fibromuscular bands can develop between the anterior and middle scalenes, or between the long transverse processes of the lower cervical vertebrae, producing entrapment. The subclavian vein is not involved, because it usually passes anterior to the anterior scalene muscle. Entrapment at this site may also result from cervical ribs. However, the presence of a cervical rib does not necessarily precipitate signs and symptoms. 2. As it passes the first rib, clavicle, and subclavius: the costoclavicular interval. Entrapment in this space between the ribcage and the posterior aspect of the clavicle may occur with clavicle depression, rib elevation caused by scalene hypertonicity, repetitive shoulder abduction, or a first ribclavicular deformity. A postfracture callus formation of the first rib or clavicle can also increase the potential for entrapment. 3. As it passes the coracoid process, pectoralis minor, and clavipectoral fascia to enter the axillary fossa. At this point, the subclavian artery and vein become the axillary artery and vein. At this third site, the neurovascular bundle can be compromised with arm abduction or elevation, especially if external rotation is superimposed on the motion. Pectoralis minor tendon compression is associated with shoulder hyperabduction. During hyperabduction, the tendon insertion and the coracoid act as a fulcrum, about

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which the neurovascular structures are forced to change direction.

1. Neurogenic TOS: Compression of the brachial plexus at the scalene triangle. Symptoms, which include either local or extremity pain, are often exacerbated by lifting the arms overhead. This type may account for about 95% of the cases. 2. Venous TOS: Compression of the subclavian vein by the structures making up the costoclavicular junction. This type may account for about 4% of the cases. 3. Arterial TOS: Compression due to abnormal bony or ligamentous structures at the thoracic outlet region.

Assessment of the scapulothoracic muscles: The anterior and middle scalenes, subclavius, pectoralis minor and major (thoracic outlet “closers”). These muscles typically are found to be adaptively shortened. ▶▶ First rib position or presence of cervical rib. ▶▶ Clavicle position and history of prior fracture, producing abnormal callous formation or malalignment. ▶▶ Scapula position, acromioclavicular joint mobility, and sternoclavicular joint mobility. ▶▶ Neurophysiologic tests, which are useful to exclude coexistent pathologies such as peripheral nerve entrapment or cervical radiculopathy. ▶▶

Intervention Conservative intervention should be attempted before surgery and should be directed toward muscle relaxation, relief of inflammation, and attention to posture. The focus of the intervention is the correction of postural abnormalities of the neck and shoulder girdle, strengthening of the scapular suspensory muscles, stretching of the scapulothoracic muscles, and mobilization of the whole shoulder complex and the first and second ribs. If symptoms progress or fail to respond within 4 months, surgical intervention is usually considered.

THERAPEUTIC TECHNIQUES

Diagnosis

Techniques to Increase Joint Mobility

TOS is a clinical diagnosis made almost entirely on the basis of the history and physical examination (see Special Tests). To help rule out other conditions that can mimic TOS, the physical examination should include the following:

Joint Mobilizations

▶▶

A careful inspection of the spine, thorax, shoulder girdles, and upper extremities for postural abnormalities, shoulder asymmetry, muscle atrophy, excessively large breasts, obesity, and drooping of the shoulder girdle.

▶▶

Palpation of the supraclavicular fossa for fibromuscular bands, percussion for brachial plexus irritability, and auscultation for vascular bruits that appear by placing the upper extremity in the position of vascular compression.

▶▶

Assessment of the neck and shoulder girdle for active and passive ranges of motion, areas of tenderness, or other signs of intrinsic disease.

▶▶

A thorough neurologic examination of the upper extremity, including a search for sensory and motor deficits and abnormalities of muscle stretch reflexes.

▶▶

Assessment of respiration to ensure the patient is using correct abdominodiaphragmatic breathing.

▶▶

Assessment of the suspensory muscles: The middle and upper trapezius, levator scapulae, and SCM

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The Cervical Spine

There may be multiple points of compression of the peripheral nerves between the cervical spine and hand, in addition to the thoracic outlet. When there are multiple compression sites, less pressure is required at each site to produce symptoms. Thus, a patient may have concomitant TOS, ulnar nerve compression at the elbow, and carpal tunnel syndrome. This phenomenon has been called the multiple crush syndrome (see Chapter 11). Symptoms vary from mild-to-limb threatening and often mimic common but difficult to treat conditions such as a tension headache or fatigue syndromes. The chief complaint is usually one of diffuse arm and shoulder pain, especially when the arm is elevated beyond 90 degrees. Potential symptoms include pain localized in the neck, face, head, upper extremity, chest, shoulder, or axilla; and upper extremity paresthesias, numbness, weakness, heaviness, fatigability, swelling, discoloration, ulceration, or Raynaud phenomenon. Illig et al.129 defines TOS as three separate entities:

(thoracic outlet “openers”). These muscles typically are found to be weak.

Most joint mobilizations use the same technique as the assessment but, by using grades, convert it into a treatment method. The purposes of joint mobilization techniques are to: reduce stresses through both the fixation and the leverage components of the spine; ▶▶ reduce stresses through hypermobile segments by mobilizing the hypomobile joints; ▶▶ reduce the overall force needed by the clinician, thus giving greater control. ▶▶

The selection of a manual technique is dependent on several factors, including: The acuteness of the condition, the cause of the restriction, and the goal of the intervention. If the structure is acutely painful (pain is felt before resistance or pain is felt with resistance), pain relief, rather than a mechanical effect, is the major goal. Joint oscillations (grades I and II) that do not reach the end of the range are used. The segment or joint is left in its neutral position, and the mobilization is carried out from that point. ▶▶ Whether the restriction is symmetric, involving both sides of the segment, or asymmetric, involving only one side of the segment. ▶▶

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THE SPINE AND TMJ

A number of specific manual techniques can be employed. Spinal locking techniques can be used to augment the comfort and safety of a manual technique. Locking is simply a method of taking up any available soft tissue tension or slack, thereby making a manual technique more specific. Two types of locking techniques are commonly advocated: craniovertebral locking and locking through segmental translation. Because of the potential for vertebral artery compromise in the craniovertebral region, the craniovertebral joints are often “locked” first before continuing motion into the middle and/or lower cervical spine joints. In the following example, a left side-bending technique is used. Although this locking technique may be used with the patient positioned in sitting or supine, if it used in supine it is important to apply a small amount of compression to compensate for the loss of the spinal loading due to the weight of the head. While palpating the C2 spinous process, the clinician slowly side-bends the patient’s head to the left. If the side bending is performed around a sagittal craniovertebral axis, the C2 spinous process should be felt to move to the right, indicating left rotation of the C2 on the C3. Maintaining the left side-bent position, the head is now rotated to the right until the C2 spinous process regains a central position. The head is again side bent slightly to the left, and the C2 spinous process de-rotated back to the midline. These motions are continued until a firm end-feel is reached. At this point, motion in the craniovertebral joints has now been exhausted, while the rest of the cervical joints remain in neutral. Being careful to maintain the position of the head, especially the right rotation, the side bending is continued left to the middle or lower cervical level required. As the cervical joints are prevented from rotating to the left, the middle cervical side bending motion is exhausted very quickly. The vast majority of biomechanical dysfunctions of the cervical spine involve the posterior quadrant (a loss of extension and a loss of side bending and rotation to one side or both). The loss of cervical flexion is usually associated with a cervical disk protrusion, a cervicothoracic dysfunction, or a craniovertebral dysfunction. However, for completeness, the techniques described here will address a loss in both the anterior and the posterior quadrants. The C4–5 level is used in the following examples. The midrange is considered the biomechanical neutral resting position of the joint, and is the ideal start point for techniques that are not intended to stress the barrier and that are intended to avoid causing pain or increasing inflammation. The various methods of grading manual therapy techniques are described in Chapter 10. Basic Techniques to Restore Motion in the Posterior Quadrant Seated Mobilization Technique to Restore Extension and Left Side Bending-Rotation VIDEO. If the clinician has large hands, mobilizing into extension can be a problem because the stabilizing hand prevents the full glide into extension from occurring. To overcome this problem, the stabilization of the inferior segment is performed by pushing the thumb

FIGURE 25-83  Seated mobilization to increase extension and left rotation.

up against the side of its spinous process, thereby preventing the rotation induced by the mobilization of the superior segment. For example, if the left side of C4–5 is being mobilized into extension, left side bending, and left rotation by the upper hand, the thumb of the inferior hand is pushed against the right side of the C5 spinous process, preventing rotation of C5 to the left (Fig. 25-83). Supine Mobilization Technique to Restore Extension and Left Side Bending-Rotation (Left Side Bending-Rotation Shown on VIDEO). The patient is positioned supine, with the head being supported. The clinician stands at the patient’s head, facing the shoulders. With the radial aspect of the right index finger, the clinician palpates the spinous process and the right inferior articular process of the C4 vertebra. With the other hand, the clinician supports the head and neck superior to the level being treated (Fig. 25-84). A lock of the superior segment is accomplished by left side bending and right rotating the C3–4 joint complex, leaving the craniovertebral joints in a neutral position. The motion barrier for extension, left side bending, and left rotation of C4–5 is then localized by pushing the right inferior articular process of C4 in a posteroinferior and medial direction on C5. Passive.  The clinician applies a grade I–V force to the C4 vertebra to produce a posteroinferior and medial glide of the left zygapophyseal joint at C4–5. ▶▶ Active.  From the motion barrier, the patient is asked to turn the eyes in a direction that facilitates further extension, left side bending, and right rotation. The isometric contraction is held for up to 5 seconds and followed by a period of complete relaxation. The joint is then passively taken to the new motion barrier. The technique is repeated three times and followed by a reexamination of joint function. Basic Techniques to Restore Motion in the Anterior Quadrant Seated Mobilization Technique to Restore Flexion and Right Rotation (Rotation Right Side Bending-Rotation Shown on VIDEO).  The patient is positioned sitting, and the clinician ▶▶

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Passive.  A grade I–IV mobilization force is applied to the C4 vertebra to produce a superoanterior glide at the zygapophyseal joints, thus flexing the C4–5 joint complex and feeling the spinous processes separate. ▶▶ Active.  At the motion barrier, the patient is instructed to turn the eyes in a direction that facilitates further flexion at C4–5. The isometric contraction is held for up to 5 seconds and followed by a period of complete relaxation. The joint is then passively taken to the new motion barrier. The technique is repeated three times and followed by a reexamination of joint function. ▶▶

The Cervical Spine

Supine Mobilization Technique to Restore Flexion and Right Side Bending-Rotation (Left Side Bending-Rotation Shown on VIDEO).  The patient is positioned supine, with the head being supported. The clinician stands at the head of the table facing the patient. The C4–5 segment is flexed, right side bent, and left translated to bring the right joint to its flexion barrier. The clinician hooks a fingertip under the right articular process and lays a fingertip pad over the articular process on the right (see Fig. 25-86). The mobilization is achieved by pulling the left process cranially, as steady light pressure is applied to the back of the left process to maintain a normal axis of motion.

FIGURE 25-84  Supine mobilization technique to restore extension and left side bending rotation.

stands on the right side. Using one hand, the clinician stabilizes the C5 segment using a lumbrical grip (Fig. 25-85). The other hand reaches around the head of the patient, securing it to the clinician’s chest, and the ulnar border of the fifth finger is applied to the left transverse process and neural arch of C4. The C4–5 segment is then flexed and rotated to the right to the barrier (see Fig. 25-85). The mobilization is carried out by the clinician applying pressure into flexion and right rotation.

FIGURE 25-85  Seated mobilization into flexion and right rotation.

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FIGURE 25-86  Supine mobilization technique to restore flexion and left side bending rotation.

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▶▶

▶▶

THE SPINE AND TMJ

Passive.  A grade I–V mobilization force is applied to the C4 vertebra to produce a superoanterior and medial glide of the right zygapophyseal joint at C4–5. Active.  At the motion barrier, the patient is instructed to turn the eyes in a direction that facilitates further flexion, right side bending, and rotation at C4–5. The isometric contraction is held for up to 5 seconds and followed by a period of complete relaxation. The joint is then passively taken to the new motion barrier. This technique is repeated three times and followed by a reexamination of function.

Techniques to Restore Motion in Bilateral Extension Hypomobility.  Bilateral hypomobilities can be treated with unilateral techniques performed to each side when only the last part of the range of movement is absent. Seated Technique for the Cervicothoracic Junction. The patient is seated with the arms behind the head. The clinician stands in front of the patient and threads the arms through the patient’s arms, before resting both of the hands on the top, and back, of each of the patient’s shoulders (Fig. 25-87). By gently leaning the patient forward, the cervical spine is extended until the stiff segment is located at the cervicothoracic junction. Gradually, the clinician increases the amount of cervicothoracic extension by gently kneading the mid-scapular area. Distraction, side flexion, or rotation motions can also be introduced. Care should be taken to avoid overextending

FIGURE 25-87  Seated technique for the cervicothoracic junction.

the lumbar spine during this technique, by pulling the patient too far forward.

Mobilizations with Movement.130 To Improve Flexion The patient is positioned sitting, with the clinician standing to the side, facing the patient. The patient’s head is held in neutral against the clinician’s lower chest, and the distal phalanx of the little finger is hooked under the spinous process of the superior vertebra of the segment being treated. The rest of the fingers wrap around the patient’s neck to provide firm support, and the wrist is extended, with the forearm placed in the plane of the facets. The lateral border of the thenar eminence of the other hand is placed below the little finger (see Fig. 25-88), and the palm of the hand rests on the upper back of the patient. The patient is asked to flex the neck, and the glide of the superior segment is produced along the correct plane by a pull from the little finger in an anterior and superior direction, while the other hand stabilizes the lower segment. This technique can be taught as part of the patient’s home exercise program using a towel, belt, or strap.

To Improve Extension The patient is positioned sitting, with the clinician standing to the side, facing the patient. The patient’s head is held in neutral against the clinician’s lower chest, and the distal phalanx of the little finger is hooked under the spinous process of the superior vertebra of the segment being treated.

FIGURE 25-88  Mobilization with movement to improve cervical flexion.

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Myofascial Trigger Point Therapy

FIGURE 25-89  Mobilization with movement to improve cervical extension.

Using a key grip between the index finger and thumb, the clinician places the grip over the articular pillar on either side of the inferior spinous process of the segment (Fig. 25-89). The patient is asked to extend the neck while the clinician simultaneously applies a glide of the inferior vertebra by pushing with the key grip hand. This technique can be taught as part of the patient’s home exercise program using a towel, belt, or a strap.

To Improve Rotation to the Right The patient is positioned sitting, with the clinician sitting behind. The clinician places the thumb of one hand over the articular pillar over the right aspect of the spinous process of the superior vertebra of the segment to be treated. The other thumb is placed over the first thumb to help reinforce. The remaining fingers of the two hands are placed around the neck and upper back. The patient is asked to rotate the head and neck slowly to the right while the clinician simultaneously applies the glide along the correct joint plane using pressure from both thumbs (see Fig. 25-90). The same technique can be used to improve cervical rotation to the left by altering the position of the thumbs. This technique can be taught as part of the patient’s home exercise program using a towel, belt, or a strap (Fig. 25-91).

Ischemic compression is advocated for myofascial trigger points and is achieved by sustaining direct pressure over a trigger point, using the thumb to apply pressure. The pressure is held for 5–7 seconds and then quickly withdrawn. The procedure is repeated for each trigger point. After each trigger point has been treated, the clinician returns to the first trigger point. The procedure is repeated three times on each trigger point. To facilitate self-treatment for inaccessible regions such as the rhomboid muscles, lying on a tennis ball, or using the handle of a cane can be substituted for direct manual compression.

The Cervical Spine

FIGURE 25-90  Mobilization with movement to improve cervical rotation to the right.

Muscle Stretching Pectoralis Minor The pectoralis minor can be stretched effectively using a corner and placing the forearms on the walls. The patient needs to avoid adopting a forward head posture during the stretch. The patient attempts a contraction of horizontal abduction and internal rotation into the wall. The clinician is cautioned against using this exercise with any patient with shoulder pathology, especially an anterior instability.

Techniques to Increase Soft Tissue Extensibility A variety of soft tissue techniques for the cervical region is available to the clinician. The choice of technique depends on the goals of the treatment and the dysfunction being treated.

FIGURE 25-91  Home exercise to improve cervical rotation to the right.

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side, until resistance is felt. The patient is then asked to look toward the treated side, a motion that is resisted by the clinician. When the patient relaxes, the clinician moves the head into further side flexion and flexion.

Upper Trapezius

THE SPINE AND TMJ

This procedure is similar to that of the levator scapulae except that the amount of neck flexion is reduced (see Fig. 25-34). The patient is positioned supine, with the head at the edge of the table. Using both hands, the clinician then flexes the neck and side bends the patient’s head to the opposite side. Rotation to the ipsilateral side is then added until resistance is felt. The patient is then asked to look toward the treated side, a motion that is resisted by the clinician. When the patient relaxes, the clinician moves the head into further flexion, side bending, and rotation. In addition to the muscles described here, the clinician should assess the following muscles for adaptive shortening: rectus capitis posterior major; ▶▶ rectus capitis posterior minor; ▶▶ obliquus capitis inferior; ▶▶

FIGURE 25-92  Pectoralis major stretch of the costosternal fibers.

Pectoralis Major The pectoralis major can be specifically stretched if the orientation of its fibers is considered (clavicular and costosternal), by having the patient lie supine and extending the arm off the table in either approximately 140 degrees of shoulder abduction (costosternal fibers) or approximately 45–50 degrees of abduction (clavicular fibers) (see Fig. 25-92).

▶▶

obliquus capitis superior. The stretches for these muscles are described in Chapter 23.

Self-Stretching Techniques Levator Scapulae The patient is seated in good posture. The patient flexes the neck fully and then side bends the head while maintaining the neck flexion (see Fig. 25-93). The side bending continues

For the following muscles, the same technique that is used to assess the length of this muscle is used for the stretch:

Sternocleidomastoid The SCM functions to flex and rotate the neck and extend the occipitoatlantal joint. The patient is positioned in sitting or supine (see Fig. 25-37). The patient is positioned supine, with the head supported. From this position, the clinician induces side bending of the neck to the contralateral side and extension of the neck. The clinician stabilizes the scapula and rotates the patient’s head and neck toward the ipsilateral side.

Anterior and Middle Scalenes The patient is positioned in supine. After stabilizing the first two ribs with the heel of one hand, the clinician performs passive cervical extension, contralateral side bending, and ipsilateral rotation (see Fig. 25-38).

Levator Scapulae

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The stretch can be passively applied by the clinician. The patient is positioned supine, with the head at the edge of the table. The elbow and hand of the side to be treated are placed on the head. The clinician stands at the head of the table and presses his or her thigh against the point of the patient’s elbow, fixing it caudally. Using both hands, the clinician then flexes the neck and side flexes the patient’s head to the opposite

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FIGURE 25-93  Self-stretch of levator scapulae.

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The Cervical Spine

FIGURE 25-95  Three-finger exercise into cervical flexion.

FIGURE 25-94  Self-stretch of upper trapezius.

until a gentle stretch is felt. Gentle overpressure can be applied using one hand. The stretch is maintained for 8–10 seconds and then the patient relaxes. The stretch is repeated 10 times.

FIGURE 25-96  Three-finger exercise into cervical side bending.

Upper Trapezius The self-stretch of the right upper trapezius depicted in Figure 25-94 is described. The stretch is maintained for 8–10 seconds, and then the patient relaxes. The stretch is repeated 10 times.

Three-Finger Exercise Active range of motion in the cervical spine can be increased through patient participation, using the three-finger exercise. The patient’s mandible rests on digits two, three, and four. The motions of flexion (Fig. 25-95), side bending (Fig. 25-96), and rotation (Fig. 25-97) can all be performed. An alternative method uses the index finger placed between the chin and the sternum to control the correct amount of flexion, with the PIP placed on the superior aspect of the manubrium and the tip of the index finger on the chin. The patient is cautioned against reproducing sharp pain while attempting to feel a stretch at the end of the available motion. With a different hand position, cervical extension can be performed in a controlled and safe manner. The fingers are interlocked and placed behind the neck, with the little fingers at the lowest segmental level of the joint restriction (at C 5 for a C4–5 restriction). Using the little finger as a fulcrum, the patient extends the cervical spine to the point just shy of pain. This position is held for a few seconds, and the neck is returned to the neutral position (Fig. 25-98).

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FIGURE 25-97  Three-finger exercise into cervical rotation.

FIGURE 25-98  Active exercise into cervical extension.

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CASE STUDY NECK PAIN AND ARM PARESTHESIA

THE SPINE AND TMJ

HISTORY

Questions

A 21-year-old woman presented to the clinic with complaints of right neck and shoulder pain, and paresthesias that often radiated into the medial arm, forearm, and fourth and fifth fingers of the right upper extremity. The patient also reported that her right upper extremity often felt tired and heavy and that her right hand occasionally would appear to have a weak grip. The patient reported that her symptoms began shortly after she was involved in an MVA about 2 months previously and have increased slightly since that time. The patient denied any history since the accident of dizziness, tinnitus, blurred vision, or headaches. No left-sided neck pain or left upper extremity symptoms were reported. The patient described her overall health as good. Her past medical history was unremarkable, and there was no past history of any surgeries.

1. What are some of the potential causes for upper extremity paresthesias? Can you rule out any of these causes from the history given? What further questions would you ask to help rule out some of the causes? 2. Which conditions could be associated with a weak grip? Could you rule these in or out with the history? 3. Which conditions could be associated with a report of a tired and heavy upper extremity? How would you rule these in or out? 4. Would the results from any imaging studies be helpful in this case? If so, which ones and why? 5. Is an upper quarter scanning examination warranted in this case? Why or why not? 6. Is this an irritable condition? Why or why not? 7. What type of conditions were the questions about dizziness, tinnitus, blurred vision, and headaches designed to help rule out?

CASE STUDY LOW NECK PAIN HISTORY

Questions

A 33-year-old woman presented with a diagnosis of low neck and upper back pain that, over the past few weeks, had become constant. Initially, the pain had been minimal, but it had worsened progressively. The pain was localized to the midline at the base of the neck, and there was no report of arm pain or symptoms. The patient worked as a computer operator for a local bank. Sleeping had become difficult, and all motions of the neck were reported to reproduce the symptoms. The patient denied any dizziness or nausea, or history of neck trauma. The patient described her overall health as excellent. The past medical history was unremarkable.

1. Make a list of all of the possible causes of midline neck pain. 2. What could the gradual onset of the pain tell the clinician? 3. What is your working hypothesis at this stage? List the tests you would use to rule out the various causes of midline neck pain. 4. Should the reports of night pain concern the clinician? 5. Does this presentation/history warrant a Cyriax upper quarter scanning examination? Why or why not?

CASE STUDY BILATERAL ARM AND WRIST WEAKNESS HISTORY

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A 36-year-old man who sustained a left tibial plateau fracture presented at the clinic with complaints of bilateral arm and wrist weakness that had worsened progressively over

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the past month since his discharge from the hospital. The patient was ambulating with crutches and non–weightbearing on the left side. There was no history of cervical trauma. The patient reported no pain in his upper extremities

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but had noticed a mild and vague numbness in his hands. There was no report or evidence of a preceding viral infection and no proximal migration of the weakness, nor did he have any other areas of weakness. The patient did complain of pain in his axillae, and commented that his crutches had been rubbing against his axillae.

Questions

The Cervical Spine

1. What structure(s) could be at fault when weakness is the major complaint? 2. Why was the history of no cervical trauma pertinent?

3. Why was the statement about preceding viral infection pertinent? 4. Why was the statement about the proximal migration of the weakness pertinent? 5. What is your working hypothesis at this stage? List the various diagnoses that could present with bilateral arm numbness and the tests you would use to rule out each one. 6. Does this presentation/history warrant a scanning exami‑ nation? Why or why not?

CASE STUDY RIGHT-SIDED NECK PAIN HISTORY

Questions

A 45-year-old woman awoke with right-sided neck pain 10 days earlier. The pain was felt over the right neck on an intermittent basis. She related that the pain was worse with head turning to the right, and further aggravated with activities involving cervical extension. She described no neurologic pain or paresthesia. The pain sites and intensity were unchanged since the onset. Further questioning revealed that the patient was otherwise in good health and had no reports of bowel or bladder impairment, night pain, dizziness, or radicular symptoms.

1. What structure(s) could be at fault with complaints of right-sided neck pain? 2. What should the motion pattern of restriction/pain tell you? 3. What is your working hypothesis at this stage? List the various diagnoses that could present with right-sided neck pain and the tests you would use to rule out each one. 4. What do the questions about night pain and dizziness pertain to? 5. Does this presentation/history warrant a scanning examination? Why or why not?

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19. Allia P, Gorniak G. Human ligamentum nuchae in the elderly: its function in the cervical spine. J Man Manipulative Ther. 2006;14:11–21. 20. Johnson GM, Zhang M, Jones DG. The fine connective tissue architecture of the human ligamentum nuchae. Spine. 2000;25:5–9. 21. Fielding JW, Burstein AA, Frankel VH. The nuchal ligament. Spine. 1976;1:3–11. 22. Keshner EA. Motor control of the cervical spine. In: Boyling JD, Jull GA, eds. Grieve’s Modern Manual Therapy: The Vertebral Column. Philadelphia, PA: Churchill Livingstone; 2004:105–117. 23. Simons DG, Travell JG, Simons SL. Myofascial Pain and Dysfunction— The Trigger Point Manual. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1998. 24. Mercer S, Campbell AH. Motor innervation of the trapezius. J Man Manip Ther. 2000;8:18–20. 25. Jull GA, Falla D, Treleaven J, Sterling M, O’Leary S. A therapeutic exercise approach or cervical disorders. In: Boyling JD, Jull GA, eds. Grieve’s Modern Manual Therapy: The Vertebral Column. Philadelphia, PA: Churchill Livingstone; 2004:451–470. 26. Mercer S. Kinematics of the spine. In: Boyling JD, Jull GA, eds. Grieve’s Modern Manual Therapy: The Vertebral Column. Philadelphia, PA: Churchill Livingstone; 2004:31–37. 27. Van Mameren H, Drukker J, Sanches H, Beurgsgens J. Cervical spine motions in the sagittal plane. I: ranges of motion of actually performed movements, an x-ray cine study. Eur J Morphol. 1990;28:47–68. 28. Blanpied PR, Gross AR, Elliott JM, et al. Neck pain: Revision 2017. J Orthop Sports Phys Ther. 2017;47:A1–A83. 29. Wang B, Liu H, Wang H, Zhou D. Segmental instability in cervical spondylotic myelopathy with severe disc degeneration. Spine. 2006;31:1327–1331. 30. Rabb CH. Cervical instability. J Neurosurg Spine. 2005;3:169; author reply. 31. Cook C, Brismee JM, Fleming R, Sizer PS Jr. Identifiers suggestive of clinical cervical spine instability: a Delphi study of physical therapists. Phys Ther. 2005;85:895–906. 32. Hardin J Jr. Pain and the cervical spine. Bull Rheum Dis. 2001;50:1–4. 33. McKenzie RA, May S. The Cervical and Thoracic Spine: Mechanical Diagnosis and Therapy. Waikanae, NZ: Spinal Publications; 2006. 34. Mottram SL. Dynamic stability of the scapula. Man Ther. 1997;2:123–131. 35. Sahrmann SA. Diagnosis and Treatment of Movement Impairment Syndromes. St. Louis, MO: Mosby; 2002. 36. Donato EB, DuVall RE, Godges JJ, Zimmerman GJ, Greathouse DG. Practice analysis: defining the clinical practice of primary contact physical therapy. J Orthop Sports Phys Ther. 2004;34:284–304. 37. Donato EB. Physical Examination Procedures to Screen for Serious Disorders of the Head, Neck, Chest, and Upper Quarter. La Crosse, WI: Orthopaedic Section, APTA, Inc; 2003. 38. American Medical Association. In: Cocchiarella L, Andersson GBJ, eds. Guides to the Evaluation of Permanent Impairment. 5 ed. Chicago, IL: American Medical Association; 2001. 39. Tousignant M, de Bellefeuille L, O’Donoughue S, Grahovac S. Criterion validity of the cervical range of motion (CROM) goniometer for cervical flexion and extension. Spine. 2000;25:324–330. 40. Tousignant M, Smeesters C, Breton AM, Breton E, Corriveau H. Criterion validity study of the cervical range of motion (CROM) device for rotational range of motion on healthy adults. J Orthop Sports Phys Ther. 2006;36:242–248. 41. Wainner RS, Fritz JM, Irrgang JJ, Boninger ML, Delitto A, Allison S. Reliability and diagnostic accuracy of the clinical examination and patient self-report measures for cervical radiculopathy. Spine. 2003;28:52–62. 42. Cyriax J. Textbook of Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions. 8th ed. London, England: Bailliere Tindall; 1982. 43. Ehrhard R, Bowling RW. Treatment of the cervical spine: APTA: Orthopedic Section; 1996. 44. Falla D, Bilenkij G, Jull G. Patients with chronic neck pain demonstrate altered patterns of muscle activation during performance of a functional upper limb task. Spine. 2004;29:1436–1440. 45. Falla D, Jull G, Edwards S, Koh K, Rainoldi A. Neuromuscular efficiency of the sternocleidomastoid and anterior scalene muscles in patients with chronic neck pain. Disabil Rehabil. 2004;26:712–717. 46. Landes P, Malanga GA, Nadler SF, Farmer J. Physical examination of the cervical spine. In: Malanga GA, Nadler SF, eds. Musculoskeletal Physical Examination—An Evidence-based Approach. Philadelphia, PA: Elsevier-Mosby; 2006:33–57.

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47. Fjellner A Bexander C, Faleij R, Strender LE. Interexaminer reliability in physical examination of the cervical spine. J Manipulative Physiol Ther. 1999;22:511–516. 48. Smedmark V, Wallin M, Arvidsson I. Inter-examiner reliability in assessing passive intervertebral motion of the cervical spine. Man Ther. 2000;5:97–101. 49. Strender LE, Lundin M, Nell K. Interexaminer reliability in physical examination of the neck. J Manipulative Physiol Ther. 1997;20: 516–520. 50. Viikari-Juntura E. Interexaminer reliability of observations in physical examinations of the neck. Phys Ther. 1987;67:1526–1532. 51. Pool JJ, Hoving JL, de Vet HC, van Mameren H, Bouter LM. The interexaminer reproducibility of physical examination of the cervical spine. J Manipulative Physiol Ther. 2004;27:84–90. 52. Yung E, Wong M, Williams H, Mache K. Blood pressure and heart rate response to posteriorly directed pressure applied to the cervical spine in young, pain-free individuals: a randomized, repeated-measures, double-blind, placebo-controlled study. J Orthop Sports Phys Ther. 2014; 44:622–6. 53. Bobos P, MacDermid JC, Walton DM, Gross A, Santaguida PL. Patientreported outcome measures used for neck disorders: an overview of systematic reviews. J Orthop Sports Phys Ther. 2018;48:775–788. 54. Hoving JL, O’Leary EF, Niere KR, Green S, Buchbinder R. Validity of the neck disability index, Northwick Park neck pain questionnaire, and problem elicitation technique for measuring disability associated with whiplash-associated disorders. Pain. 2003;102:273–281. 55. Fejer R, Jordan A, Hartvigsen J. Categorising the severity of neck pain: establishment of cut-points for use in clinical and epidemiological research. Pain. 2005;119:176–182. 56. Pinfold M, Niere KR, O’Leary EF, Hoving JL, Green S, Buchbinder R. Validity and internal consistency of a whiplash-specific disability measure. Spine. 2004;29:263–268. 57. Niere K. The Whiplash Disability Questionnaire (WDQ). Aust J Physiother. 2006;52:151. 58. Fankhauser CD, Mutter U, Aghayev E, Mannion AF. Validity and responsiveness of the Core Outcome Measures Index (COMI) for the neck. Eur Spine J. 2012;21:101–114. 59. Bolton JE, Humphreys BK. The Bournemouth Questionnaire: a shortform comprehensive outcome measure. II. Psychometric properties in neck pain patients. J Manipulative Physiol Ther. 2002;25:141–148. 60. Hall T, Robinson K. The flexion-rotation test and active cervical mobility—a comparative measurement study in cervicogenic headache. Man Ther. 2004;9:197–202. 61. Tong HC, Haig AJ, Yamakawa K. The spurling test and cervical radiculopathy. Spine. 2002;27:156–159. 62. Lindgren KA, Leino E, Manninen H. Cervical rotation lateral flexion test in brachialgia. Arch Phys Med Rehabil. 1992;73(8):735–737. 63. Roos DB. Congenital anomalies associated with thoracic outlet syndrome. J Surg. 1976;132:771–778. 64. Wright IS. The neurovascular syndrome produced by hyperabduction of the arms. Am Heart J. 1945;29:1–19. 65. Saturno PJ, Medina F, Valera F, Montilla J, Escolar P, Gascon JJ. Validity and reliability of guidelines for neck pain treatment in primary health care. A nationwide empirical analysis in Spain. Int J Qual Health Care. 2003;15:487–493. 66. Hoving JL, de Vet HC, Koes BW, et al. Manual therapy, physical therapy, or continued care by the general practitioner for patients with neck pain: long-term results from a pragmatic randomized clinical trial. Clin J Pain. 2006;22:370–377. 67. Gross AR, Aker PD, Goldsmith CH, Peloso P. Physical medicine modalities for mechanical neck disorders. Cochrane Database Syst Rev. 2000;(2):CD000961. 68. Falla D. Unravelling the complexity of muscle impairment in chronic neck pain. Man Ther. 2004;9:125–133. 69. Falla DL, Jull GA, Hodges PW. Patients with neck pain demonstrate reduced electromyographic activity of the deep cervical flexor muscles during performance of the craniocervical flexion test. Spine. 2004;29:2108–2114. 70. Cleland JA, Childs JD, McRae M, Palmer JA, Stowell T. Immediate effects of thoracic manipulation in patients with neck pain: a randomized clinical trial. Man Ther. 2005;10:127–135. 71. Cleland JA, Glynn P, Whitman JM, Eberhart SL, MacDonald C, Childs JD. Short-term effects of thrust versus nonthrust mobilization/manipulation directed at the thoracic spine in patients with neck pain: a randomized clinical trial. Phys Ther. 2007;87:431–440.

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95. Ligthart L, Gerrits MM, Boomsma DI, Penninx BW. Anxiety and depression are associated with migraine and pain in general: an investigation of the interrelationships. J Pain. 2013;14:363–370. 96. Collins JJ, Baase CM, Sharda CE, et al. The assessment of chronic health conditions on work performance, absence, and total economic impact for employers. J Occup Environ Med. 2005;47:547–557. 97. Boudreau SA, Farina D, Falla D. The role of motor learning and neuroplasticity in designing rehabilitation approaches for musculoskeletal pain disorders. Man Ther. 2010;15:410–414. 98. Rao R. Neck pain, cervical radiculopathy, and cervical myelopathy: pathophysiology, natural history, and clinical evaluation. J Bone Joint Surg Am. 2002;84-A:1872–1881. 99. Chen TY. The clinical presentation of uppermost cervical disc protrusion. Spine. 2000;25:439–442. 100. Young WF. Cervical spondylotic myelopathy: a common cause of spinal cord dysfunction in older persons. Am Fam Phys. 2000;62:1064–1070, 1073. 101. Cleland JA, Fritz JM, Whitman JM, Palmer JA. The reliability and construct validity of the Neck Disability Index and patient specific functional scale in patients with cervical radiculopathy. Spine. 2006;31:598–602. 102. Johnson JP, Filler AG, McBride DQ, Batzdorf U. Anterior cervical foraminotomy for unilateral radicular disease. Spine. 2000;25:905–909. 103. Panjabi MM. Clinical spinal instability and low back pain. J Electromyogr Kinesiol. 2003;13:371–379. 104. Crowe H, ed. Injuries to the Cervical Spine. Presentation to the annual meeting of the Western Orthopaedic Association: San Francisco; 1928. 105. Walton DM, Elliott JM. An integrated model of chronic whiplashassociated disorder. J Orthop Sports Phys Ther. 2017;47:462–471. 106. Zaloshnja E, Miller TR, Blincoe LJ. Costs of alcohol-involved crashes, United States, 2010. Ann Adv Automo Med. 2013;57:3–12. 107. Ferrari R, Russell AS. Epidemiology of whiplash: an international dilemma. Ann Rheum Dis. 1999;58:1–5. 108. Lankester BJ, Garneti N, Gargan MF, Bannister GC. Factors predicting outcome after whiplash injury in subjects pursuing litigation. Eur Spine J. 2006;15:902–907. 109. Sarrami P, Armstrong E, Naylor JM, Harris IA. Factors predicting outcome in whiplash injury: a systematic meta-review of prognostic factors. J Orthop Traumatol. 2017;18:9–16. 110. Fritz J. Toward improving outcomes in whiplash: implementing new directions of care. J Orthop Sports Phys Ther. 2017;47:447–448. 111. Elliott JM, Walton DM. How do we meet the challenge of whiplash? J Orthop Sports Phys Ther. 2017;47:444–446. 112. Nordhoff LS Jr. Cervical trauma following motor vehicle collisions. In: Murphy DR, ed. Cervical Spine Syndromes. New York: McGraw-Hill; 2000:131–150. 113. Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders. Spine. 1995;20:33S, 8S–9S. 114. Nikolai MD, Teasell R. Whiplash: the evidence for an organic etiology. Arch Neurol. 2000;57:590–591. 115. McGwin G Jr., Metzger J, Alonso JE, Rue LW, III. The association between occupant restraint systems and risk of injury in frontal motor vehicle collisions. J Trauma. 2003;54:1182–1187. 116. Segui-Gomez M. Driver air bag effectiveness by severity of the crash. Am J Public Health. 2000;90:1575–1581. 117. Elliott J, Pedler A, Kenardy J, Galloway G, Jull G, Sterling M. The temporal development of fatty infiltrates in the neck muscles following whiplash injury: an association with pain and posttraumatic stress. PLoS One. 2011;6:e21194. 118. Elliott JM, Courtney DM, Rademaker A, Pinto D, Sterling MM, Parrish TB. The rapid and progressive degeneration of the cervical multifidus in whiplash: an MRI study of fatty infiltration. Spine. 2015;40:E694–E700. 119. Sterling M, Ng TS, Walton D, Smith A. Whiplash-associated disorders. In: Jull G, Moore A, Falla D, Lewis J, McCarthy C, Sterling M, eds. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. London, England: Elsevier; 2015:423–432. 120. Leeuw M, Goossens ME, Linton SJ, Crombez G, Boersma K, Vlaeyen JW. The fear-avoidance model of musculoskeletal pain: current state of scientific evidence. J Behav Med. 2007;30:77–94. 121. Turk DC. A diathesis-stress model of chronic pain and disability following traumatic injury. Pain Res Manag. 2002;7:9–19. 122. Martin AL, Halket E, Asmundson GJ, Flora DB, Katz J. Posttraumatic stress symptoms and the diathesis-stress model of chronic pain and disability in patients undergoing major surgery. Clin J Pain. 2010;26:518–527.

The Cervical Spine

72. Cleland JA, Mintken PE, Carpenter K, et al. Examination of a clinical prediction rule to identify patients with neck pain likely to benefit from thoracic spine thrust manipulation and a general cervical range of motion exercise: multi-center randomized clinical trial. Phys Ther. 2010;90:1239–1250. 73. Dunning JR, Cleland JA, Waldrop MA, et al. Upper cervical and upper thoracic thrust manipulation versus nonthrust mobilization in patients with mechanical neck pain: a multicenter randomized clinical trial. J Orthop Sports Phys Ther. 2012;42:5–18. 74. Masaracchio M, Cleland JA, Hellman M, Hagins M. Short-term combined effects of thoracic spine thrust manipulation and cervical spine nonthrust manipulation in individuals with mechanical neck pain: a randomized clinical trial. J Orthop Sports Phys Ther. 2013;43:118–127. 75. Kennedy CN. The cervical spine. In: Hall C, Thein-Brody L, eds. Therapeutic Exercise: Moving Toward Function. Baltimore, MD: Lippincott Williams & Wilkins; 2005:582–609. 76. Bird SP, Tarpenning KM, Marino FE. Designing resistance training programmes to enhance muscular fitness: a review of the acute programme variables. Sports Med. 2005;35:841–851. 77. Alves-Guerreiro J, Noble JG, Lowe AS, Walsh DM. The effect of three electrotherapeutic modalities upon peripheral nerve conduction and mechanical pain threshold. Clin Physiol. 2001;21:704–711. 78. Barati K, Arazpour M, Vameghi R, Abdoli A, Farmani F. The effect of soft and rigid cervical collars on head and neck immobilization in healthy subjects. Asian Spine J. 2017;11:390–395. 79. Stanton D, Hardcastle T, Muhlbauer D, van Zyl D. Cervical collars and immobilisation: a South African best practice recommendation. Afr J Emerg Med. 2017;7:4–8. 80. Lee H, Nicholson LL, Adams RD. Cervical range of motion associations with subclinical neck pain. Spine. 2004;29:33–40. 81. Roddey T, Olson S, Grant S. The effect of pectoralis muscle stretching on the resting position of the scapula in persons with varying degrees of forward head/rounded shoulder posture. J Man Manipulative Ther. 2002;10:124–128. 82. Wright E, Domenech M, Fischer J. Usefulness of posture training for patients with temporomandibular disorders. J Am Dent Assoc. 2000;131:202–210. 83. Harman K, Hubley-Kozey CL, Butler H. Effectiveness of an exercise program to improve forward head posture in normal adults: a randomized, controlled 10-week trial. J Man Manipulative Ther. 2005;13:163–176. 84. Humphreys BK, Irgens PM. The effect of a rehabilitation exercise program on head repositioning accuracy and reported levels of pain in chronic neck pain subjects. J Whiplash Relat Disord. 2002; 1:99–112. 85. de Jager JP, Ahern MJ. Improved evidence-based management of acute musculoskeletal pain: guidelines from the National Health and Medical Research Council are now available. Med J Aust. 2004;181:527–528. 86. Jull G, Falla D, O’Leary S, McCarthy C. Cervical spine: idiopathic neck pain. In: Jull G, Moore A, Falla D, Lewis J, McCarthy C, Sterling M, eds. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. London, England: Elsevier; 2015:410–422. 87. Farioli A, Mattioli S, Quaglieri A, Curti S, Violante FS, Coggon D. Musculoskeletal pain in Europe: the role of personal, occupational, and social risk factors. Scand J Work Environ Health. 2014;40:36–46. 88. Martin BI, Deyo RA, Mirza SK, et al. Expenditures and health status among adults with back and neck problems. JAMA. 2008;299:656–664. 89. Carroll LJ, Holm LW, Hogg-Johnson S, et al. Course and prognostic factors for neck pain in whiplash-associated disorders (WAD): results of the Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders. Spine. 2008;33:S83–S92. 90. Wakaizumi K, Yamada K, Oka H, et al. Fear-avoidance beliefs are independently associated with the prevalence of chronic pain in Japanese workers. J Anesth. 2017 31:255–262. 91. Linton SJ, Shaw WS. Impact of psychological factors in the experience of pain. Phys Ther. 2011;91:700–711. 92. Lozada HL. Addressing yellow flags in the care of a patient with chronic neck pain: a case report. Ortho Phys Ther Pract. 2017;29:44–51. 93. Cleland JA, Childs JD, Fritz JM, Whitman JM, Eberhart SL. Development of a clinical prediction rule for guiding treatment of a subgroup of patients with neck pain: use of thoracic spine manipulation, exercise, and patient education. Phys Ther. 2007;87:9–23. 94. Pelletier R, Higgins J, Bourbonnais D. Addressing neuroplastic changes in distributed areas of the nervous system associated with chronic musculoskeletal disorders. Phys Ther. 2015;95:1582–1591.

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123. Scholten-Peeters GG, Verhagen AP, Bekkering GE, et al. Prognostic factors of whiplash-associated disorders: a systematic review of prospective cohort studies. Pain. 2003;104:303–322. 124. Rebbeck T. The role of exercise and patient education in the noninvasive management of whiplash. J Orthop Sports Phys Ther. 2017;47: 481–491. 125. Neck Pain Guidelines: Revision 2017: Using the Evidence to Guide Physical Therapist Practice. J Orthop Sports Phys Ther. 2017;47: 511–512. 126. Elliott J, Cannata E, Christensen E, et al. MRI analysis of the size and shape of the oropharynx in chronic whiplash. Otolaryngol Head Neck Surg. 2008;138:747–751.

127. Elliott JM, Pedler AR, Theodoros D, Jull GA. Magnetic resonance imaging changes in the size and shape of the oropharynx following acute whiplash injury. J Orthop Sports Phys Ther. 2012;42:912–918. 128. Cassidy JD, Carroll LJ, Cote P, Lemstra M, Berglund A, Nygren A. Effect of eliminating compensation for pain and suffering on the outcome of insurance claims for whiplash injury. N Engl J Med. 2000;342:1179–1186. 129. Illig KA. Thoracic outlet syndrome in adolescents is real: comment on “Spectrum of thoracic outlet syndrome presentation in adolescents.” Arch Surg. 2011;146:1388. 130. Mulligan BR. Manual Therapy: “NAGS”, “SNAGS”, “PRP’S” etc. Wellington: Plane View Series; 1992.

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C H A P T E R 2 6

CHAPTER OBJECTIVES At the completion of this chapter, the reader will be able to: 1. Describe the anatomy of the temporomandibular joint (TMJ), including the bones, ligaments, muscles, and blood and nerve supply. 2. Describe the biomechanics of the TMJ, including the movements, normal and abnormal joint barriers, kinesiology, and reactions to various stresses. 3. Summarize the various causes of temporomandibular dysfunction (TMD). 4. Describe the close association between the TMJ, the middle ear, and the cervical spine. 5. Perform a comprehensive examination of the temporomandibular musculoskeletal system, including palpation of the articular and soft-tissue structures, specific passive mobility, and passive articular mobility tests, and stability tests. 6. Evaluate the total examination data to establish a diagnosis. 7. Recognize the manifestations of abnormal TMJ function and develop strategies to correct these abnormalities. 8. Apply active and passive mobilization techniques to the TMJ, using the correct grade, direction, and duration. 9. Describe and demonstrate intervention strategies and techniques based on clinical findings and established goals. 10. Evaluate the intervention effectiveness in order to progress or modify an intervention. 11. Plan an effective home program and instruct the patient in this program.

The Temporomandibular Joint

OVERVIEW Approximately 50–75% of the general population has experienced unilateral temporomandibular joint dysfunction (TMD) on a minimum of one occasion and that at least 33% have reported a minimum of one continuing persistent symptom.1,2 The American Academy of Orofacial Pain uses orofacial pain as a collective term for a number of dysfunctions and sensory complaints associated with the TMJ, the masticatory muscles, and associated structures.3 It encompasses terms such as Costen syndrome, TMD, craniomandibular disorders, and mandibular dysfunction. TMD is a collective term used to describe a number of related disorders affecting the stomatognathic system and its related structures, all of which may have common symptoms. The term TMJ dysfunction as an overall descriptor of stomatognathic system dysfunction has been discontinued because it implies structural problems when none may exist, and does not include the many other factors that may be involved. Housed within the skull are the components of the stomatognathic system, which includes the TMJ, the masticatory systems, and the related organs and tissues such as the inner ear and salivary glands.4 An interrelationship exists between the stomatognathic system and the head and neck due to their proximity and shared embryological development. An understanding of this relationship is vital to understand the reasons for the myriad of symptoms that this region can exhibit. The embryological structures from which the head, the face, and the neck originate are segmentally organized during development with the appearance and modification of six paired branchial or pharyngeal arches.4 These branchial arches contain the cranial nuclei of the trigeminal nerve (ophthalmic; maxillary and mandibular), the facial, the glossopharyngeal, and the laryngeal branch of the vagus nerve as well as the hypoglossal nerve. The first of these arches, the mandibular arch, consists of a large anterior (ventral) part (the mandibular process of Meckel’s cartilage) and a small posterior (dorsal) (maxillary) process. As development progresses, both processes disappear

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except for two small portions at the posterior (dorsal) ends, which persist. The first brachial arch forms the mandible; the rudiments of the inner ear bones, the malleus, and incus; ▶▶ the anterior malleolar and sphenomandibular ligaments of the TMJ; ▶▶ the tensor tympani and the tensor veli palatini of the inner ear; ▶▶ the mylohyoid and the anterior belly of the digastric muscle; and ▶▶ the trigeminal mandibular nerve. ▶▶ ▶▶

THE SPINE AND TMJ

The second pharyngeal arch (the hyoid arch) consists of Reichert’s cartilage. This arch is involved in the formation of the superior component of the hyoid bone and the lesser cornu bone; ▶▶ the stapes muscle; ▶▶ the temporal styloid process; ▶▶ the stylohyoid ligament; ▶▶

the stapedius muscle; the stylohyoid muscle; ▶▶ the posterior belly of the digastric muscle; ▶▶ the muscles of facial expression and mastication; ▶▶ the platysma muscle; and ▶▶ ▶▶

▶▶

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the glossopharyngeal nerve.

The third pharyngeal arch is involved in the formation of the greater cornu of the hyoid and its body, the stylopharyngeal muscle, and the sensory apparatus of the posterior onethird of the tongue. The fourth pharyngeal arch combines with the sixth arch to form the thyroid, cricoid, and arytenoid cartilages of the larynx. The muscles derived from this arch are the pharyngeal constrictors (the cricothyroid) and the intrinsic muscles of the larynx. The pharyngeal constrictors are innervated by the superior laryngeal branch of the vagus nerve. The intrinsic muscles of the larynx are innervated by the recurrent laryngeal branch of the vagus nerve. In primitive creatures, and the human fetus, vibrations through the jaw are used as a basis for hearing. At around 8½ weeks, the small bones of the inner ear (the malleus, incus, and stapes) can be seen as distinct entities. The development of the malleus bone and the tensor tympani is intimately related to that of the lateral pterygoid muscle. Due to this embryological relationship, it is theorized that a spasm of the lateral pterygoid muscle can increase the tension within the tensor tympani (similar to that of a drum skin)4 resulting in increased sensitivity to pitch and vibration. Theoretically, this increased tension could produce sensorineural tinnitus, or ringing in the ears, a common associated symptom of a TMD, and an injury to the craniovertebral region. The diagnosis of TMD, like that of whiplash syndrome, remains controversial. This is due in part to a paucity of studies regarding the incidence, course, management, and prognosis of claimed TMDs. However, reports of TMD appear to

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be quite common. TMD tends to affect women more often than men,5 specifically women over the age of 55.6 Headaches, orofacial pain, earache, and neck pain are common complaints. Clinical and research report indicate that head and orofacial pain around the TMJ may or may not be related to TMD.7,8 Due to the complex interplay between the sympathetic and trigeminal nervous systems and an increased understanding of the centralization of pain, TMD is best approached as a cluster of related disorders that have many causes and common symptoms. There are likely four etiologic characteristics of TMD: (1) myogenic, (2) traumatic, (3) arthrogenic, and (4) neurogenic factors3: Myofascial TMD pain, which is often described as pain around the TMJ without reference to a particular pathophysiological mechanism, can occur during orofacial activities such as chewing, swallowing, sucking, speaking, and facial expression. Dental occlusion, parafunctional activities, neuroendocrine factors, genetic factors, and stress that pass a certain threshold have all been associated with chronic TMD pain. ▶▶ Traumatic factors generally fall into the following three categories: (1) overt, extrinsic trauma to the head, the neck, or the jaw; (2) repeated low-grade extrinsic trauma, such as nail biting and chewing gum; and (3) repeated low-grade intrinsic trauma such as teeth clenching or bruxism (grinding teeth). ▶▶

Arthrogenic causes of TMD include hypermobility/ dislocation, osteoarthrosis/itis, disk displacements, joint adhesions, and ankylosis. ▶▶ Neurogenic causes of TMD, which include trigeminal, laryngeal, and glossopharyngeal neuralgia, are characterized by unpredictable episodic sharp, stabbing facial pain. Thus, given the number of potential causes of jaw and face pain, a diagnosis of TMD can rarely be ascribed solely to the TMJ. A diagnosis of TMD must, therefore, include an examination of all of the following: ▶▶

Jaw and facial muscles ▶▶ Bone and cartilage joint structures ▶▶ Facial structures ▶▶ Soft-tissue joint structures, including the articular disk and synovium ▶▶ TMJ function ▶▶ Cervical and upper thoracic spine function ▶▶ Postural dysfunction ▶▶ Systemic disease ▶▶ Psychosocial issues ▶▶

Nonsurgical interventions such as counseling, physical therapy, pharmacotherapy, and occlusal splint therapy continue to be the most effective way of managing the vast majority of patients with TMD. Although dentists are the primary professionals involved in the examination and intervention of TMD, physical therapists can play an important role in assisting the dentist in restoring function to the stomatognathic

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ANATOMY

Bony Anatomy A number of bony components make up the masticatory system: the maxilla and the mandible, which support the teeth, and the temporal bone, which supports the mandible at its articulation with the skull. The sphenoid bone and the hyoid bone also could be included, because they provide important anatomic and functional links to the TMJ. Zygomatic arch (cut)

The borders of the maxillae extend superiorly to form the floor of the nasal cavity as well as the floor of each orbit (Fig. 26-1). Inferiorly, the maxillary bones form the palate and the alveolar ridges, which support the teeth. The maxillae and mandible each contains 16 permanent teeth. The structure of each tooth reflects its function in mastication.

Sphenoid Bone The greater wings of the sphenoid bone form the boundaries of the anterior part of the middle cranial fossa. From these greater wings, the pterygoid laminae serve as the attachments for the medial and lateral pterygoid muscles.

Hyoid Bone The U-shaped hyoid bone (Fig. 26-2), also known as the skeleton of the tongue, serves as the attachment for the infrahyoid muscles and for some of the extrinsic tongue muscles. The hyoid bone is involved with the mandible to provide reciprocal stabilization during swallowing and chewing. Theoretically, due to its muscle attachments, the position of the hyoid bone can be affected by cervical and shoulder positions, as occurs during forward head posture (FHP), which changes the length–tension relationships.

The Temporomandibular Joint

The TMJ (Fig. 26-1) is a synovial, compound, modified ovoid bicondylar joint, which is formed between the articular eminence of the temporal bone, the intra-articular disk, and the head of the mandible. The TMJ is unique in that, even though the joint is synovial, the articulating surfaces of the bones are covered not by hyaline cartilage but by fibrocartilage.4 Fibrocartilage has the same general properties found in hyaline cartilage but tends to be less distensible, owing to a greater proportion of dense collagen fibers (see Chapter 1). The development of fibrocartilage over the load-bearing surface of the TMJ indicates that the joint is designed to withstand large and repeated stresses and that this area of the joint surface has a greater capacity to repair itself than would hyaline cartilage.4 The area of load bearing is affected by the congruity of the contacting tooth surfaces (occlusion), head position, and the coordination of muscle function. The fibrocartilage is at its thinnest at the roof of the fossa, but load bearing here occurs only in the presence of dysfunction. The mandible works like a class-three lever (see Chapter 1), with its joint as the fulcrum.

Maxilla

ANATOMY

system. However, the procedures in physical therapy intervention are not well described in the literature.

Mandible The mandible, or jaw (Fig. 26-1), which supports the lower teeth, is the largest and the strongest bone in the face. It is suspended below the maxillae by muscles and ligaments that provide it with both mobility and stability. The medial surface of the mandible serves as the attachment for the medial pterygoid and the digastric muscles. The platysma, mentalis, and buccinator gain attachment on its lateral aspect. Two broad, vertical rami extend upward from the mandible: the condyle and the coronoid process. The anterior of the two processes, the coronoid, serves as the attachment for the temporalis and masseter muscles.4 The condyle process articulates with the temporal bone. The bony surfaces of the condyle and the articular portion of the temporal bone are made of dense cortical bone. The articulating surface of the condyle is flattened from front to back with its medial–lateral length twice as long as its anterior–posterior length. The condyles are generally convex, possessing short bony projections known as medial and lateral poles.9

Temporal Bone

Mastoid process Styloid process

Pterygomaxillary fissure and pterygoid plate Maxilla

Infratemporal fossa

FIGURE 26-1 The temporomandibular joint. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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The mandibular fossa of the temporal bone is divided into two surfaces: articular and nonarticular.9 The articulating surface of the temporal bone is made up of a concave mandibular, or glenoid fossa, and a convex bony prominence called the articular eminence.4 The articular tubercle, situated anterior to the glenoid fossa, serves as an attachment for the temporomandibular (or lateral) ligament.4 The nonarticular surface of the fossa consists of a very thin layer of bone and fibrocartilage that occupies much of the superior and posterior walls of the fossa.9

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ANATOMY

Mastoid process

Styloid process

THE SPINE AND TMJ

Digastric m. (posterior belly) Mandible Stylohyoid m.

Hyoglossus m. Mylohyoid m.

Digastric, intermediate tendon

Digastric m. (anterior belly)

Connective-tissue sling

Hyoid bone Infrahyoid mm.

FIGURE 26-2  The hyoid bone and related muscles. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

Fibrocartilaginous Disk Located between the articulating surface of the temporal bone and the mandibular condyle is a fibrocartilaginous disk (sometimes inappropriately referred to as “meniscus”) (Fig. 26-3). The biconcave shape of the disk is determined by the shape of the condyle and the articulating fossa. The fibrocartilaginous disk has three clearly defined transverse, ellipsoidal zones that are divided into three regions— posterior band, intermediate zone, and anterior band—of which the intermediate zone makes contact with the articular surface of the condyle.4 Both the disk and the lateral pterygoid muscle develop from the first branchial arch, and there is very little differentiation among the muscle, the disk, and the joint capsule. The fibrocartilaginous disk is tethered by a number of structures10,11: Medial and lateral collateral diskal ligaments firmly attach the fibrocartilaginous disk to the medial and lateral poles of the condyle, permitting anterior and posterior rotation of the disk on the condyle during mouth opening and closing. ▶▶ Posteriorly, the disk is attached by fibroelastic tissue to the posterior mandibular fossa and the back of the mandibular condyle. ▶▶ Anteriorly, the disk is attached to the upper part of the tendon of the lateral pterygoid muscle (Fig. 26-3). ▶▶

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The disk usually is located on top of the condyle in the 12 o’clock to 1 o’clock position on the mandibular head when the jaw is closed. Since the only firm attachment of the disk to

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the condyle occurs medially and laterally, the disk can move somewhat independently of the condyle. The disk effectively divides the TMJ into a lower and an upper joint cavity (see Fig. 26-3):4 Lower compartment.  This compartment, bordered by the mandibular condyle and the inferior surface of the articular disk, is where, under normal conditions, the osteokinematic spin (rotation) of the condyle occurs. ▶▶ Upper compartment.  This compartment, bordered by the mandibular fossa and the superior surface of the articular disk, primarily allows only translation of the disk and condyle along the fossa, and onto the articular eminence. ▶▶

Blood vessels and nerves are found only in the thickened periphery of this disk, especially its posterior attachment; its middle articular portion is avascular and aneural.4

Supporting Structures The supporting structures of the TMJ consist of periarticular connective tissue (ligament, tendon, capsule, and fascia). As its name implies, the periarticular connective tissue serves to keep the joints together and to limit the ranges of motion at the joint. For example, the ligaments of the TMJ protect and support the joint structures and act as passive restraints to joint movement. The synovial cavities are surrounded by loose connective tissue rather than by ligaments. The intercapsular structures are located posteriorly to the condyle. Anterior to the joint are the muscles of the medial

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Articular disk

Superior compartment of joint capsule Inferior compartment of joint capsule Lateral pterygoid m.

ANATOMY

Mandibular fossa

Capsule

A Lateral pterygoid m.

Protrusion of articular disk and mandibular condyle

The Temporomandibular Joint

Mandibular condyle

Protrusion Depression

B Hinge movement FIGURE 26-3  The TMJ disk and the pterygoid. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

and lateral pterygoid (see next section). There are no welldefined anterior or posterior ligaments between the mandibular condyle and the temporal bone. However, two strong ligaments help to provide joint stability: 1. Joint capsule or capsular ligament. This structure, which surrounds the entire joint, is thought to provide proprioceptive feedback regarding the joint position and movement. 2. Temporomandibular (or lateral) ligament. The capsule of the TMJ is reinforced laterally by an outer oblique portion and an inner horizontal portion of the temporomandibular ligament, which function as a suspensory mechanism for the mandible during moderate opening movements. The ligament also functions to resist rotation and posterior displacement of the mandible. Two other ligaments assist with joint stability: ▶▶

Stylomandibular ligament.  The stylomandibular ligament is a specialized band that splits away from the superficial lamina of the deep cervical fascia to run deep to both pterygoid muscles.4 This ligament becomes taut and acts as a guiding mechanism for the mandible,

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keeping the condyle, disk, and temporal bone firmly opposed. ▶▶ Sphenomandibular ligament.  The sphenomandibular ligament is a thin band that runs from the spine of the sphenoid bone to a small bony prominence on the medial surface of the ramus of the mandible, called the lingula. This ligament acts to check the angle of the mandible from sliding as far forward as the condyles during the translatory cycle and serves as a suspensory ligament of the mandible during wide opening.4 It is this ligament that hurts with any prolonged jaw opening, such as that which occurs at the dentist.

CLINICAL PEARL Pinto’s ligament is a vestige of Meckel’s cartilage, an embryological tissue. It arises from the neck of the malleus of the inner ear and runs in a medial-superior direction to insert into the posterior aspect of the TMJ capsule and disk. While the role of this ligament in mandibular mechanics is thought to be negligible, its relationship to the middle ear and the TMJ could be a basis for the middle ear symptoms, which are often present with TMD.

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Temporalis m. (cut)

ANATOMY

Temporalis m.

THE SPINE AND TMJ

Lateral pterygoid mm.

Medial pterygoid m.

A

Masseter m.

B

Buccinator m. (not a muscle of mastication)

Masseter m. (cut)

FIGURE 26-4  Lateral view of TMJ. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

Muscles The muscles of mastication are the key muscles when discussing TMD. Three of these muscles, the masseter, the medial pterygoid, and the temporalis (Fig. 26-4), function to raise the mandible during mouth closing. The lateral pterygoid and digastric muscles work together to depress the mandible during mouth opening. Although these muscles work most efficiently in groups, an understanding of the specific anatomy and action(s) of the individual muscles is necessary for an appreciation of their coordinated function during masticatory activity (Tables 26-1 and 26-2).

Temporalis The temporalis muscle (Fig. 26-4) has its origin from the floor of the temporal fossa and the temporal fascia. The muscle travels inferiorly and anteriorly to insert on the anterior border of the coronoid process and the anterior border of the ramus of the mandible. The temporalis muscle is innervated by a branch of the mandibular division of the trigeminal nerve. In addition to assisting with mouth closing and sideto-side grinding of the teeth, the temporalis muscle provides a good deal of stability to the joint.

The Masseter

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The masseter (Fig. 26-4) is a two-layered quadrilateral-shaped muscle. The superficial portion arises from the anterior twothirds of the lower border of the zygomatic arch. The deep portion arises from the medial surface of the zygomatic arch. Both sets of fibers blend anteriorly and form a raphe with the medial pterygoid.4 The masseter inserts on the lateral surface of the coronoid process of the mandible, the upper half of the ramus and angle of the mandible. The masseter

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muscle is innervated by a branch of the mandibular division of the trigeminal nerve. The major function of the masseter is to elevate the mandible, thereby occluding the teeth during mastication.

The Medial Pterygoid The medial pterygoid muscle is a thick quadrilateral muscle, with a deep origin situated on the medial aspect of the mandibular ramus (Fig. 26-4). The muscle travels posteriorly to insert on the inferior and posterior aspects of the medial subsurface of the ramus and angle of the mandible. The medial pterygoid muscle is innervated by a branch of the mandibular division of the trigeminal nerve. Working bilaterally, and in association with the masseter and temporalis muscles, the medial pterygoids assist in mouth closing. Individually, the medial pterygoid muscle is capable of deviating the mandible toward the opposite side. The medial pterygoid muscle also acts as an assistance to the lateral pterygoid and anterior fibers of the temporalis muscle to produce protrusion of the mandible.

The Lateral Pterygoid Two divisions of the lateral pterygoid muscles are recognized, each of which is functionally and anatomically separate (Figs. 26-3 and 26-4). The superior head arises from the infratemporal surface of the greater wing of the sphenoid. The inferior head arises from the lateral surface of the lateral pterygoid plate. The most commonly described insertion is at the anterior aspect of the neck of the mandibular condyle and capsule of the TMJ. The lateral pterygoid muscle is innervated by a branch of the mandibular division of the trigeminal nerve. The superior head of the lateral pterygoid is involved mainly with chewing and functions to rotate the disk

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Muscles of the Temporomandibular Joint Proximal

Distal

Innervation

Medial pterygoid

Medial surface of lateral pterygoid plate and tuberosity of maxilla

Medial surface of mandible close to angle

Mandibular division of trigeminal nerve

Lateral pterygoid

Greater wing of sphenoid and lateral pterygoid plate

Neck of mandible and articular cartilage

Mandibular division of trigeminal nerve

Temporalis

Temporal cranial fossa

By way of a tendon into medial surface, apex, and anterior and posterior borders of mandibular ramus

Anterior and posterior deep temporal nerves, which branch from anterior division of mandibular branch of trigeminal nerve

Masseter

Superficial portion: from anterior two-thirds of lower border of zygomatic arch; deep portion from medial surface of zygomatic arch

Lateral surfaces of coronoid process of mandible, upper half of ramus, and angle of mandible

Masseteric nerve from anterior trunk of mandibular division of trigeminal nerve

Mylohyoid

Medial surface of mandible

Body of hyoid bone

Mylohyoid branch of trigeminal nerve and mandibular division

Geniohyoid

Mental spine of mandible

Body of hyoid bone

Anterior (ventral) ramus of C1 via hypoglossal nerve

Stylohyoid

Styloid process of temporal bone

Body of hyoid bone

Facial nerve

Anterior and posterior digastric

Internal surface of mandible and mastoid process of temporal bone

By intermediate tendon to hyoid bone

Anterior: mandibular division of trigeminal nerve; posterior: facial nerve

Sternohyoid

Manubrium and medial end of clavicle

Body of hyoid bone

Ansa cervicalis

Omohyoid

Superior angle of scapula

Inferior body of hyoid bone

Ansa cervicalis

Sternothyroid

Posterior surface of manubrium

Thyroid cartilage

Ansa cervicalis

Thyrohyoid

Thyroid cartilage

Inferior body and greater horn of hyoid bone

C1 via hypoglossal nerve

anteriorly on the condyle during the closing movement. It has also been suggested that in normal function of the craniomandibular complex, the superior lateral pterygoid plays an important role in stabilizing and controlling the movements of the disk. The inferior head of the lateral pterygoid muscle exerts an anterior, lateral, and inferior pull on the mandible, thereby opening the jaw, protruding the mandible, and deviating the mandible to the opposite side.

Infrahyoid or “Strap” Muscles The infrahyoid muscles comprise the sternohyoid, omohyoid, sternothyroid, and thyrohyoid muscles (Fig. 26-5). Sternohyoid.  The sternohyoid muscle is a strap-like muscle that functions to depress the hyoid and assist in speech and mastication.

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Omohyoid.  The omohyoid muscle, situated lateral to the sternohyoid, consists of two bellies and functions to depress the hyoid. In addition, the muscle has been speculated to tense the inferior aspect of the deep cervical fascia in prolonged inspiratory efforts, thereby releasing tension on the apices of the lungs and on the internal jugular vein, which are attached to this fascial layer.4 Sternothyroid and Thyrohyoid. The sternothyroid and thyrohyoid muscles (see Fig. 26-5) are located deep to the sternohyoid muscle. The sternothyroid muscle is involved in drawing the larynx downward, whereas the thyrohyoid depresses the hyoid and elevates the larynx. These infrahyoid muscles are innervated by fibers from the upper cervical nerves. The nerves to the lower part of these muscles are given off from a loop, the ansa cervicalis (cervical loop) (see Chapter 3).

The Temporomandibular Joint

Muscle

ANATOMY

TABLE 26-1

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ANATOMY



TABLE 26-2

Actions of the Temporomandibular Joint Muscles

THE SPINE AND TMJ

Action

Muscles Acting

Opening of mouth      

Lateral pterygoid Mylohyoid Geniohyoid Digastric

Closing of mouth    

Masseter Temporalis Medial pterygoid

Protrusion of mandible              

Lateral pterygoid Medial pterygoid Masseter Mylohyoid Geniohyoid Digastric Stylohyoid Temporalis (anterior fibers)

Retraction of mandible          

Temporalis (posterior fibers) Masseter Digastric Stylohyoid Mylohyoid Geniohyoid

Lateral deviation of mandible  

Lateral pterygoid (ipsilateral muscle) Medial pterygoid (contralateral muscle) Temporalis Masseter

   

Suprahyoid Muscles The suprahyoid muscles (Fig. 26-2), working with the infrahyoid muscles, play a major role in coordinating mandibular function, by providing a firm base on which the tongue and mandible can be moved. Geniohyoid.  The geniohyoid muscle is a narrow muscle situated under the mylohyoid muscle. The muscle functions to elevate the hyoid bone. Digastric.  As its name suggests, the digastric muscle consists of two bellies. The posterior belly arises from the mastoid notch of the temporal bone, while the anterior belly arises from the digastric fossa of the mandible. The posterior belly is innervated by a branch of the facial nerve. The anterior belly is innervated by the inferior alveolar branch of the trigeminal nerve. The two bellies of the digastric muscle are joined by a rounded tendon that attaches to the body and greater cornu of the hyoid bone through a fibrous loop or sling.4 Bilaterally, the two bellies of the digastric muscle assist in forced mouth opening by stabilizing the hyoid. The posterior bellies are especially active during coughing and swallowing.4

CLINICAL PEARL The muscles of the TMJ, working in combinations, are involved as follows: ▶▶ Mouth opening—bilateral action of the lateral pterygoid and digastric muscles. ▶▶ Mouth closing—bilateral action of the temporalis, masseter, and medial pterygoid muscles. ▶ ▶ Lateral deviation—action of the ipsilateral masseter, and contralateral medial and lateral pterygoid muscles. ▶▶ Protrusion—bilateral action of the lateral pterygoid, medial pterygoid, and anterior fibers of the temporalis muscles. ▶▶ Retrusion—bilateral action of the posterior fibers of the temporalis muscle, the digastric, stylohyoid, geniohyoid, and mylohyoid muscles.

Mylohyoid.  This flat, triangular muscle is functionally a muscle of the tongue, stabilizing or elevating the tongue while swallowing and elevating the floor of the mouth in the first stage of deglutition.4 Stylohyoid.  The stylohyoid muscle elevates the hyoid and base of the tongue and has an undetermined role in speech, mastication, and swallowing.

Nerve Supply The TMJ is primarily supplied by three nerves that are part of the mandibular division of the fifth cranial (trigeminal) nerve (Fig. 26-6) (Box 26-1). Portions of the middle ear ossicles, middle ear musculature, and muscles of mastication all originate from the first branchial arch and are innervated by this nerve. Therefore, in a patient with altered bite mechanics, spasm of the muscles of mastication caused by a displaced condyle may cause neuromuscular dysfunction of all the muscles innervated by the trigeminal nerve. There is considerable clinical interest in the interactions between the cervical and craniofacial regions. This interest stems from a number of reports concerning patients who have pain in the cervical and craniofacial areas simultaneously.3 In the suboccipital region, a series of dense neural connections, called the trigeminocervical complex, exists among trigeminal, facial, glossopharyngeal, and vagus nerves, with those of the upper C1–4 cervical spinal nerves (Fig. 26-7).4 Postural abnormalities resulting from various acute or chronic etiologies that produce suboccipital compression may, therefore, be responsible for craniofacial pain anywhere in the head, in addition to symptoms of dizziness or nystagmus.3 TMJ-related headaches usually include pain near the TMJ and ear, ear fullness, temporal headaches, and facial pain.3

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Mylohyoid m. Stylohyoid m. Digastric m. (posterior belly)

Hyoid bone

BIOMECHANICS

Digastric m. (anterior belly)

Thyrohyoid m.

Upper Sternothyroid m.

Lower

Sternohyoid m.

Sternohyoid m. (cut)

The Temporomandibular Joint

Omohyoid m.:

FIGURE 26-5  The infrahyoid muscles. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

BIOMECHANICS The movements that occur at the TMJ are extremely complex. The TMJ has three degrees of freedom, with each of the degrees of freedom being associated with a separate axis of rotation. Two primary arthrokinematic movements (rotation and anterior translation) occur at this joint around three planes: sagittal, horizontal, and frontal. Rotation occurs from the beginning to the midrange of movement. In addition to the rotational motions during mouth opening and closing and lateral deviations, movements at the TMJ involve arthrokinematic rolls and slides. Gliding, translation, or sliding movements occur in the upper cavity, whereas rotation or hinged movement occurs in the lower cavity. The motions of protrusion and retrusion are planar glides. Thus, mouth opening, contralateral deviation, and protrusion all involve an anterior osteokinematic rotation of the mandible and an anterior, inferior, and lateral glide of the mandibular head and disk; and ▶▶ mouth closing, ipsilateral deviation, and retrusion all involve a posterior osteokinematic rotation of the mandible and an anterior, inferior, and lateral glide of the mandibular head and disk. ▶▶

Occlusal Position Occlusal positions are functional positions of the TMJ. The occlusal position is defined as the point at which contact

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between some or all of the teeth occurs. Under normal circumstances, the upper molars rest directly on the lower molars and the upper incisors slightly override the lower incisors. The ideal position provides mutual protection of the anterior and posterior teeth, comfortable and painless mandibular function, and stability. The median occlusal position corresponds to the position in which all of the teeth are fully interdigitated and is considered the start position for all mandibular motions. The median occlusal position is dependent on the presence, shape, and position of the teeth. Protrusion of the upper or lower incisors, failure of the upper incisors to overlap with the lower incisors, absent or abnormally shaped teeth, and back teeth that do not meet are all causes of malocclusion. ▶▶ The centric position is considered to be the position that implies the most retruded, unstrained position of the mandible from which lateral movements are possible, and the components of the oral apparatus are the most balanced. Ideally, the centric position should coincide with the median occlusal position. It is worth remembering that malocclusion is probably very common in the general nonsymptomatic patient and may or may not be relevant to the presenting symptoms.12 Rather than being a primary etiologic factor in TMD, malocclusion is likely to have a secondary or contributory role.3 ▶▶

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BIOMECHANICS

Superior orbital fissure Foramen rotundum Trigeminal ganglion CN V-1 ophthalmic branches

THE SPINE AND TMJ

CN V

Foramen ovale

CN V-2 maxillary branches

CN V-3 Branchial motor innervation to muscles of mastication CN V-3 mandibular branches

A

CN V-1

CN V-2

CN V-3

B FIGURE 26-6  The trigeminal nerve. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

Mouth Opening

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Mouth opening occurs in a series of steps (Table 26-3). In the erect position, the condyles begin to rotate anteriorly and translate inferiorly and laterally during the first 25 degrees of opening as the jaw opens. The upper head of the lateral pterygoid muscle and the anterior head of the digastric muscle draw the disk anteriorly and prepare for condylar rotation during movement.10,11 This initial condylar rotation occurs as the mandibular elevators (masseter, temporalis, and medial pterygoid muscles) gradually relax and lengthen, allowing

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gravity to depress the mandible (see Fig. 26-8). The directions of the fibers of the lateral and medial temporomandibular ligaments also keep the condyle from moving posteriorly. The fibrous capsule and parts of the temporomandibular ligament limit excessive lateral movement of the condyle. The rotation occurs through the two condylar heads between the articular disk and the condyle. As the mandible moves forward on opening, the disks move medially and posteriorly until the collateral ligaments and the lateral pterygoid stop their movement. During the last 15 degrees of opening, the

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Motor Nucleus The anterolateral upper pons Sensory Nucleus There are two nuclei: (1) the chief sensory nucleus in the posterior (dorsal)–lateral pons and (2) the mesencephalic nucleus, which extends from the chief sensory nucleus upward through the pons to the midbrain.

Nerves ▶▶ Mandibular ▶▶ Ophthalmic ▶▶ Maxillary Termination ▶▶ Muscles of mastication, both pterygoids, tensor veli palatini, tensor tympani, mylohyoid, and anterior belly of digastric. ▶▶ Skin of vertex, temporal area, forehead, and face; mucosa of sinuses, nose, pharynx, anterior two-thirds of tongue, and oral cavity. ▶▶ Lacrimal, parotid, and lingual glands; dura of anterior and middle cranial fossae. ▶▶ External aspect of tympanic membrane and external auditory meatus, TMJ, and teeth. ▶▶ Dilator pupillae and probably proprioceptors of extraocular muscles. ▶▶ Sensation from upper three or four cervical levels.

rotation ceases due to tightening of the collateral ligaments, and is replaced by an anterior translation of the condyles (see Fig. 26-8).10,11 During this translation, the condyle and disk move together. The anterior translation, which is produced mainly by muscle contraction, serves to prevent mandibular encroachment of the anterior neck structures. Opening is also assisted by the other suprahyoid muscles.4 In extremely wide opening, such as that occurs with yawning, the functional joint contact is on the distal aspect of the condyle, and the anterior lateral aspect of the condyle contacts the posterior part of the masseter muscle. In this position, the soft-tissue structures are in a position of stretch, making them more prone to dysfunction.

Mouth Closing Closing of the mouth involves a reversal of the movements described for mouth opening. The condyles translate

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Protrusion Protrusion is a forward movement of the mandible that occurs at the superior joint compartments, which consists of the disk and condyle moving downward, forward, and laterally. The muscles responsible for protrusion are the anterior fiber of the temporalis and the medial and lateral pterygoid muscles.

Retrusion Retrusion is a backward movement of the mandible, produced by the posterior fiber of the temporalis and assisted by the suprahyoid muscles. The retrusive range is limited by the extensibility of the temporomandibular ligaments.

The Temporomandibular Joint

Spinal Nucleus The spinal tract consists of small- and medium-sized myelinated nerve fibers and runs caudally to reach the upper cervical segments of the spinal cord. The lowest nerve fibers in the tract mix with the spinal fibers in the tract of Lissauer.

posteriorly as a result of an interaction between the retracting portions of the masseter and temporalis muscle and the retracting portions of the mandibular depressors (see Fig. 26-8).10,11 As the condyles translate posteriorly and glide medially, they hinge on the disks. The disks then glide posteriorly and superiorly on the temporal bone along with the condyles (as a result of the actions of the masseter, medial pterygoid, and temporalis muscles).10,11 When the jaws are closed to maximal occlusal contact, the condyles contact the disks, and the disks contact the posterior slopes of the articular tubercles and the glenoid fossae.

BIOMECHANICS

Box 26-1  Characteristics of the Trigeminal Nerve

Lateral Excursion If a protrusion movement occurs unilaterally, it is called a lateral excursion, or deviation. For example, if only the left TMJ protrudes, the jaw deviates to the right. Lateral movements of the mandible are the result of asymmetric muscle contractions (Fig. 26-9). During a lateral excursion to the right, the condyle and the disk on the left side glide inferiorly, anteriorly, and laterally in the sagittal plane and medially in the horizontal plane along the articular eminence. The condyle and the disk on the right side rotate laterally on a sagittal plane and translate medially in the horizontal plane while remaining in the fossa.

CLINICAL PEARL The translation of the human condyle during jaw opening and lateral jaw movements is referred to as the Bennett shift.

The Close- and Open-Packed (Resting) Positions The close-packed position of the TMJ is difficult to determine because the position of maximal muscle tightness is also the position of least joint surface congruity and vice versa. The most commonly cited close-packed position is with the teeth clenched. The open-packed position is with the mouth slightly open, the lips together, and the teeth not in contact. The significance of this position is that it permits the tissues of the stomatognathic system to rest and undergo repair.

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EXAMINATION

Main trunk of CN V-3 entering the infratemporal fossa via the foramen ovale

Temporalis m. (cut)

Auriculotemporal n. branching around the middle meningeal a. Lateral and medial pterygoid mm.

THE SPINE AND TMJ

Chorda tympani n. (CN VII)

(Long) buccal n.

Inferior alveolar n.

Tongue

Mandibular foramen Lingual n.

Nerve to the mylohyoid m.

Mental n.

Internal carotid a.

Submandibular ganglion

A

Mylohyoid and anterior digastric mm.

Superior salivatory nucleus

V-1 V-2 CN V V-3

Solitary nucleus Geniculate ganglion

General sensory (CN V-3)

Stylomastoid foramen

Special sensory taste (CN VII)

Chorda tympani (CN VII)

General sensory

B

Sublingual gland (visceral motor innervation)

Lingual n. Submandibular ganglion and gland (visceral motor innervation) Inferior alveolar n.

FIGURE 26-7  Neurology of the TMJ. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

Capsular Pattern The capsular pattern of the TMJ is a limitation of mouth opening. If one joint is more involved than the other, the jaw will laterally deviate to the same side during opening.

EXAMINATION

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Currently, clinical examination is the gold standard for diagnosing TMDs. Given the multifactorial causes of TMD, a comprehensive examination of the entire upper quadrant, including the cervical spine and shoulders, usually is warranted. In general, the TMJ and the upper three cervical joints all refer symptoms to the head, whereas the mid-to-low cervical spine typically refers symptoms to the shoulder and

Dutton_Ch26_p1259-p1294.indd 1270

the arm.13 An accurate diagnosis of TMD involves a careful evaluation of the information gleaned from the history, systems review, and tests and measures. In most chronic cases, a behavioral or psychological examination is required.13 Since postural dysfunctions are closely related to TMJ symptoms, the clinician should always perform a postural examination as part of a comprehensive examination of this joint. An examination form for the TMJ examination is shown in Table 26-4.

History A comprehensive history will help identify the possible source(s) of the orofacial pain and provide a screen for other causative or contributing factors.14 During the history, the clinician should observe whether the patient’s mouth moves comfortably. The severity of the symptoms and the time

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TABLE 26-3

 rthrokinematic Steps of the A Temporomandibular Joint

Step

Movement

Rest position

Joint is in an open-packed position.

Rotation  

There is a mid-opening. Condylar joint surfaces glide forward, inferior joint surface of disk has a relative posterior glide, upper lateral pterygoid relaxes, inferior pterygoid contracts, and posterior connective tissue is in a functional state of rest. Disk and condyle experience a short anterior translatory glide; superior and inferior heads of lateral pterygoid contract to guide disk and condyle forward. Posterior connective tissue is in a functional tightening.

  Translation    

There is full opening. Disk and condyle glide anteriorly and caudally. Superior and inferior heads of lateral pterygoid contract to guide disk and condyle fully forward. Posterior connective tissues tighten.

  Closure

Surface of condyle joint glides posteriorly, and disk glides relative to anterior surface. Superior head of lateral pterygoid contracts and inferior head relaxes. Posterior connective tissue returns to its functional length.

   

Data from Gelb H. Clinical Management of Head, Neck and TMJ Pain and Dysfunction. Philadelphia, PA: WB Saunders; 1985.

1. Restricted jaw function. Limited mouth opening, which may be reported as intermittent or progressive, is a key feature of TMD. A key question to determine restricted jaw function is, “Have you ever had your jaw lock or catch so that it would not open all the way? If so, was this limitation in jaw opening severe enough to interfere with your ability to eat? Have you ever noticed clicking, or popping, or other sounds in your joint?”16 Patients may describe a generalized tight feeling, which may indicate a muscular disorder, or capsulitis, or the sensation that the jaw suddenly “catches” or “locks,” which usually is related to a mechanical interference within the joint (an internal derangement).3 Associated signs of an internal derangement include pain and deviation of mandibular movements during opening and closing (refer to Practice Pattern 4D, under “Intervention Strategies” section later), and biting firm objects. Pain in the fully open position is probably caused by an extra-articular problem. Locking may imply that the mouth does not fully open or does not fully close and is often related to problems of the disk or joint degeneration. A gradual onset of symptoms after minor or prolonged physical activity may be indicative of a mechanical derangement. Symptoms of a mechanical nature generally are eased with rest. The irritability of a disorder is determined by the degree of activity necessary to provoke a symptom response.

Opening the mouth

Closing the mouth Lateral pterygoid (superior head)

Mandibular fossa

Temporalis

Lateral pterygoid plate

Masseter

Lateral pterygoid (Inferior head)

Medial pterygoid

en

e

Op

C

los

Suprahyoids

The Temporomandibular Joint

Functional opening

before the symptoms subside can provide the clinician with valuable information regarding possible pathology. Red flags related to cardiac history (e.g., angina, or history of myocardial infarction) and brain function (e.g., sudden-onset severe headaches, weakness, or slurred speech) must be investigated early in the history taking.15 The clinician should determine from the patient the main reason for the visit. There are three cardinal features of TMDs, which can be local or remote:

EXAMINATION



Hyoid bone

A

Infrahyoids

B

FIGURE 26-8  Mouth opening and closing.

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EXAMINATION Temporalis

THE SPINE AND TMJ

Zygomatic bone

Lateral pterygoid Pterygoid plate Medial pterygoid

Masseter

FIGURE 26-9  Lateral deviation to the left.

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2. Joint noises. Joint noises (crepitus) of the TMJ may or may not be significant, as they occur frequently in healthy populations. Some joint sounds are not audible to the clinician, so a stethoscope may be required. “Hard” crepitus is a diffuse sustained noise that occurs during a significant portion of the opening or closing cycle, or both and is an evidence of a change in bone structure and shape. Clicking describes a brief noise that occurs at some point during opening, closing, or both (see the discussion of range of motion testing, later). Jaw clicking during mouth opening or closing may be suggestive of an internal derangement consisting of an anterior disk displacement with reduction. However, joint noise is, of itself, of little clinical importance in the absence of pain.3 3. Orofacial pain. TMJ pain should be evaluated carefully in terms of its onset, nature, intensity, site, duration, aggravating and relieving factors, and how it relates to joint noise and restricted mandibular movements. Information about the nature of the pain will be critical in determining the possibility of primary headaches (migraine, cluster) and secondary headaches related to the eyes, ears, sinus, dental structures, medication complications, and/ or neurologic types of pain. Unrelenting pain unrelated to musculoskeletal function is an indication for referral. Key questions have been examined and determined to have strong sensitivity and specificity in incriminating TMDs as the source of pain.17 The initiating question should be, “Have you had pain or stiffness in the face, jaw, temple, in front of the ear, or in the ear in the past month?”15 A positive response should be followed by a question about whether the symptoms are altered by any of the following

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jaw activities: chewing, talking, singing, yawning, kissing, and moving the jaw.14 Specific questions about activities and postures of a sustained nature, such as sitting, sleeping, and driving, should be asked. Orofacial pain associated with mouth opening or closing and jaw crepitus is suggestive of osteoarthrosis, capsulitis, or internal derangement consisting of an anterior disk displacement with reduction.3 Information about cervical dysfunction is essential to determine whether the cervical spine is causing or exacerbating the headache/facial pain.15 In addition, it is important to determine: If the presenting symptoms were caused by trauma or surgery, or if the onset of pain occurred gradually. Questions should focus on any history of trauma during birth or childhood, as well as more recently. ▶▶ If there are any emotional factors in the patient’s background that may provoke habitual protrusion or muscular tension. Chronic head, neck, and back pain often are associated with psychogenic causes. Psychiatric disorders, usually, are manifested in patients whose afflictions seem to be excessive or persist beyond what would be normal for that condition. The clinician should listen for reports of psychological stress overload, malaise, anxiety, sleep problems, changes in eating patterns, weight changes, unexplained fatigue, and other signs of depression, which might exacerbate pain through central mechanisms.18 The checklist outlined in Table 26-5 can be used by the clinician to identify factors that may warrant an examination by a mental health professional. ▶▶

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EXAMINATION

TABLE 26-4

Temporomandibular Examination Form

Name:

General Dentist:

Patient’s Physician:

Phone (home):

Age:

Phone (bus):

Address:

Chief Complaint:

Occupation: Phone: Check all applicable

The Temporomandibular Joint

I.  MEDICAL HISTORY Arthritic Disease 1.  Traumatic arthritis: 2. Osteoarthritis: 3.  Rheumatoid arthritis: 4.  Psoriatic arthritis: 5. Other: ENT. Disorders 1.  Salivary gland disorders: 2. Cysts: 3.  Ear problems: 4. Polyps: 5.  Nose/throat problems: 6. Allergies: 7.  Sinusitis: 8.  Other: Vascular Disease and Blood Dyscrasias Head/Neck Trauma Date:   __________________ Description: Headache/Neuralgia (location, character, frequency, duration) Medication (current and past) 1. Type: 2.  Allergy to medication: Additional Medical Information (past and present)  1. Surgery:  2. Psychiatric:  3. ENT:  4. Orthopaedic:  5. Neurologic:  6. Internist:  7. Rheumatologic:   8.   Chiropractic:  9. Physical therapy: 10.  Endocrine: a.  Do your nails break easily? b.  Is your skin dry? c.  Do you tire easily? d.  Does the cold weather bother you? 11.  Osteopathic: 12.  Other: 13.  Nutritional state: (Continued)

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EXAMINATION

TABLE 26-4

Temporomandibular Examination Form (Continued) II. DENTAL HISTORY

A. Oral Conditions (describe general condition, presence of fixed or removable prosthesis, periodontal problems, and vertical dimension discrepancies) B.  Last Dental Examination and Films: C.  Recent Dental Treatment:

THE SPINE AND TMJ

D.  Previous Orthodontic Therapy Dates:   _______________ Bicuspid Extraction? E.  Previous TMJ Treatment and Results (date/doctor): F.  Pain Symptoms:   1.  Date of onset:   2.  Area of onset  _________________________________ Righ t _________________ Left   3.  Type: superficial, deep, sharp, dull   4.  Quality: burning, aching  5. Frequency:   6.  Duration: constant, intermittent   7. Period of greatest intensity:   8.  Status of pain: increased, decreased, unchanged   9.  Onset: abrupt, gradual 10.  Disappearance: abrupt, gradual 11.  Factors alleviating pain: 12.  Triggering devices: eating, yawning, speaking, singing, shouting 13.  Pain in specific teeth: 14.  Additional pain information: G.  Oral Symptoms (other than pain) 1.  Jaws clenched upon awakening 2.  Clenching and grinding during sleep 3.  Clenching and grinding during waking hours 4.  Muscle fatigue H.  Vertigo, Syncope, Meniere Disease (frequency, duration, circumstances): I.  Ear Symptoms/Joint Noises 1. Tinnitus:

(R) (L)

2.  Popping, clicking, or grating noises on opening and closing:

(R) (L)

3.  Stuffiness of ears:

(R) (L)

J.  Skeletal–Facial Deformity: K.  Other Complaints: III.  CLINICAL EXAMINATION Reported Pain   1.  Temporomandibular joint

(R) (L)

 6. Shoulder

(R) (L)

 2. Upper back

(R) (L)

 7. Arm

(R) (L)

 3. Middle back

(R) (L)

 8. Fingers

(R) (L)

 4. Lower back

(R) (L)

 9. Chest

(R) (L)

 5. Scapula area

(R) (L)

10.  Occipital area

(R) (L)

Tenderness and Pain on Palpation 1. Temporalis a.  Anterior Fibers

(R) (L)

b.  Middle Fibers

(R) (L)

c.  Posterior Fibers

(R) (L)

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(Continued)

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Temporomandibular Examination Form (Continued)

 2. Masseter

III.  CLINICAL EXAMINATION (Continued)  

 a. Zygoma

(R) (L)

 b. Body

(R) (L)

  c.  Lateral surface of angle of mandible

(R) (L) (R) (L)

 4. Posterior cervicals

(R) (L)

 5. Trapezius

(R) (L)

 6. Sternocleidomastoid

(R) (L)

  7.  Lateral pterygoid: insertion

(R) (L)

  8.  Medial pterygoid: insertion

(R) (L)

 9. Mylohyoid

(R) (L)

10.  Coronoid process

(R) (L)

11.  TMJ lateral aspect

(R) (L)

Lateral/posterior aspect

(R) (L)

3a. Ear (anterior wall tenderness)

(R) (L)

TMJ Sounds (Stethoscopic and/or digital palpation) 1. Crepitation

(R) (L)

2. Sagittal opening click:

 

Immediate

(R) (L)

Intermediate

(R) (L)

Full opening

(R) (L)

3. Sagittal closing click:

The Temporomandibular Joint

 3. Digastric

EXAMINATION

TABLE 26-4

 

Immediate

(R) (L)

Intermediate

(R) (L)

Terminal closure

(R) (L)

4.  Nature of click (soft/loud)

(R) (L)

B.  Occlusal Interferences

 

Left nonworking side

Right nonworking side

Protrusive

Centric Occlusion

Occlusion: Angle’s class Extruded labial or lingual version teeth Clinical Postural Observation 1.  Head posture (at rest): 2.  Range of motion: Summary of TMJ Imaging Findings: Mandibular Movement 1.  Widest interincisal opening 2.  Right lateral ________________________________________________ Left lateral 3.  Pain present with movement? Diagnosis: Plan of Treatment: Prognosis: Remarks: ENT, ear, nose, and throat; TMJ, temporomandibular joint. Data from Fain WD, McKinney JM. The TMJ examination form. Cranio. 1985 Mar-May;3(2):138–144.

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EXAMINATION



TABLE 26-5

 hecklist of Psychological and C Behavioral Factors

THE SPINE AND TMJ

Inconsistent, inappropriate, or vague reports of pain Overdramatization of symptoms Symptoms that vary with life events Significant pain of >6 months’ duration Repeated failures with conventional therapies Inconsistent response to medications History of other stress-related disorders Major life events (e.g., new job, marriage, divorce, and death) Evidence of drug abuse Clinically significant anxiety or depression Evidence of secondary gain Note: The significance of these factors depends on the particular patient. Reproduced with permission from McNeill C, Mohl ND, Rugh JD, et al. Temporomandibular disorders: diagnosis, management, education, and research. J Am Dent Assoc. 1990 Mar;120(3):253, 255, 257.

Tests and Measures ▶▶

If the patient is aware of any parafunctional habits (cheek biting, nail biting, pencil chewing, teeth clenching, or bruxism). For example, does the patient chew on one side more than the other? Chewing more on one side versus the other is typically the result of malocclusion (see later). In addition, favoring one side can lead to a loss of vertical dimension (the distance between any two arbitrary points on the face). A simple way to measure the aforementioned is to measure from the lateral edge of the eye to the corner of the mouth and from the base of the nose to the chin.

The behavior of symptoms over a 24-hour period. This information assists the clinician in formulating causal relationships. ▶▶ Whether the symptoms are improving or worsening. ▶▶ The relationship of eating to the symptoms. Alcohol, chocolate, and other foods such as ice cream can cause head pain in some individuals, suggesting a vasomotorrelated pain. ▶▶ The patient’s past dental and orthodontic history. ▶▶

Systems Review

1276

other symptoms similar to TMD, a cervicogenic headache (see Chapter 23), or a primary headache (see Chapter 5).15 Unexplained weight loss, ataxia, weakness, fever with pain, nystagmus, and neurologic deficits are characteristic of intracranial disorders. Neurovascular disorders are associated with a migraine headache and its variants, carotidynia, and cluster headaches (see Chapter 5). Neuropathic disorders include trigeminal neuralgia, glossopharyngeal neuralgia, and occipital neuralgia. A cranial nerve screen (see Chapter 3) should be completed on each patient presenting with orofacial pain with particular attention on the fifth cranial nerve (trigeminal), which supplies motor and sensory innervation to the masticatory region. Once the possibility of cervical, systemic, psychogenic, or ear or sinus problems has been ruled out, the next step is to consider the possibility of orofacial pain and impairment.

Pain or dysfunction in the orofacial region often results from nonmusculoskeletal causes such as otolaryngologic, neurologic, vascular, neoplastic, psychogenic, and infectious diseases. Clinicians often see patients with a TMD who present with nonspecific symptoms such as neck pain, headaches (see Chapter 5), earaches, tinnitus, and sinusitis.15 Patients with sinusitis complain of acute facial pain or pressure type headaches, and may present with nasal congestion, a reduced sense of smell, postnasal drip, fever or malaise, and aching teeth associated with certain weather conditions or times of the year.19 Ear disorders, such as an inner or outer ear infection, can produce preauricular symptoms in around the TMJ.20 Conversely, hyperactivity of the masticatory and tensor tympani muscles can cause ear pain, tinnitus, and feelings of fullness in the ear.21 Finally, patients with eye disorders may experience pain around the eye, numbness, a headache, and

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Examination of the TMJ structures includes observation, and a thorough mobility and palpation examination to identify impairments and functional limitations.

Observation The posture of the head and neck is assessed for asymmetry. The FHP (see Chapters 6 and 25) has been frequently associated with TMD. This is likely because of the direct impact an FHP can have on oral symmetry during occlusion. Nevertheless, there is still debate regarding whether or not head posture is directly related to TMD and orofacial pain.3 Occlusion occurs when the teeth are in contact, and the mouth is closed—when tapping the teeth together in the neutral position, all of the teeth appear to strike simultaneously. However, if the same task is attempted while placing the head forward, it is the anterior teeth that occlude first. A deviation from normal occlusion is defined as malocclusion—improper positioning of the teeth and jaws. The potential consequences of this repetitive functional malocclusion during food or gum chewing should be apparent and, although most people have some degree of malocclusion, it is not usually serious enough to require treatment. Even though evidence at present is somewhat inconclusive, it is still recommended that the clinician assesses the influence of the individual patient’s head posture on their symptoms—if changing head posture improves a patient’s complaints, it may be reasoned that it has a role in the symptoms.3 The clinician should also note whether the teeth are normally aligned or whether there is any crossbite, underbite, or overbite. Crossbite: This occurs when the teeth of the mandible are lateral to the upper maxillary teeth on one side and medial on the opposite side. An anterior crossbite occurs when the lower incisors are anterior to the upper incisors, whereas a posterior crossbite occurs when there is an abnormal transverse relationship of the teeth. ▶▶ Underbite: This occurs when the mandibular teeth are anterior to the maxillary teeth either unilaterally, bilaterally, or in pairs. ▶▶

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Overbite: This occurs when the anterior maxillary incisors extend below the anterior mandibular incisors when the jaw is in central occlusion.

CLINICAL PEARL

The face is also assessed for asymmetry, such as swelling or flattening of the cheek. Asymmetry is an important finding, because developmentally the facial structures evolve in a proportional relationship, some determined by genetics, others in response to the physical environment. Orthognathy relates to the amount of projection of the lower face in relation to an imaginary perpendicular line from the eyes when viewed from the side. Three types of facial profile are recognized: Orthognathic: A straight facial profile in which the upper and lower lips are in line with the tip of the chin. ▶▶ Retrognathic: Describes a facial profile in which the tip of the chin is posterior to the upper and lower lips. ▶▶ Prognathic: Describes a facial profile in which the tip of the chin is anterior to the upper and lower lips. ▶▶

In addition, the clinician should note the presence of any abnormal jaw deviation, unusual dryness of the lips, and signs of tissue stress such as overdeveloped masseter and mentalis muscles. A lateral deviation of the jaw, evidenced by a malalignment or malocclusion of the upper and lower teeth, or hypertonus of one of the masseter muscles, may cause an adaptive shortening of the mastication muscles on the ipsilateral side of the deviation, and a lengthening of the muscles on the contralateral side. Since the role that malocclusion plays in TMD remains unclear, the relevance of the malalignment to the patient’s symptoms must be determined by passively attempting to correct the deformity. An increase in pain with the correction suggests the presence of a protective deformity. The teeth should be examined for symmetry. Cavities, wear patterns, and restored, and missing teeth should be noted. Tooth wear and fracture are often destructive signs of parafunctional habits (abrasive diet, bruxism, and teeth clenching). Loss of teeth can cause disruption in the working and nonworking interfaces of the teeth, which may cause unilateral function and subsequent overloading of the remaining teeth and the TMJ. The clinician should also ask the patient if there are any painful or sensitive teeth, which can lead to incorrect biting and subsequent abnormal loading of the TMJs. The tongue should be examined. The tongue should appear dull red, moist, and glistening. Its anterior portion should have a smooth yet roughened appearance. The posterior portion should have a smooth, slightly uneven appearance. A large tongue can exert excessive pressure against the teeth and may interfere with occlusion, resulting in bite marks.

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Range of Motion The range of motion of the TMJ, the cervical spine, the craniovertebral joints, and the shoulders should be assessed with active range of motion (AROM), and then with passive overpressure, to assess the end-feel. During cervical flexion, the mandible moves superiorly and anteriorly, whereas, during cervical extension, the mandible moves inferiorly and posteriorly. The patient should be able to open and close the mouth while keeping a fist in place under the chin. During side bending or rotation of the cervical spine, a maximum occlusion occurs on the ipsilateral side. Although it is unclear how the individual components of the examination contribute to the final diagnosis, most clinicians would agree that substantially reduced mandibular motion is a strong indicator of the presence of a serious TMD and helps to distinguish TMD patients from non-TMD controls.22,23 However, there is little evidence to suggest that mandibular motion measurements add critical information to the process of differential diagnosis among the common TMD subgroups.22,23 The clinician observes the opening and closing of the mouth, noting both the range and the quality of movement. All movements of the TMJ should be smooth and without noise or pain. Normally, the mandible should open and close in a straight line. To help detect crepitus, the clinician can palpate over the mandible heads during opening and closing (Fig. 26-10). If crepitus or clicking occurs on opening and/ or closing, the clinician notes where they occur in the range. If pain occurs, a determination should be made as to where in the range the pain occurs, and the location of the pain. A Boley gauge, T-bar, or ruler can be used to measure the range of the TMJ in millimeters. The type and temporal sequence of joint clicking can provide the clinician with the following information15: 1. Reciprocal clicking is defined as clicking that occurs during opening and again during closing. The opening click occurs when the condyle moves under the posterior band of the disk until it snaps into its normal relationship on the concave surface of the disk, whereas the closing click reflects the reversal of this process. Reciprocal clicks may be early, intermediate, or late, depending on the degree of opening at which they occur. a. Early clicking usually indicates a small anterior displacement. b. Late clicking usually indicates that the disk has been further displaced.   Reciprocal clicking is a common finding in patients with a posterosuperior condylar positioning.

The Temporomandibular Joint

Overjet, not to be confused with an overbite, is a measure of how far the top incisor teeth are ahead of the bottom incisors. Normally, the top and bottom front teeth should be touching upon closure leaving no or zero overjet. If the top teeth are ahead by some distance, this is referred to as positive overjet. If the top teeth are behind the bottom teeth are referred to as negative overjet or underjet.

The rest position of the TMJ should be noted. The clinician can locate the rest position of the TMJ by gently placing the little finger with the palmar portion facing anteriorly into the external auditory meatus. From an open-mouth position, the patient is asked to slowly close the mouth. At the point of resting position, the patient’s mandibular heads are felt to gently touch the finger. The space between the upper and lower incisors should be 2–4 mm. A greater distance may indicate hypermobility of both TMJs.

EXAMINATION

▶▶

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EXAMINATION THE SPINE AND TMJ

FIGURE 26-11  Mouth closing with overpressure.

Depression of the Mandible (Mouth Opening)

Palpation during opening FIGURE 26-10 Palpation of TMJ during mouth opening and deviation.

2. Clicking that occurs at the end of opening often results from articular hypermobility and is accompanied by a deviation of the jaw toward the contralateral side. 3. The “soft” and “popping” opening and closing clicks associated with muscular incoordination are usually intermittent and inconsistent. They are thought to be caused by ligament movement or articular surface separation. Muscle tenderness to palpation is a frequently associated symptom.

The opening of the mouth is considered the most revealing and diagnostic movement for TMD. While approximately only 25–35 mm of mouth opening measured between the maxillary and mandibular incisors is required for everyday activities, the maximum range of motion is approximately 40–50 mm.22,23 At this extreme, the periarticular structures are stretched to 100% of their total length. The functional range of motion is considered to be closer to 40 mm, or approximately a two-to-three-knuckle width of the nondominant hand (see Fig. 26-12). At this point in the range, the periarticular structures are stretched to 70–80% of their total length. In myogenic TMD, the typical pattern is that in restricted mouth opening, overpressure beyond the active range results in more mouth opening (10– 15 mm).3 Excessive opening is indicated when the patient is able to insert three or more knuckles between the incisors. Excessive opening is associated with large anterior translatory movements at the beginning of mouth opening, accompanied by excessive protrusive movements of the mandible. Linear ruler measurement of mandibular opening has good intrarater and interrater reliability (intraclass correlation coefficient [ICC] = 0.70–0.99 and 0.90–1.00, respectively).24 If a deviation occurs to the left on opening (a C-type curve) or to the right (a reverse C-type curve), hypomobility is evident toward the side of the deviation. If, during mouth opening, an S-type or reverse S-type curve is noted, the problem is

Elevation of the Mandible (Mouth Closing)

1278

The primary muscles involved with mouth closing are the masseter, the temporalis, and the medial pterygoid. Since the maxillary teeth are fixed, the upper midline of the incisors can be used as a landmark to assess lower jaw deviation during mouth closing. Under normal conditions, the midline relationship between the upper and lower incisors should remain constant in the closed and open positions. Overpressure can be applied to the mouth closing by placing the fingers under the chin and pushing superiorly in a controlled fashion (Fig. 26-11). The normal end-feel for mouth closing should be bone-on-bone (teeth contact).

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Finger width test FIGURE 26-12  Three-knuckle width of mouth opening.

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Limited opening with deviation to one side should alert the clinician to an internal derangement without reduction, which limits the translation on the involved side and causes the jaw to deviate toward the less-mobile side, even if that is the normally mobile side and the other side is hypermobile. Early deviation suggests hypomobility, and late deviation indicates hypermobility.

If hypomobility resulting from internal derangement with reduction of one TMJ is present, the mandible will deviate in a C pattern of motion to that side of the open mouth in the midrange of opening before returning to normal. ▶▶ The patient who demonstrates an S movement of the jaw while opening the mouth may have a muscle imbalance (often caused by trigeminal facilitation and masticatory hypertonicity), or it may be a momentary locking of a deranged disk. Lateral excursion of the mandible with mouth opening implicates contralateral structures such as the contralateral disk, the masseter, the medial and lateral pterygoid, or the lateral ligaments. ▶▶

Overpressure can be applied to the opening movement using a lumbrical grip placed on the patient’s chin, under the bottom lip (Fig. 26-13). The overpressure is applied to ensure that the jaw is maximally depressed. The normal end-feel should be tissue stretch. Locking of the jaw can be associated with three main types of abnormal end-feel:

FIGURE 26-13  Mouth opening with overpressure.

Protrusion of the Mandible.  The patient opens the mouth slightly and protrudes the lower jaw. The normal movement of the lower teeth is greater than 7 mm, measured from the resting position to the protruded position. This equates to the mandibular teeth being able to protrude past the top teeth. The amount and direction of the protrusion are noted: An abnormal protrusive position may be associated with a residual pediatric tongue thrust (deviant swallowing), or an acquired adult tongue thrust secondary to a FHP or habitual protrusion. ▶▶ Any lateral excursion of the mandible during protrusion may indicate the involvement of the contralateral structures, such as the contralateral disk, the masseter, the medial and lateral pterygoid, or the lateral ligaments. ▶▶

The Temporomandibular Joint

▶▶

EXAMINATION

probably a muscular imbalance or medial displacement of the disk. Reduced mouth opening can result from a number of disorders including chronic muscle contraction, joint hypomobility, muscle tightness, or the presence of trigger points within the elevator muscles: the temporalis, the masseter, and the medial pterygoid. If contracture of the masticatory muscles is present, the mandibular opening can be as limited as 10–20 mm between the incisors.23 Acute disk displacement without reduction and trismus are difficult to distinguish because both conditions present with recent onset and painful limitation of jaw opening. To be certain of the anatomic basis of acute disk displacement without reduction, most clinicians feel that joint imaging with magnetic resonance of the disk is required.22,23 Translation of the lateral pole of the condyle should occur after 11 mm of mouth opening. If an opening deviation occurs, it is important to note where in the opening cycle it occurs. Opening and closing deviations are observed simply by taking a small ruler or tongue depressor and laying the edge down the midline of the face. While the clinician “eyes” the straight edge, the patient opens and closes the mouth slowly:

The clinician can apply overpressure by grasping the patient’s mandible with the index and the middle fingers behind the mandibular angles and the thumbs on the patient’s cheeks, and then gently pulling the jaw anteriorly (Fig. 26-14). Retrusion of the Mandible.  The patient is asked to retrude the jaw as far back as possible. The normal movement is 3–4 mm. Pain at the end range of retrusion may indicate an intracapsular injury.22,23 Overpressure can be applied using a lumbrical grip positioned under the patient’s bottom lip and pushing the mandible posteriorly (Fig. 26-15).

Hard.  This type of end-feel is associated with osseous abnormalities. ▶▶ Springy.  This type of end-feel is associated with a displacement of the disk. ▶▶ Capsular.  This type of end-feel is associated with adaptive shortening of the periarticular tissues. ▶▶

Excursion of the Mandible The superior and inferior incisors are assessed for any deviation of the jaw laterally (cross-bite) or anteroposteriorly (overbite or underbite).

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FIGURE 26-14  Manual jaw protrusion.

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EXAMINATION THE SPINE AND TMJ

and during maximum-assisted opening, and the presence of click and crepitus sounds demonstrated an accuracy of 78.7% to predict TMJ effusion. Among the single clinical symptoms, the most reliable predictor of TMJ effusion was found to be the presence of pain with lateral palpation (accuracy 76.2%; kappa [κ] = 0.53).26 The two primary positive findings with palpation in this region are local tenderness and pain referral, although it is difficult to determine whether the muscle pain is the primary source of the problem or a secondary condition contributing to the overall pain condition.27 The TMJ should be palpated at rest and during mandibular motion. For comparison and expediency, palpation of the lateral and posterior aspects of the TMJs is performed bilaterally and simultaneously. FIGURE 26-15  Manual jaw retrusion.

Lateral Deviation of the Mandible.  The patient opens the mouth slightly and moves the lower jaw to the left and to the right. The right and left motions are compared. Normal range of motion for lateral deviation is approximately one-fifth of the opening range (8–11 mm).25 Lateral deviation can be measured as the amount of lateral excursion between the center of the mandibular incisors and the center of the maxillary incisors. An appreciable difference between the two sides is more significant than a limited range occurring bilaterally.22,23 Passive overpressure can be applied in a lateral direction. Pain reported on the side away from the direction of overpressure may indicate ligamentous or joint capsule damage.23 Tongue Movements. Tongue movements give valuable information about the function of the hypoglossal nerve (CN XII). Any deviation or atrophy of the tongue during tongue protrusion may indicate a lesion of this nerve. A unilateral weakness of the tongue is manifested by a deviation of the protruded tongue toward the weaker side. A test for a weakness of the tongue is to ask the patient to stick the tongue into the cheek while the clinician presses against the bulging cheek. A comparison is made between both sides.

Palpation

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Palpation of the TMJ can be used to assess tenderness, patterns of pain referral, skin temperature, muscle tone, swelling, skin moisture, and the location of trigger points. The palpation examination begins with a gentle touch and light pressure because the muscles of mastication can be highly sensitive if they are in spasm. Schiffman et al.16 found that a range of about 1–1.8 kg (approximately 2–4 lb of force) is appropriate for masticatory joint and muscle palpation examination. The clinician should use a slight blanching of the pad of the distal phalanx as a guideline for appropriate amounts of pressure during the palpation examination.15 In a study by Manfredini et al.,26 61 patients with TMJ pain were assessed by means of a standardized clinical examination and magnetic resonance imaging (MRI). The aim of this work was to evaluate the predictive value of clinical symptoms for MRI findings of TMJ effusion. The study reported that a clinical examination based on the assessment of pain in the TMJ with lateral palpation, with posterior palpation, during motion,

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Anterior Aspect Zygomatic Arch.  The zygomatic arch is located anterior to the condylar process of the mandible. The temporal muscle lies above, and the masseter muscle lies below the zygomatic arch. Hyoid Bone.  The hyoid bone, located anterior to the C2 and C3 vertebrae, is palpated for normal, painless movement as the patient swallows. Digastric Muscle (Anterior Belly).  The anterior belly of the digastric muscle can be palpated from its origin on the lingual side of the mandible to its tendinous insertion on the hyoid bone. Thyroid.  The thyroid cartilage, located anterior to the C4 and C5 vertebrae, is palpated and moved. Crepitation of this structure may be felt during neck extension as the cartilage becomes taut.

Lateral Aspect Temporomandibular Joint.  The clinician palpates the lateral aspect of the TMJ by placing the tip of the forefinger just anterior to the tragus of the ear (see Fig. 26-10). During mouth opening, the lateral pole of the condyle is the most palpable osseous structure. As the individual opens the mouth wide, the clinician’s finger will identify a depression posterior to the condylar head (the posterior aspect of the joint) and overlying the joint that is created by the translating condyle. Tenderness in this depression may indicate inflammation. Alternatively, the lateral aspect of the joint capsule can be palpated on the lateral pole of the condyle just anterior to the tragus. To facilitate identification of the lateral pole, the patient is asked to open and lightly hold a cotton roll in the premolar region.28 Palpation around the lateral pole has excellent interrater reliability for pain reproduction (κ = 0.89)16 and is part of the diagnostic criteria/temporomandibular disorders (DC/TMD) classification algorithm for any joint pain, with a sensitivity and specificity of 0.92 and 0.96 when using the expert driven diagnosis as the gold standard (and high patient accuracy).16 Mandible.  The mandible should be palpated along its entire length. Any asymmetry from side to side should be noted. The mandibular angle serves as an important landmark for orientation. The mandibular ramus is covered by the masseter muscle. The condylar process of the mandible is located just in front of the ear. The parotid gland is located anterior

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Trapezius Muscle.  The trapezius muscle is palpated from its origin on the acromion process to its insertion along the midline of the spine to the base of the skull. The trapezius is perhaps the most common site for muscular trigger points and often refers pain to the base of the skull and the temporal region. Masseter Muscle.  Both the superficial and deep portions of the masseter run from the zygomatic arch to the mandibular ramus. Palpation begins at the superior attachment along the zygomatic arch and continues inferiorly along the muscle belly to its inferior attachment on the ramus of the mandible. Trigger points in the masseter muscle can refer pain to the teeth, ear, and sinus areas. Temporalis Muscle.  The temporalis muscle can be palpated in front of, and above, the ear. The clinician places a finger against the temporal region and then asks the patient to gently open and close the mouth. The anterior vertical, middle oblique, and posterior horizontal fibers clench the teeth and should all be palpated. The temporalis can refer pain to the teeth, the joint, and the retro-orbital area. The tendon can be palpated intraorally and extraorally during mandibular depression to bring the coronoid process inferior to the zygomatic arch.20 Posterior Aspect of the Joint.  Posterior TMJ palpation is performed by placing the tip of the little finger in the patient’s external auditory canal and exerting anterior pressure as the patient repeatedly opens and closes the mouth. Alternatively, the palpation can be performed with the teeth in the intercuspal position.28 If inflammation is present, pain is felt on jaw closing as the tissue is compressed between the clinician’s finger and the condyle. The examination also may reveal a posterosuperiorly positioned condyle and disk dysfunction. This posterosuperior position of the condyle can be a result of occlusal factors or trauma. The position results in an anteriorly displaced disk and an impingement by the condyle on the space normally occupied by the disk. This displacement may cause reciprocal clicking or locking. The masseter, temporalis, and perihyoid muscles are palpated extraorally for hypertonicity and tenderness. In addition, the lateral aspect of the joint capsule and the lateral TMJ ligament are palpated for tenderness. Medial and Lateral Pterygoid.  It is questionable whether the medial and lateral pterygoid can be palpated due to the depth of their location and adjacent overlying structures.

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Muscle Tests It is important to be able to stress the muscles of mastication and facial expression selectively to determine whether they are implicated in the symptoms. All these tests cannot replace a thorough palpation of the muscles. All test positions, resisted motions, and attempted facial expressions may be used as exercises to rehabilitate any identified deficits. For each of the following, the patient is seated.

Temporalis The clinician palpates the side of the head in the temporal fossa region. The patient is asked to elevate and retract the mandible. Resistance can be applied using a tongue depressor placed between the teeth. Both sides are tested.

The Temporomandibular Joint

Sternocleidomastoid Muscle.  The sternocleidomastoid is palpated from its dual origin on the sternum and the clavicle along its course upward and posteriorly to its insertion on the mastoid process.

Nonetheless, descriptions detailing palpation of these muscles exist. For the medial pterygoid, the patient is asked to move the tongue to the opposite side. The clinician slides a thumb onto the medial aspect of the lower gum and toward the back of the mouth and angle of the mandible. The thumb is maintained at the bottom of the mouth to prevent the gag reflex. The insertion site for the medial pterygoid is located on the medial aspect of the mandibular angle. The lateral pterygoid is said to be palpated by sliding a thumb back to the medial aspect of the base of the upper molars. The patient is asked to open the mouth wider, and the clinician slides the thumb back and up at an angle of 45 degrees and inspects the muscle and area for tenderness.

EXAMINATION

to and below the auricle, and normally extends from the sternomastoid muscle anteriorly to the masseter muscle. Enlargement of the parotid gland causes the earlobe to move outward on the involved side. Enlargement of the parotid gland can have a number of medical causes, prompting a referral. The submandibular gland is palpable in front of the mandibular angle and underneath the mandibular body, about halfway between the chin and the mandibular angle. Normally, the gland has a firm, irregular consistency.

Masseter The clinician palpates the cheek, just above the angle of the mandible. The patient is asked to elevate the mandible, as in closing the jaw. Resistance can be applied using a tongue depressor placed between the teeth.

Lateral Pterygoid The clinician palpates the pterygoid at the neck of the mandible and joint capsule. The patient is asked to protrude and depress the mandible against manual resistance.

Medial Pterygoid The patient is asked to elevate and protrude the mandible. Resistance can be applied using a tongue depressor placed between the teeth.

Suprahyoid Muscles The clinician palpates the floor of the mouth. The patient is asked to press the tip of the tongue against the front teeth. Resistance can be applied to the surface of the hyoid bone in an attempt to protrude the tongue.

Infrahyoid Muscles The clinician palpates below the hyoid bone, immediately lateral to the midline. The patient is asked to swallow while the clinician palpates for the movement of the hyoid and the larynx.

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EXAMINATION

TABLE 26-6

Muscles of Facial Expression

THE SPINE AND TMJ

Muscle

Action

Innervation

Occipitofrontalis

Wrinkles forehead by raising eyebrows

Facial nerve

Corrugator

Draws eyebrows together, as in frowning

Facial nerve

Procerus

Draws skin on lateral nose upward, forming transverse wrinkles over bridge of the nose

Facial nerve

Nasalis

Dilates and compresses aperture of the nostrils

Facial nerve

Orbicularis oculi

Closes eyes tightly

Facial nerve

Superior levator palpebrae

Lifts upper eyelid

Oculomotor nerve

Orbicularis oris

Closes and protrudes lips

Facial nerve

Major and minor zygomatic

Raises corners of mouth upward and laterally, as in smiling

Facial nerve

Levator anguli oris

Raises upper border of lip straight up, as in sneering

Facial nerve

Risorius

Draws corners of mouth laterally

Facial nerve

Buccinator

Presses cheeks firmly against teeth

Facial nerve

Levator labii superioris

Protrudes and elevates upper lip

Facial nerve

Depressor anguli oris and platysma

Draws corner of mouth downward and tenses skin over neck

Facial nerve

Depressor labii inferioris

Protrudes lower lip, as in pouting

Facial nerve

Mentalis

Raises skin on chin

Facial nerve

Muscles of Facial Expression

Joint Capsule

This group of muscles, most of which are innervated by the facial nerve, can be assessed by having the patient attempt to make the specific facial expression attributed to each muscle (Table 26-6). A number of scoring systems have been developed for the clinical assessment of facial nerve function, of which the House–Brackmann score (Table 26-7), and its various modifications (Facial Nerve Grading Scale 2.0), has been the most widely accepted system.

The clinician stands at the head of the patient. The patient’s mandible is closed. The clinician places one hand on top of the patient’s head, and the other hand on the ramus and angle of one side. The clinician then applies a contralateral protrusion and ipsilateral deviation force (Fig. 26-16).

Ligament and Capsule Stress Tests The ligament stress tests assess the integrity of the capsule and ligaments. Positive findings include excessive motion compared with the other side, or pain. The patient is seated.

Temporomandibular (Lateral) Ligament

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This test is only performed if there is a painful loss of AROM of the TMJ. The purpose of the test is to determine if the painful restriction is caused by damage to one of the ligaments or the joint capsule. The clinician cradles and stabilizes the patient’s head with one hand. The index and middle fingers of this hand can be used to palpate the joint line. The patient is asked to open their mouth to the point of restriction; mandible is positioned slightly open. The clinician places the thumb of the mobilizing hand on the ipsilateral molars of the side to be tested. The clinician then applies a downward force on the molars creating a caudal shear (Fig. 26-14). There should be slight movement with this technique, and the end-feel should be capsular.

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Joint Loading Tests Selective loading of the TMJ may be used to help determine the presence of an intracapsular pathology. A positive finding is a pain with the test. These tests include dynamic loading and joint compression.

Dynamic Loading The patient is asked to bite forcefully on a cotton roll or tongue depressor on one side. This maneuver loads the contralateral TMJ.

Joint Compression The patient is positioned supine, with the clinician standing at the head of the bed. The clinician places the fingers of each hand under each side of the mandible, with the thumbs resting on the ramus. The mandible is then tipped posteriorly and inferiorly to compress the joint surfaces.

Passive Articular Mobility Testing The passive articular mobility tests assess the joint glides and the end-feels. The patient and clinician setup are identical

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House–Brackmann Facial Nerve Grading System Grade I

Grade II

Grade III

Grade IV

Grade V

Grade VI

Overall appearance

Normal

Slight weakness on close inspection

Obvious but not disfiguring difference between both sides

Obvious weakness and/or disfiguring asymmetry

Only barely perceptible motion

No movement

At rest

Normal symmetry

Normal symmetry Normal symmetry Normal symmetry

Asymmetry

Asymmetry

Forehead movement

Normal with excellent function

Moderate-togood function

Slight-tomoderate function

None

None

None

Eyelid closure

Normal closure

Complete with minimum effort

Complete with maximal effort

Incomplete closure with Incomplete maximal effort closure with maximal effort

Mouth

Normal and Slight asymmetry symmetric

Slight asymmetry Asymmetry with with maximum maximum effort effort

Synkinesis contracture and/or hemifacial spasm

None

Obvious but not disfiguring synkinesis contracture and/or hemifacial spasm

May have very slight synkinesis; no contracture or hemifacial spasm

Synkinesis contracture and/or hemifacial spasm disfiguring or severe enough to interfere with function

No movement

Slight movement

No movement

Synkinesis contracture and/or hemifacial spasm usually absent

No movement

The Temporomandibular Joint

Parameter

EXAMINATION

TABLE 26-7

Modified with permission from House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg. 1985 Apr;93(2):146–147.

to that described above for the temporomandibular (lateral) ligament stress test. From the end-range position (or as close as possible, given that the thumb is in the patient’s mouth), the following maneuvers are performed assessing for range and end-feel. Findings are compared with each side. Pain, or a restricted glide, are positive findings and may indicate articular involvement or a capsular restriction. It is important to check the specific glides that are related to the loss of active motion. For example, if a patient demonstrated diminished mouth

Medial-lateral FIGURE 26-16  Contralateral protrusion and ipsilateral deviation force to TMJ.

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opening, the combined anterior, inferior, and lateral glide is assessed at each joint. Limited opening can be caused by anterior disk displacement without reduction, elevator muscle spasm, or capsular restraint. By inducing a passive stretch to the joint after the patient has actively opened the mouth to the full extent, the “end-feel” can be used to differentiate between these causes. For example, if a displaced disk is responsible for limited opening, there will be a hard end-feel with little or no play. In contrast, a gummy end-feel is present when muscle spasm or capsular connective tissue is preventing full opening. Passive motions can be used to help differentiate between an elevator muscle spasm and a capsular restriction. With elevator muscle spasm, only the vertical movement is restricted, and protrusive and lateral excursions are normal. Anterior disk displacement without reduction, however, exhibits restrictions in both protrusive movements and contralateral excursions. The movement to the side of the involved joint is usually not mechanically restricted because the main movement occurring in the joint is a rotation. While hypomobility may be apparent with passive articular mobility testing, hypermobility is difficult to determine with these tests. Most of the mobility tests can also be used for mobilizations by changing the grade and the intent. The clinician should remove the thumb from the patient’s mouth every 10–15 seconds to allow the patient to swallow. ▶▶

Distraction (Fig. 26-14). The mandible is moved inferiorly in a direction perpendicular to the joint surface.

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THE SPINE AND TMJ

Medial-lateral (alternate position)

Anterior glide (see Fig. 26-14). The mandible is moved anteriorly. ▶▶ Medial glide (see Fig. 26-17). The clinician stands to the side of the patient and stabilizes the patient’s head. A medial force is applied by the other hand. This glide assesses the ability of the TMJ to side glide to the contralateral side from the side of the joint being tested. ▶▶ Posterior glide with a lateral excursion for the posterior ligaments. ▶▶

Neurologic Tests Trigeminal Nerve (CN V) Sensation.  The skin near the midline (there is overlap from the anterior [ventral] rami of C2 and C3 if tested too laterally) of the forehead and face can be stroked with cotton wool or tissue paper or can be tested for pinprick sensation. It is best if the testing is carried out bilaterally and simultaneously. Reflex.  The jaw jerk can be used to test trigeminal function. A lesion superior to the pons would produce hyperreflexia, and a lesion below the pons would result in hyporeflexia or areflexia. The patient’s mouth is relaxed and open in the resting position. The clinician places a thumb on the mandible and then lightly taps the thumb with the pointed end of a reflex hammer (Fig. 26-18). A normal response is one in which the mouth closes.

Facial Nerve (CN VII) The facial nerve can be tested using the Chvostek (Weiss sign) test. The patient is positioned sitting. The clinician taps the parotid gland overlying the mass of the muscle. If the facial muscles twitch (typically a twitch of the nose or lips), the test is considered positive for hypocalcemia (i.e., from hypoparathyroidism, pseudohypoparathyroidism, hypovitaminosis D) with resultant hyperexcitability of the nerves.

Special Tests 1284

FIGURE 26-18  Jaw jerk test.

FIGURE 26-17  Medial glide.

At the time of writing, no routine special tests for the TMJ exist. Most, if not all, of the structures of the TMJ are isolated

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and tested during the standard examination previously described. Although cranial nerve testing (see Chapter 3) is not, strictly speaking, a special test, this testing should be performed if an injury to a cranial nerve is suspected. In addition, the special tests for thoracic outlet syndrome, brachial plexus stretching, and dural mobility should be performed to help rule out any referral of symptoms.

Imaging Studies With the rapid progress made in TMJ imaging techniques, many studies have focused on the importance of internal derangement and osteoarthrosis as the underlying mechanisms in the etiology of TMJ-related pain and dysfunction. Despite the limitations, plain radiographs of the TMJ, such as high-level orthopantomograms and transcranial projections, are useful ways of visualizing any gross pathologic, degenerative, or traumatic changes in the bony component of the TMJ complex.20 MRI is currently the most accurate imaging modality for the identification of disk positions of the TMJ and may be regarded as the gold standard for disk position identification purposes.

INTERVENTION STRATEGIES The lack of a consistent method for identifying and diagnosing TMD in a research setting, varying durations of treatment, lack of control groups, lack of objective-dependent measures, and lack of specification of symptom duration have prevented significant research on the effectiveness of various treatment modalities for TMD.29 Complicating matters is the fact that the majority of the symptoms associated with TMD are selflimiting and resolve without active intervention.3 The chronic pain associated with TMD most likely occurs because of secondary factors. These factors include a fixed FHP, abnormal stress levels, depression, or oral parafunctional habits (such as bruxism). This prolonged pain is frequently due to adaptive shortening of the tissues, or from a secondary hypermobility. It is likely that the longer the duration of the symptoms, the smaller the likelihood that the patient will benefit from a conservative intervention.

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TABLE 26-8

 iagnostic Classification of Physical D Conditions Associated with TMD

Group I: Masticatory Muscle Disorders

Group III: Joint Dysfunction

Ia—with normal opening

IIa—disk displacement with reduction

IIIa—arthralgia

Ib—with limited opening

IIIb—osteoarthritis IIb—disk displacement without reduction with limited opening IIIb—osteoarthrosis IIc—disk displacement without reduction without limited opening

Data from Schiffman EL, Ohrbach R, Truelove EL, et al. The research diagnostic criteria for temporomandibular disorders. V: methods used to establish and validate revised axis I diagnostic algorithms. J Orofac Pain. 2010 Winter;24(1): 63–78; Schiffman EL, Truelove EL, Ohrbach R, et al. The research diagnostic criteria for temporomandibular disorders. I: overview and methodology for assessment of validity. J Orofac Pain. 2010 Winter;24(1):7–24.

In 2010, an interprofessional consortium revised the criteria to improve the reliability, validity, sensitivity, and specificity of the examination algorithms for TMDs, resulting in the DC/TMD (Table 26-8). The DC/TMD provides a valid diagnostic classification based on the more common body structure/function impairments and activity limitations seen with TMD patients. The DC/TMD describes two axes of focus for examination30,31: Axis I. This encompasses a physical examination of body structure/functional impairments in the muscle and joint domains with diagnostic classifications as the outcome. Three broad classification groups are contained: (1) masticatory muscle disorders; (2) joint disorders related to temporomandibular disk derangements (disk displacement with reduction, disk displacement without reduction); and (3) joint disorders related to TMD arthropod arthritis, and arthrosis (Table 26-8). ▶▶ Axis II. This focuses on identifying psychosocial characteristics that play a foundational or indictment in prior complaints. ▶▶

Recently, there has been an interest in the relative effectiveness of specific conservative interventions for TMD and, as a result, a number of systematic reviews have been performed in the area. In 2006, two systematic reviews concluded that, despite the criticisms about reliability, validity, outcome measurements, and inclusion and exclusion criteria for TMD, exercises, manual therapy, electrotherapy, relaxation training, and biofeedback seem to have the best outcomes in TMD treatment.32,33 In addition, Gatchel et al.29 conducted a randomized clinical trial with a 1-year follow-up to evaluate the efficacy of a biopsychosocial intervention for patients who were at high risk of

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Acute Phase Acute injuries to the TMJ most frequently have a traumatic origin, such as a direct blow, or from a sudden locking of the jaw caused by an internal derangement. The typical patient presentation for an acute injury demonstrates a capsular pattern of restriction (decreased ipsilateral opening and lateral deviation to the involved side), with pain and tenderness on the same side.

Physical Therapy POLICE (protection, optimal loading, ice, compression, elevation—see Chapter 8) are recommended during the acute phase, with the exception of elevation, which is neither appropriate nor feasible. Cold is applied to reduce edema, inflammation, and muscle spasm. No single drug has been proved to be effective for all cases of TMD. Thus, a wide variety of drug classes have been described for chronic orofacial pain, ranging from short-term treatment with nonsteroidal antiinflammatory drugs (NSAIDs), corticosteroids, and muscle relaxants for pain of muscular origin to chronic administration of antidepressants for less well-characterized pain. The analgesic effect of NSAIDs is specific only in cases of TMD, in which pain is the result of an inflammatory process such as synovitis or myositis. The patient should receive instruction on how to obtain the rest position of the TMJ. The motion of the TMJ should be restricted to pain-free movements to allow the rest or immobilization of any painful muscular and articular structures. However, very gentle and pain-free active exercises should be frequently performed (every hour or so) to help stimulate the mechanoreceptors and modulate pain, as well as improve vascularization. Kropmans et al.34 report that at least 6 mm of change has to be seen to be a detectable difference when doing more than one measurement or to determine the effect of treatment. Appropriate exercises during the acute stage are designed to aid in muscle control, range of motion, coordination, and the reduction of muscle spasm. The patient should be instructed to perform the following exercises 10 times each at a frequency of three times per day. 1. Tongue rest position and nasal breathing. The patient places the tip of the tongue on the roof of the mouth, just behind the front teeth. With the tongue in this position, the patient is asked to breathe through the nose and to use the diaphragm muscle for expiration only (no accessory breathing muscles).

The Temporomandibular Joint

Group II: Disk Displacements

progressing from acute to chronic TMD-related pain. The study reported that the group who received behavioral skills training and biofeedback demonstrated reduced pain levels, improved coping abilities, and reduced emotional distress at the 1 year point. It should be clear from the studies that TMD is complex and that there is a clear need for further well-designed RCTs examining physical therapy interventions for TMD, which include valid and reliable outcome measures.

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THE SPINE AND TMJ

2. Controlled opening. The patient positions the tongue in the rest position and practices opening the mouth without shift or sound to the point where the tongue begins to leave the roof of the mouth. 3. Joint mobility. The “cork” exercise is a gentle technique to help increase joint mobility and articulation. The size (width) of the cork depends on the available motion. The patient holds the cork between his or her teeth. To help increase joint mobility, the patient rolls the cork between the teeth to one side and then the other. To aid in improving articulation, the patient talks for approximately 2 minutes while holding the cork between his or her teeth (Fig. 26-19). The talking exercise is then repeated with the cork removed. 4. Rhythmic stabilization. The patient positions the tongue in the rest position and grasps the chin with one or both hands. The patient then applies a resistance sideways to right deviation and then left deviation. The patient then applies a resistance against mouth opening and closing. Throughout all of these exercises, the patient must maintain the resting jaw position. 5. Craniocervical extension. The patient places both hands behind the neck and interlaces the fingers to stabilize the entire cervical region. The patient performs craniovertebral extension (see Chapter 23) without increased activity of the mandible. 6. Isolated controlled protrusion of the mandible. The patient is asked to actively protrude the mandible without associated movement of the facial muscles and the craniocervical region. 7. Shoulder retraction and thoracic extension. The patient is asked to pull the shoulders back and downward in one motion while squeezing the shoulder blades together to help restore the shoulder girdle to an ideal postural position and to extend the thoracic spine. Neuromuscular education techniques can be used to control premature or excessive translation. If premature translation has been found to be occurring, the patient is taught to maintain the tongue on the posterior portion of the palate and to monitor the lateral pole of the condyles during

opening to ensure that only rotation occurs during the early phase of opening.

Patient Education The clinician should explain the cause and nature of the disorder to the patient, and to reassure him or her of the benign nature of the condition. A successful self-care program allows healing and prevents further injury and is often enough to control the problem. A typical self-care home program includes the following: Limitation of mandibular function (rest). The patient is advised to eat soft foods and avoid those that need a lot of chewing and is discouraged from wide yawning, singing, chewing gum, and any other activities that would cause excessive jaw movement. ▶▶ An exercise program, consisting of the exercises described above. ▶▶ Habit awareness and modification. ▶▶ Stress avoidance. Patients should be advised to identify any source(s) of stress and to try to change their lifestyle accordingly. ▶▶

▶▶

The patient’s sleeping position. If the intrinsic ligaments are injured, the patient should be advised to sleep on the back, with the neck supported by a cervical pillow. The prone position should be avoided as it compresses the TMJ and stresses the cervical spine by extending and rotating it.

Occlusal Appliance Therapy Occlusal appliances include bite-raising appliances, occlusal splints, or bite guards. These removable custom-made appliances are usually made of hard acrylic, which are custom made to fit over the occlusal surfaces of the teeth in one arch. The function of the occlusal device is to provide a stable jaw posture by creating single contacts for all of the posterior teeth in centric relation and centric occlusion. Although occlusal appliance therapy has been shown clinically to alleviate symptoms of TMD, malocclusion, in itself, is not established as an important factor in TMD, because very few patients with malocclusion actually go on to develop TMD. In an evidence-based assessment of occlusal adjustment as a treatment for TMDs, Tsukiyama et al.12 concluded that the experimental evidence reviewed was neither convincing nor powerful enough to support the performance of occlusal therapy as a general method for treating a nonacute TMD, bruxism, or a headache.12

Functional Phase The interventions described for this phase are best used in combination and are dependent on the patient’s needs.

Postural Education FIGURE 26-19  Cork exercise.

The focus of the postural intervention should be to educate the patient on the correct posture of the head, neck, shoulder, and tongue, in order to help minimize symptoms.

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Oftentimes, the focus of the education is to teach the patient mental reminders to reduce the times spent in habitual positions during work and recreation.

Psychotherapy

Manual Therapy The specific manual techniques for the TMJ are described under “Therapeutic Techniques” section later.

Trigger Point Therapy One of the most common interventions for masticatory muscle disorders is trigger point therapy.2 Chapter 11 reviews the basis for the various intervention procedures for trigger points, which include deep massage, soft-tissue mobilizations, postural exercises, ultrasound, acupuncture, and trigger point injections. Spray and stretch techniques may also be used. These techniques involve the application of a vapocoolant spray during the stretching of soft tissues to reduce trigger points and eliminate referred pain. Vapocoolants may also be applied to cool the skin and overlying musculature rapidly during stretching. When using vapocoolants in this region, care must be taken to cover the patient’s eyes and to prevent any inhalation of the vapors.

Exercise Some evidence suggests that exercise of the specific painful area during the functional phase is effective in strengthening the muscles, improving function, and reducing pain.2 Because of the association of TMD and poor posture, the prescribed exercises for TMD include strengthening exercises for the cervicothoracic stabilizers (see Chapter 25) and the scapular stabilizers (see Chapter 16). Stretching exercises are prescribed for the scalene, trapezius, pectoralis minor, levator scapulae (see Chapter 25), and the suboccipital extensors (see Chapter 23). A restriction of mouth opening is treated with range-ofmotion exercises to elongate the soft tissues and with joint mobilizations. The patient should be encouraged to begin full active range-of-motion exercises as early as tolerated (see the discussion of automobilizations under “Therapeutic Techniques” section later). However, if jaw deviation is occurring, the exercises should be performed in a range in which the patient can control the deviation.

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Thermal and Electrotherapeutic Modalities A multitude of electrotherapeutic modalities, especially ultrasound and electrical stimulation, have been applied to patients with TMDs, but there appears to be little evidence that passive modalities alone can cause long-lasting reductions, and very few studies have systematically evaluated the effect of these treatments.2 Moist Heat Packs.  Conventional hot packs or face packs may be used in the functional stage and are applied for approximately 15 minutes. Thermotherapy is used to help the soft tissues relax and to increase circulation. High-Voltage Electric Stimulation.  High-voltage stimulators deliver a monophasic, twin-peak waveform. Because of the short duration of this twin-peak wave, high voltages with high-peak current but low average current can be achieved. These electrical characteristics provide patient comfort and safety in the application. In addition, in contrast to lowvoltage direct-current devices, thermal and galvanic effects are minimized. High-voltage stimulators can been applied clinically to reduce or eliminate muscle spasm and soft-tissue edema, as well as for muscle reeducation (non–CNS-produced muscle contraction), trigger point therapy, and increasing blood flow to tissues with decreased circulation.20

The Temporomandibular Joint

Researchers in orofacial pain acknowledged the importance of the psychological domain in causing and/or maintaining pain, and in regulating peripheral and central neural structures involved in nociception. Some studies suggest that, on occasion, TMD may be the somatic expression of an underlying psychological or psychiatric disorder such as depression.35 Where persistent habits exacerbate or maintain the TMD, a more structured program of behavioral therapy may be required. Such behavioral therapy may include counseling on lifestyle, relaxation therapy, sleep interruption devices, or hypnosis.2 Medical hypnosis has been demonstrated to be an effective treatment modality for TMD, in terms of reducing both symptoms and medical use.36

Excessive mandibular motion is treated by muscle reeducation, with isometrics performed at the desired opening range.

Ultrasound.  The effects of ultrasound are partly thermal, because of the increase in blood flow and tissue temperature produced. Thus, ultrasound may be used to help the soft tissues relax and to increase circulation. Ultrasound is an ideal modality both before and during joint and soft-tissue mobilization. There is also a mechanical effect associated with ultrasound because the sound waves produce pressure changes in the tissues, which may result in a micromassage of the tissues. A 3-MHz frequency is recommended, with an intensity of between 0.75 and 1.0 W/cm2. Tongue depressors can be inserted in the patient’s mouth to apply a gentle stretch during the ultrasound treatment. Iontophoresis.  Iontophoresis may be used to introduce medications such as cortisol, dexamethasone, salicylates, and analgesics.

Surgical Intervention A range of surgical procedures is currently used to treat TMD, ranging from TMJ arthrocentesis and arthroscopy to the more complex open joint surgical procedures, referred to as arthrotomy. The proximity of the medial aspect of the TMJ to the structures of the infratemporal fossa raises the possibility of complications associated with TMJ surgery on the medial aspect of the joint. In terms of intervention, the postsurgical patient is treated as though in the acute phase of healing and is progressed gradually, as outlined under “Intervention Strategies” section earlier.

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PRACTICE PATTERN 4D: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, AND RANGE OF MOTION ASSOCIATED WITH CONNECTIVE TISSUE DYSFUNCTION Internal Derangement: Intra-Articular Disk Displacement THE SPINE AND TMJ

Impairments of the TMJ may involve the temporomandibular disk, joint surfaces, joint capsule, or synovium, or any combination of these structures. The DC/TMD categories of group II (disk displacement) and group III (joint dysfunction) are integrated here, because disk disorders become problematic for patients primarily when these result in joint pain (arthralgia) or functional motion restrictions.15 TMJ internal derangement is one of the most common forms of TMD and is associated with characteristic clinical findings such as pain, joint sounds, and irregular or deviating jaw function. The term internal derangement when related to TMD denotes an abnormal positional relationship of the articular disk to the mandibular condyle and the articular eminence. This abnormal positional relationship may result in mechanical interference and restriction of the normal range of mandibular activity. Theoretically, internal derangement of the TMJ involves the anterior (and medial) displacement of the disk, resulting from the action of the upper head of the lateral pterygoid muscle, a tear or thinning of the disk, osteoarthrosis, or malocclusion.37 Macrotrauma, as may occur from opening the mouth for dental procedures, intubations, and blows to the face, can result in plastic deformation and injury to the retrodiskal tissue and/or the collateral ligaments that anchor the disk to the condyle.15 Alternately, repeated microtrauma, as occurs with parafunctional activities of gritting, grinding, and bruxism, can cause excessive force on the disk, resulting in disk thinning or perforations and disk displacement.15

Disk Incoordination

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Disk incoordination may occur when the intra-articular disk adheres to the eminence that usually occurs after a prolonged period of TMJ inactivity, such as that occurs with postsurgical immobilization. Other causes of this condition include occlusion, bruxism, excessive biting force, and trauma. The adhesion can result in a loss of the translatory glide of the condyle, which in turn can result in excessive pressure between the disk and the eminence and a strain on the diskal ligaments, predisposing the patient to a true disk displacement of the joint. Clinical findings with this condition may include a discrete opening click with momentary discomfort while the remainder of the translatory cycle is accomplished without difficulty.22 The click associated with a deviation in the form usually occurs at the same point in the range of opening and closing. The conservative intervention for this condition should focus on the elimination of any occlusal disharmony, the reduction of parafunctional habits, and methods to prevent the disk–condyle complex from returning to the closed position. The latter goal can be accomplished by applying a

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permanent stabilization splint for a few months. When symptoms have been reduced, the patient should be weaned from the splint during the day and, eventually, night.

Articular Surface Defects An articular surface defect located on the articulating surface of the eminence, the superior surface of the disk, or both, may cause an obstruction to the normal translatory movement of the disk.8 The defect may be caused by trauma to the mandible when the teeth are apart, habitual abuse, or developmental and growth anomalies. Clinical findings for articular surface defects include a reciprocal click at the same point during both opening and closing movements. In addition, a lateral deviation frequently occurs on opening, as the patient attempts to circumvent the interference. Although the condition itself is painless, it can be worsened by any activities that increase intra-articular pressure.20 Conservative intervention for this condition includes habit training to develop a path of mandibular movement that avoids the interference. In addition, the patient is asked to make a conscious effort to reduce the force of chewing and eliminate parafunctional habits. Chewing on the affected side, by decreasing the intra-articular pressure, may also be helpful. A stabilization splint may serve to reduce pressure on the joint structures.

Disk Thinning and Perforation Disk thinning can result from the application of excessive pressure on the TMJ and can lead to a deformation of the joint structures. The continuous pressure eventually may cause perforation of the disk. The symptoms of disk thinning and perforation depend on the extent of disk damage. Theoretically, thinning of the central part of the disk should be painless because that part of the disk is not innervated. However, variables such as joint tenderness and muscle pain often are associated with any activity that deepens the central bearing area of the disk. If the disk should perforate, grating sounds or crepitus during the translatory cycle are likely because of damage of the articular surfaces.20 The diagnosis of disk perforation usually is made by imaging, arthrography, or arthroscopy. Conservative intervention for disk thinning usually involves the application of a stabilization splint to prevent a perforation. If perforation has occurred, and the patient can no longer tolerate the symptoms, surgical intervention is indicated.

Disk Displacements Anterior disk displacement is the most common type of disk displacement.20 A pathologic click in a disk displacement occurs when the condyle glides onto the middle aspect of the displaced disk later than normal in the opening cycle. A reciprocal click, sometimes muted, occurs during mouth closing as the condyle slips posteriorly on the anteriorly displaced disk, or it may represent the sudden snapping back of the disk by the less than adequately elastic posterior ligament of the disk.

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Partial Anteromedial Disk Displacement

Anteromedial Intra-Articular Disk Displacement with Reduction Disk displacement with reduction is both an anatomic and functional disorder that is cyclic in nature.38 Anteromedial disk displacement with reduction is described as an unexpected alteration or interference of the disk–condyle structural relation during mandibular translation with mouth opening and closing.15 The misalignment of the disk is thought to be the result of articular surface irregularity, disk– articular surface adherence, synovial fluid degradation, or myofascial imbalances around the joint.20 The temporarily misaligned disk reduces or improves its structural relationship with the condyle when mandibular translation occurs with mouth opening. This change often is associated with an “opening click,” and a reciprocal “closing click,” which occurs just before the teeth occlude during mouth closing. Pain, if present, usually occurs at the time of the disk reduction. Disk displacement with reduction may be characterized by five progressive stages.20 Stage I.  In stage I, the disk may be positioned slightly anteromedially on the mandibular head. Pain is usually mild or absent. As the disk becomes deformed from the repetitive microtrauma, it begins to interfere with the normal translation of the condyle. ▶▶ Stage II.  In this stage, the disk slips further anteromedially on the mandibular head. The reciprocal click may occur in the early phase of opening and late in the phase of closing. Stage II is characterized by a loss of integrity of the ligamentous and intracapsular structures. This loss of integrity may result in increased mobility and a decrease in control of the disk, which increases the potential for impingement and deformation of the disk, resulting in severe pain, and increasing the potential for intermittent open locking or subluxation of the joint. An open lock is characterized by two opening clicks, and two clicks on closing. During opening, the first click occurs when the condyle moves over the posterior rim of the disk and the second click as the condyle moves over the anterior rim. If, after the second click occurs on opening, the disk lies posterior to the condyle, the condyle may be prevented from sliding back. ▶▶ Stage III.  Stage III, often the most painful stage, is characterized by a reciprocal click that occurs later ▶▶

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The Temporomandibular Joint

In a healthy joint, the center of the posterior band of the disk is in the 12 o’clock position on the condyle when the teeth are occluded. With partial anterior disk displacement, the disk is permitted to slide anteriorly on the condyle, and the terminal position of the posterior band of the disk occurs anteriorly to its normal position on the condyle in the closed-joint position. The anterior displacement is thought to occur because of two factors: some thinning of the posterior band and minimal elongation of the diskal ligaments. The conservative intervention for partial displacements should focus on preventing any worsening of the disk displacement. This can be achieved using intraoral appliances in combination with psychological stress reduction.

in the opening cycle and earlier in the closing cycle. Occasionally, the intra-articular disk becomes adherent to the mandibular condyles in both the open and closed positions. This is known as a closed-lock position. The sustained closed-lock condition produces a sudden limitation of opening, as the disk becomes permanently lodged anteriorly, thereby interfering with the normal condylar rotation and translation. This closed-lock condition results in a hard end-feel in the joint when the clinician attempts to induce a passive stretch to the joint. The impingement on the posterior attachment of the disk by the condylar head may result in a prolonged stretching of the tissue. The limitation of opening usually is restricted to 25–30 mm. Since condylar translatory mobility commonly is hindered only on the affected side, the mandible may deviate away from the midline toward the affected side with maximal jaw opening. However, if this condition is chronic, there may be no deviation or limitation of jaw opening because of progressive tearing in the retrodiskal lamina. Tenderness of the masticatory muscles may also occur as a result of the protective splinting of the joint. ▶▶ Stage IV.  In this stage, clicking is rare because the disk position is usually so incompatible. If clicking does occur, it is usually a single opening click because of the irregularities in translations. Chronic locking with softtissue remodeling can occur as a result of routine daily jaw function on the posteriorly or anteriorly positioned disk. Known as rotational displacement, this condition is associated with pain and, commonly, with anterior displacement of the disk. ▶▶ Stage V.  This stage is characterized by radiographic degenerative changes on the condylar head and, occasionally, on the articular eminences, with evidence of remodeling and osteophytosis.38 Marked deformity and thickening of the disk may occur, and the shape of the disk may change in configuration from biconcave to biconvex. The joint space typically is narrowed to the point where bone-on-bone contact is evident, resulting in coarse crepitus with jaw motions. Stages I and II usually are amenable to physical therapy intervention. The focus for these stages is on reducing muscle dysfunction and improving the biomechanics of the joint. The intervention usually involves using mandibular-repositioning appliances that stabilize a protrusive position to keep the disk in a more optimal relationship with the condyle. The primary purpose of protrusive splint therapy may be to allow repair and regeneration to occur in the retrodiskal tissue and, possibly, in the diskal ligaments. The intervention for stages III–V, and for those patients who are postsurgical, is directed at promoting and progressing the healing, restoring joint range of motion, and reducing the inflammation associated with capsulitis.

Anteromedial Disk Displacement with Intermittent Locking As mentioned in the previous section, if the disk remains displaced for longer periods of time, its shape becomes deformed and may slowly change from biconcave to biconvex. This change

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THE SPINE AND TMJ 1290

in shape makes the passage of the condyle under the disk more difficult. To return the disk, the patient must learn to move the mandible to the opposite side in order to activate the superior retrodiskal lamina. Unfortunately, at this point, the retrodiskal tissue has thinned considerably and lost much of its elasticity, making disk reduction difficult to achieve. The intermittent locking may occur at any time, but it most often occurs in the morning upon awakening, after a prolonged period of clenching, or after chewing on the involved side. Conservative intervention usually involves a mandibularrepositioning appliance to keep the disk in correct alignment with the condyle.

Intra-Articular Disk Displacement without Reduction Although some patients may show progression through the various stages of disk displacement, it is unclear why some patients remain in the category of anterior disk displacement with reduction for years, whereas others proceed to intermittent locking and anterior disk displacement without reduction within a matter of months. Disk displacement without reduction is described as an alteration or interference of the disk–condyle structural relation that is maintained during mandibular translation. As a result of continued disk deformation along with elongation of diskal ligaments and a loss of tension in the posterior attachment, the disk may remain anteromedially displaced creating a “closed lock.”20 Contact is lost among the condyle, disk, and articular eminence, and the articular disk space collapses, trapping the disk in front of the condyle and thereby preventing translation. Usually, the displacement of the disk becomes worse with jaw motions. Initially, there may be an associated locking with a sudden and marked limited jaw motion. In addition, there may be a deviation of the mandible toward the involved side during mouth opening, and a marked limitation of lateral deviation to the contralateral side. The limited opening resulting from anterior disk displacement without reduction may have a variety of causes. In addition to the more common causes, including muscle spasm and capsular tightness, limited mouth opening may occur when either the disk is lodged anteriorly to the condyle or the TMJ is dislocated or subluxed. Limited mouth opening as a result of elevator muscle spasm or capsular restraint can be differentiated by determining the end-feel. Elevator muscle spasm tends to limit only vertical movement; the protrusive and lateral excursions are usually normal. Anterior disk displacement without reduction, however, exhibits restrictions in both protrusive movements and contralateral excursions. The movement to the side of the involved joint is usually not mechanically restricted because the main movement occurring in the joint is a rotation. Painful restriction may be the result of impingement on inflamed retrodiskal tissues. Secondary muscle spasm of the elevator muscles may add to the restricted opening as well as capsular involvement. In the acute phase, joint noise is usually absent. However, crepitus may be detected as the displacement becomes chronic, and changes occur on the articular surfaces. As the condition becomes chronic, the pain often is markedly reduced, and the range of motion may approach normal dimensions.

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The intervention for the acute phase of this type of disk displacement should focus on a reduction of the displaced disk through mobilization of the joint. Since secondary elevator muscle spasm is usually present, as well as some inflammation of joint structures, it may be of benefit for the patient to take a skeletal muscle relaxant and an NSAID prior to the physical therapy session. The reduction procedure involves the patient opening the mouth as wide as comfortable and then moving the mandible toward the opposite joint. If unsuccessful, the clinician may then attempt to reduce the disk manually through downward pressure on the last molar on the involved side.20 Success in reducing the disk usually can be clinically determined by comparing the amount of vertical opening and contralateral movement after mobilization with the amount of movement before mobilization. This difference should be verified through imaging because clinical criteria alone may not be accurate. Generally speaking, reductive mobilization is more successful in the more acute conditions. In cases in which changes in the connective tissue capsule may be contributing factors, manual stretching of the vertical fibers of the capsule may be indicated.

Adhesive Disk Although many cases of intracapsular restriction of mandibular movement or closed lock are caused by an anterior disk displacement without reduction, another frequent abnormality of the TMJ is the formation of intra-articular adhesions. The restriction may also be caused by an adhesion occurring in the superior joint cavity between the disk and the eminence, resulting in a loss of condylar translation. In addition, an adhesion may result in condylar displacement of the disk, with distortion of the disk itself on mandibular opening.38 Trauma frequently is implicated as a causative factor. If the trauma is slight, only mild surface damage to the disk may occur, resulting in disk incoordination or an articulating surface defect. A more severe episode could cause intracapsular bleeding and effusion. Fibrosis may result, producing a reduction in the range of motion as well as degeneration. The condylar translation may be lost as a result of disk adhesion. Clinically, adhesive disk hypomobility is indistinguishable from acute anterior disk displacement without reduction. Since translation does not occur, opening is limited. Pain is variable and may be caused by stretching of the diskal ligaments, as forced opening is attempted. The conservative intervention for adhesive disk hypomobility is specific joint mobilizations (see “Therapeutic Techniques” section later).

Displacement of the Disk–Condyle Complex Subluxation Subluxation between the disk and the articular eminence may occur as a result of excessive opening, which can force the condyle and the disk anteriorly beyond the normal limits of the translatory cycle. If the disk cannot rotate any farther posteriorly, and the condyle continues to translate, a partial dislocation or subluxation can occur. Usually, the patient has a history of jaw clicking with wide mouth opening.

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Intervention for this condition includes habit training to limit mouth opening voluntarily within normal limits. This training should be accompanied by exercises that strengthen the elevator muscles.

Dislocation

Alteration to the ligaments can be achieved by the introduction of a sclerosing agent into the capsular space of the TMJ. ▶▶ Alteration of the associated musculature can be achieved by exercise. Strengthening the suprahyoid muscles to counterbalance the action of the lateral pterygoid muscles could, theoretically, reduce the likelihood of dislocation. The equipment to perform this type of exercise, however, is elaborate and involves considerable compliance by the patient. A more recently reported treatment modality for alteration of the musculature is the use of type A botulinum toxin. If the dislocation is chronic, the patient should be taught how to self-reduce the mandible. Habit training similar to that employed for subluxation should be instituted. ▶▶ An alteration of bony anatomy requires a surgical eminectomy. ▶▶

Arthritis The TMJ, like other joints in the body, can become a site of osteoarthritis. Osteoarthritis and osteoarthrosis represent degeneration of the articular surface of the TMJ, with the former being associated with inflammatory processes. Degenerative osteoarthritis may be secondary to excessive loading, prolonged chemical irritation (i.e., inflammation), trauma, surgery, congenital malformation, or, most commonly,

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Pigmented Villonodular Synovitis Pigmented villonodular synovitis (PVNS) is a proliferative but nonneoplastic disorder of unknown pathogenesis that affects the synovial membranes of joints.40 Eighty percent of cases involve the knee, followed in order of frequency by the hip, ankle, and shoulder, with the involvement of the TMJ being very rare.41 The disorder is generally thought to be a benign, inflammatory process, although it may develop as an aggressive local process. PVNS is described as expressing multiple manifestations of a histologic lesion occurring in the synovial membrane of joints. PVNS is subdivided into diffuse and localized forms, depending on the extent of synovial involvement. PVNS may extend into bone, and, in most instances, the diffuse form probably represents aggressive extra-articular extension and occasional recurrence after surgical intervention.41 The symptoms of PVNS of the TMJ vary but typically include swelling in the preauricular area, progressive TMJ pain during mastication, and a history of progressive difficulty in opening of the mouth.40 The recommended intervention for PVNS lesions involves synovectomy at all sites involved.41

The Temporomandibular Joint

Dislocation of the TMJ is caused by additional rotation of the mandibular condyle beyond its biomechanical limit, resulting in an anterior displacement of the disk beyond the articular eminence and in direct contact between the condyle and the eminence. As opposed to subluxation, which is a partial loss of contact between the disk and the eminence, dislocation involves a collapse of the articular disk space. Some factors associated with the onset of habitual dislocation include, but are not limited to, yawning, singing, sleeping with the head resting on the forearm, manipulation of the mandible while the patient is under general anesthesia, excessive tooth abrasion, severe malocclusion, loss of dentition (leading to overclosure), and trauma.39 Clinical findings include an inability of the patient to close the mandible after wide mouth opening so that the mouth becomes locked open and cannot be moved vertically. Pain may be variable, which increases as the patient attempts to close, thus straining the inferior retrodiskal lamina and the collateral diskal ligaments. The main focus of the intervention is to widen the articular disk space to allow the superior retrodiskal lamina to retract the disk. For recurrent dislocations, the approach is addressed according to the stability factors into (1) alteration of the ligaments, (2) alteration of the associated musculature, and (3) alteration of the bony anatomy39:

long-standing disk derangement. Marginal osteophyte formation, bony erosion sclerosis, and subchondral or subcortical formation may be observed.38 The temporomandibular disk may become distorted in shape secondary to adhesions seen in osteoarthritis.20 Other arthritides are known to affect the TMJ, including rheumatoid arthritis, systemic lupus erythematosus, synovial chondromatosis, ankylosing spondylitis, psoriasis, and crystalline arthritides such as calcium pyrophosphate deposition disease and gout. The patient may report joint pain and crepitus or a grating feeling throughout the entire joint movement.15 To date, no intervention exists that can reverse the anatomic and biochemical alterations of osteoarthrosis. Thus, the intervention approach has to be aimed at restoring function and managing pain through the acute phase of the disease.

PRACTICE PATTERN 4E: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, AND RANGE OF MOTION ASSOCIATED WITH LOCALIZED INFLAMMATION Masticatory Muscle Disorders The masticatory muscles include the masseter, lateral pterygoid, the temporalis, and the medial pterygoid. Masticatory muscles may be directly injured through overuse and/or tensile strain, and indirectly through muscle guarding and centrally mediated myalgia.15 Such dysfunctions include trauma, occlusal imbalance, changes in the vertical dimensions between the teeth, immobilization, prolonged dental procedures, chronic teeth clenching, and disease. Centrally mediated myalgia is a process that involves chronic overactivation of muscle, as a result of central sensitization (see Chapter 3).42

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The following descriptions outline the common referral patterns of the TMJ muscles.

Temporalis Referred pain from the temporalis muscle may extend over the temporal region, to the eyebrow and the upper teeth, and to the maxilla and TMJ. A headache caused by temporalis muscle spasm is common. The patient also may feel pressure behind the eye or have increased eye fatigue.

Lateral Pterygoid THE SPINE AND TMJ

Spasm of the lateral pterygoid may cause a deep ache in the cheek area, maxilla, TMJ, or ear. Pain also is felt with chewing.

Medial Pterygoid

Trigeminal Neuralgia

The medial pterygoid may refer pain behind the TMJ, deep in the ear, to the tongue, and to the back of the mouth.

Trigeminal neuralgia is an intensely painful disorder of the face of brief duration (30 seconds). The pain is spontaneous and can be triggered by touch, cold, shaving, brushing teeth, or make-up application. The cause of trigeminal neuralgia is at present unknown, although most authors place the site of disturbance in the region of the posterior root or in the spinal tract of the nerve.43 Injuries to nerves and soft and hard tissues as a result of repeated traumas have been reported to produce persistent pain because of sensitization of both peripheral and central neurons.43 The sensitization process has been shown to influence subsequent pain experience. Increased postoperative pain resulting from insufficient preemptive analgesia, such as incomplete use of local anesthetics or pain medication before surgery, has been well documented.

Masseter Referred pain from a masseter muscle spasm may be projected to the eyebrow, maxilla, anterior mandible, and upper and lower molars. The intervention for these muscle spasms includes application of moist heat to promote muscle relaxation; massage of the affected muscles; ▶▶ passive and active self-stretch exercises; and ▶▶ spray and stretch techniques. ▶▶ ▶▶

Forced mouth opening should be avoided. In the absence of joint hypomobility, yawning exercises are recommended as a home exercise, because this activity produces a strong reflex inhibition of the mandibular elevators. The lateral pterygoid can be passively stretched with maximal retrusion, followed by rhythmic sideways oscillations. The medial pterygoid can be passively stretched with jaw opening exercises.

INTEGRATION OF PRACTICE PATTERNS 4B, 4C, AND 4F: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE AND RANGE OF MOTION SECONDARY TO IMPAIRED POSTURE, SYSTEMIC DYSFUNCTION (REFERRED PAIN SYNDROMES), SPINAL DISORDERS, AND MYOFASCIAL PAIN DYSFUNCTION Cervical Spine Disorders

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constitutes an FHP. This posture is considered to be minimal at 60 degrees, moderate at 60–75 degrees, and maximal at 75–90 degrees.3 Associated signs include a decrease or reversal in the cervical lordosis and an increase in cranial rotation at the occipitoatlantal joint, resulting in a shortening and excessive activity of the posterior cervical muscles. The FHP can place undue stress on both the posterior cervical muscles and the anterior submandibular muscles, by increasing their normal resting lengths. This stress may also stretch the TMJ capsule and alter the bite biomechanics of the TMJ, resulting in a posterior migration of the mandible and an altered occlusal contact pattern.

Patients with TMD frequently report symptoms related to cervical spine disorders, and vice versa. The most common postural abnormality in the cervical spine with direct impact on the craniofacial area and temporomandibular arthralgia is the FHP. Any increase in the sternocleidomastoid angulation, or distance from the thoracic apex to the midcervical region,

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Myofascial Pain and Dysfunction Many clinicians over the years have described numerous conditions that share features such as fatigue, pain, and other symptoms in the absence of objective findings. These include illnesses such as chronic fatigue syndrome, fibromyalgia, and TMD. Myofascial pain and dysfunction associated with TMD generally present with diffuse pain that is cyclic and found in several sites in the head and neck, particularly the muscles of mastication. Pain is frequently at its worst in the morning, the patient often reports sore teeth from clenching, and there is often a history of stress and difficulty sleeping. The intervention for myofascial pain syndromes requires a comprehensive, and often a multidisciplinary, approach. The role of physical therapy in these syndromes is one of patient education, manual therapy techniques, and electrotherapeutic modalities to reduce pain, and exercises to improve posture, reduce the adaptive shortening of tissues, and improve the strength of the postural stabilizers.

THERAPEUTIC TECHNIQUES Manual Therapy The aim of manual therapy in TMD is to restore normal mandibular function using a number of techniques that serve to relieve musculoskeletal pain and promote the healing of tissues. In the acute phase, manual techniques, if used at all, should be very low grade and very carefully performed, because

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this joint tends to be very reactive and can flare up easily. To reduce hypomobility and acute locking of the TMJ, mobilization and massage can be applied to the TMJ, as well as to the muscles of mastication to stretch and relax them. Muscle relaxation and soft-tissue techniques often are required before mobilizations of the TMJ can be performed.

Myofascial Release

Muscle Stretching Muscle stretching techniques can be used if the examination shows that the restriction of movement is a result of shortened muscles (or other structures). Techniques to increase the extensibility of the cervical structures are described in Chapters 23 and 25.

Joint Mobilizations Specific joint mobilizations of the craniovertebral and cervical regions are described in Chapters 23 and 25, respectively. Specific mobilization techniques of the TMJ are indicated for decreased range of motion and pain caused by muscle contracture, disk displacement without reduction, and fibrous adhesions in the joint. During these procedures, the patient’s mandible should be completely relaxed, and the patient should not attempt to open his or her mouth until instructed to do so.

Techniques to Increase Mouth Opening Distraction  This technique is performed to separate the joint surfaces of the TMJ to allow the disk to start repositioning on the condyle and to start realigning the fibers of the tissue caudally. The patient is positioned sitting, and the clinician stands to the patient’s side. The clinician grips the patient’s head, using his or her forearm and hand, fingers against the patient’s forehead. The clinician stabilizes the patient’s head with his or her hand, arm, and chest. With a medical-gloved hand, the clinician places his or her thumb on the patient’s lower molars on the involved side, as far back in the mouth as possible. The clinician’s index and middle fingers grip the angle of the patient’s mandible of the involved side, with the ring or little fingers held under the patient’s mandible (depending on the size of the clinician’s hand and patient’s mandible). Using this grip, the clinician applies light distraction inferiorly to the patient’s involved TMJ by pressing his or her thumb inferiorly against the lower molars (see Fig. 26-14). Distraction, Anterior Glide, and Lateral Stretch This technique is performed to increase the anterior and inferior movement of the mandible for the patient who can only achieve slight opening of the mouth. The patient and clinician positions are the same as those described for the distraction

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Technique to Increase Full Mouth Closing This technique is used to increase the posterior movement of the mandible (retraction) for the patient, with an inability to fully close the mouth. The patient and clinician position is the same as described for the techniques to increase mouth opening. Using the same grip described for those techniques, the clinician gradually and maximally pushes posteriorly against the patient’s involved mandible to produce a posterior glide of the head of the mandible at the TMJ (see Fig. 26-15). Note: If the restriction of movement is bilateral, the same intervention may be performed on the patient’s opposite side.

The Temporomandibular Joint

Myofascial release is a combination of direct, indirect, and reflex neural release procedures. The basis of this technique is sensing palpable changes at various tissue levels and manually directing a gentle force to assist in releasing restricted tissues.

technique. Using the same grip as described earlier, the clinician applies light distraction inferiorly to the patient’s involved TMJ by pressing his or her thumb inferiorly against the lower molars. In addition to the distraction, the clinician gradually superimposes an anterior glide of the head of the mandible at the TMJ and a lateral stretch to the joint on the opposite side. Following the technique, the patient is asked to open his or her mouth as much as possible, and the newly acquired range is assessed. The procedure is repeated gradually until the patient is able to open his or her mouth fully, or considerable improvement is attained. Note: If the restriction of movement is bilateral, the technique may be performed on the opposite side.

Extraoral Lateral Glide This technique is used in the presence of severe pain, spasm, and marked limitation of movement caused by recent trauma. The patient is positioned in supine, with the head being supported on a pillow. The patient is asked to rotate the head in the opposite direction of the involved TMJ. The clinician places the thumbs of both hands over the lateral pole of the condyle. Gentle oscillations are performed over the lateral pole, or more distally depending on patient tolerance.

Extraoral Depression This technique also is used in the presence of severe pain, spasm, and marked limitation of movement caused by recent trauma. The patient is positioned in supine, with the head being supported on a pillow. The clinician gently grasps the angle of the mandible with the index and the thumb bilaterally. Gentle oscillations are then performed in the direction of mandibular depression.

Automobilizations Toothpick Exercise This exercise can be used for patients who demonstrate lateral deviation with mouth opening or closing. The patient stands or sits facing a mirror. A thick line is drawn down the mirror using a wax crayon. The patient wedges a toothpick between the lower incisors and lines up the toothpick with the line on the mirror. As the patient opens and closes the jaw, if the line becomes visible, the patient corrects the deviation before

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continuing the movement. If correction is not possible, the exercise is stopped to prevent incorrect learning by the controlling muscles.

Distraction Mobilization

THE SPINE AND TMJ

This technique can be taught to patients who demonstrate or report recurrent dislocations. To self-reduce a dislocation, the patient is instructed to place a gauze roll on the back inferior molars of both sides and to place his or her index fingers on the gauze. The patient opens the mouth as wide as possible and then applies a downward force on the gauze and the molars, thereby creating a joint distraction. Following a successful reduction, ice or heat (whichever produces the optimal therapeutic effect) should be applied around the TMJ.

REFERENCES 1. Nassif NJ, Al-Salleeh F, Al-Admawi M. The prevalence and treatment needs of symptoms and signs of temporomandibular disorders among young adult males. J Oral Rehabil. 2003;30:944–950. 2. Reneker J, Paz J, Petrosino C, et al. Diagnostic accuracy of clinical tests and signs of temporomandibular joint disorders: a systematic review of the literature. J Orthop Sports Phys Ther. 2011;41:408–416. 3. von Piekartz H. Temporomandibular disorders: neuromusculoskeletal assessment and management. In: Jull G, Moore A, Falla D, Lewis J, McCarthy C, Sterling M, eds. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. London, England: Elsevier; 2015:433–443. 4. Standring S, Gray H. Gray’s Anatomy: The Anatomical Basis of Clinical Practice. 41st ed. London, England: Elsevier; 2015. 5. Warren MP, Fried JL. Temporomandibular disorders and hormones in women. Cells Tissues Organs. 2001;169:187–192. 6. Johansson A, Unell L, Carlsson GE, et al. Gender difference in symptoms related to temporomandibular disorders in a population of 50-year-old subjects. J Orofac Pain. 2003;17:29–35. 7. Marklund S, Wanman A. Incidence and prevalence of temporomandibular joint pain and dysfunction. A one-year prospective study of university students. Acta Odontol Scand. 2007;65:119–127. 8. Perez CV, de Leeuw R, Okeson JP, et al. The incidence and prevalence of temporomandibular disorders and posterior open bite in patients receiving mandibular advancement device therapy for obstructive sleep apnea. Sleep Breath. 2013;17:323–332. 9. Neumann DA. Kinesiology of mastication and ventilation. In: Neumann DA, ed. Kinesiology of the Musculoskeletal System: Foundations for Physical Rehabilitation. 3rd ed. St. Louis, MO: Mosby; 2016:437–468. 10. Tanaka E, Koolstra JH. Biomechanics of the temporomandibular joint. J Dent Res. 2008;87:989–991. 11. Ingawale S, Goswami T. Temporomandibular joint: disorders, treatments, and biomechanics. Ann Biomed Eng. 2009;37:976–996. 12. Tsukiyama Y, Baba K, Clark GT. An evidence-based assessment of occlusal adjustment as a treatment for temporomandibular disorders. J Prosthet Dent. 2001;86:57–66. 13. Armijo Olivo S, Magee DJ, Parfitt M, et al. The association between the cervical spine, the stomatognathic system, and craniofacial pain: a critical review. J Orofac Pain. 2006;20:271–287. 14. de Leeuw R, Klasser GD. Orofacial Pain: Guidelines for Assessment, Diagnosis, and Management. Hanover Park, IL: Quintessence Publishing; 2013. 15. Harrison AL, Thorp JN, Ritzline PD. A proposed diagnostic classification of patients with temporomandibular disorders: implications for physical therapists. J Orthop Sports Phys Ther. 2014;44:182–197. 16. Schiffman EL, Ohrbach R, Truelove EL, et al. The research diagnostic criteria for temporomandibular disorders. V: methods used to establish and validate revised axis I diagnostic algorithms. J Orofac Pain. 2010;24:63–78. 17. Gonzalez YM, Schiffman E, Gordon SM, et al. Development of a brief and effective temporomandibular disorder pain screening questionnaire: reliability and validity. J Am Dent Assoc. 2011;142:1183–1191.

18. Zakrzewska JM. Facial pain: neurological and non-neurological. J Neurol Neurosurg Psychiatry. 2002;72 (Suppl 2):ii27–ii32. 19. Ah-See KW, Evans AS. Sinusitis and its management. BMJ. 2007;334:358–361. 20. Okeson JP. Management of Temporomandibular Disorders and Occlusion. 7th ed. St Louis, MO: Mosby Year Book; 2013. 21. Pekkan G, Aksoy S, Hekimoglu C, et al. Comparative audiometric evaluation of temporomandibular disorder patients with otological symptoms. J Craniomaxillofac Surg. 2010;38:231–234. 22. Okeson JP, de Leeuw R. Differential diagnosis of temporomandibular disorders and other orofacial pain disorders. Dent Clin North Am. 2011;55:105–120. 23. Kumar A, Brennan MT. Differential diagnosis of orofacial pain and temporomandibular disorder. Dent Clin North Am. 2013;57:419–428. 24. Walker N, Bohannon RW, Cameron D. Discriminant validity of temporomandibular joint range of motion measurements obtained with a ruler. J Orthop Sports Phys Ther. 2000;30:484–492. 25. Skaggs CD. Diagnosis and treatment of temporomandibular disorders. In: Murphy DR, ed. Cervical Spine Syndromes. New York, NY: McGrawHill; 2000:579–592. 26. Manfredini D, Tognini F, Zampa V, et al. Predictive value of clinical findings for temporomandibular joint effusion. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2003;96:521–526. 27. Schiffman EL, Truelove EL, Ohrbach R, et al. The research diagnostic criteria for temporomandibular disorders. I: overview and methodology for assessment of validity. J Orofac Pain. 2010;24:7–24. 28. Masumi S, Kim YJ, Clark GT. The value of maximum jaw motion measurements for distinguishing between common temporomandibular disorder subgroups. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2002;93:552–559. 29. Gatchel RJ, Stowell AW, Wildenstein L, et al. Efficacy of an early intervention for patients with acute temporomandibular disorder-related pain: a one-year outcome study. J Am Dent Assoc. 2006;137:339–347. 30. Ohrbach R, Turner JA, Sherman JJ, et al. The research diagnostic criteria for temporomandibular disorders. IV: evaluation of psychometric properties of the axis II measures. J Orofac Pain. 2010;24:48–62. 31. Truelove E, Pan W, Look JO, et al. The research diagnostic criteria for temporomandibular disorders. III: validity of axis I diagnoses. J Orofac Pain. 2010;24:35–47. 32. McNeely ML, Armijo Olivo S, Magee DJ. A systematic review of the effectiveness of physical therapy interventions for temporomandibular disorders. Phys Ther. 2006;86:710–725. 33. Medlicott MS, Harris SR. A systematic review of the effectiveness of exercise, manual therapy, electrotherapy, relaxation training, and biofeedback in the management of temporomandibular disorder. Phys Ther. 2006;86:955–973. 34. Kropmans T, Dijkstra P, Stegenga B, et al. Smallest detectable difference of maximal mouth opening in patients with painful restricted temporomandibular joint function. Eur J Oral Sci. 2000;108:9–13. 35. Younger JW, Shen YF, Goddard G, et al. Chronic myofascial temporomandibular pain is associated with neural abnormalities in the trigeminal and limbic systems. Pain. 2010;149:222–228. 36. Simon EP, Lewis DM. Medical hypnosis for temporomandibular disorders: treatment efficacy and medical utilization outcome. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;90:54–63. 37. Cleland J. Temporomandibular joint. In: Orthopedic Clinical Examination: An Evidence-Based Approach for Physical Therapists. Carlstadt, NJ: Icon Learning Systems, LLC; 2005:39–89. 38. Hayt MW, Abrahams JJ, Blair J. Magnetic resonance imaging of the temporomandibular joint. Top Magn Reson Imaging. 2000;11:138–146. 39. Shorey CW, Campbell JH. Dislocation of the temporomandibular joint. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;89:662–668. 40. Aimoni C, Ciorba A, Cappiello L, et al. Pigmented villonodular synovitis of the temporomandibular joint. J Craniofac Surg. 2012;23:e168–e170. 41. Giannakopoulos H, Chou JC, Quinn PD. Pigmented villonodu lar synovitis of the temporomandibular joint. Ear Nose Throat J. 2013;92:E10–E103. 42. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain. 2011;152:S2–S15. 43. Bennetto L, Patel NK, Fuller G. Trigeminal neuralgia and its management. BMJ. 2007;334:201–205.

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C H A P T E R 2 7

CHAPTER OBJECTIVES At the completion of this chapter, the reader will be able to: 1. Describe the vertebrae, ligaments, muscles, and blood and nerve supply that comprise the thoracic intervertebral segment. 2. Outline the coupled movements of the thoracic spine, the normal and abnormal joint barriers, and the responses of the various structures to loading. 3. Perform a detailed objective examination of the thoracic musculoskeletal system, including palpation of the articular and soft-tissue structures, combined motion testing, position testing, passive articular mobility tests, and stability tests. 4. Evaluate the total examination data to establish the diagnosis and estimate the prognosis. 5. Describe the common pathologies and lesions of this region. 6. Apply a variety of manual techniques to the thoracic spine using the correct grade, direction, and duration. 7. Describe intervention strategies based on clinical findings and established goals. 8. Design an intervention plan based on patient education, manual therapy, and therapeutic exercise. 9. Evaluate intervention effectiveness in order to progress or modify an intervention. 10. Plan an effective home program, including spinal care and therapeutic exercise, and instruct the patient in this program.

OVERVIEW The thoracic spine serves as a transitional zone between the lumbosacral region and the cervical spine and has a significant influence on both regions. Despite the fact that the thoracic

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The Thoracic Spine

spine has not enjoyed the same attention as other regions of the spine in terms of research, it can be a significant source of local and referred pain. The thoracic spine is the most rigid region of the spine and, in this area, protection of the thoracic viscera takes precedence over segmental spinal mobility. In addition, the thorax is an important region of load transfer between the upper body (the head, cervical spine, and upper extremities) and the lower body (the lumbopelvic region and lower extremities).1 As each thoracic vertebra is involved in at least six articulations, and as many as 13, establishing the specific cause of thoracic dysfunction may not always be possible. This task is made more difficult because of the inaccessibility of most of these joints.

ANATOMY The thoracic spine (Fig. 27-1) forms a kyphotic curve between the lordotic curves of the cervical and lumbar spines. The curve begins at T1–2 and extends down to T12, with the T6–7 disk space as the apex. The thoracic kyphosis is a structural curve that is present from birth. Unlike the lumbar and cervical regions, which derive their curves from the corresponding differences in intervertebral disk (IVD) heights, the thoracic curve is maintained by the wedge-shaped vertebral bodies, which are about 2 mm higher posteriorly than anteriorly. The thoracic spine can be divided into five regions based on anatomical and biomechanical differences: Cervicothoracic: This region comprises the C7–T1 segment and the first rib. ▶▶ Vertebromanubrial: This region, which has a slight overlap with the cervicothoracic region, includes the first two thoracic vertebrae, ribs one and two, and the manubrium. ▶▶ Vertebrosternal: This region includes T3–T7, the third to seventh ribs and the sternum. ▶▶ Vertebrochondral: This region includes T8–10, together with the eighth, ninth, and tenth ribs. ▶▶ Thoracolumbar: This region includes T11 and T12, and the 11th and 12th ribs. At the thoracolumbar junction, typically located between T11 and L1, the changes in ▶▶

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ANATOMY

Vertebral body Costal facets

Head of rib

Tubercle of rib Costal facets

THE SPINE AND TMJ

Rib shaft Transverse process

A

Spinous process

Costochondral joint 1

1 2

Scapula

2

True ribs (1–7)

3 4

3 4

5

Thoracic vertebra

6

5

7

Sternum

6

8

7

9

False ribs (8–10)

10 11

11

8 12 9 10

12

Floating ribs (11–12)

B

Costal cartilage Jugular notch

Head Neck Internal surface Costal groove

Rib 1 Manubrium Sternal angle

Costal cartilage

Rib 2 Costal cartilage Sternal body

External surface

Neck

C

Second intercostal space

Tubercle

Articular facets

D

Xiphoid process

FIGURE 27-1  The thoracic spine and rib cage. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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Thoracic Vertebra The thoracic vertebrae consist of the usual elements: the vertebral body (centrum), transverse processes, and spinous process (Fig. 27-1).

Vertebral Body

Intervertebral Disk The IVDs of the thoracic spine have been poorly researched, although preliminary studies seem to indicate that the typical thoracic disk appears to have been adapted from a cervical design rather than from a lumbar design.4 The vertebral bodies of thoracic vertebrae 2–10 increase in size and change shape down the vertebral column, and, importantly, each has two demifacets for the attachment of ribs.4 The IVDs of this region are narrower and flatter than those in the cervical and lumbar spine and contribute approximately one-sixth of the length of the thoracic column.2 Disk size in the thoracic region gradually increases from superior to inferior. The disk height to body height ratio is 1:5, compared to 2:5 in the cervical spine, and 1:3 in the lumbar spine, making it the smallest ratio in the spine and affording the least amount of motion.2 Motion is further restricted by the orientation of the lamella of the annulus fibrosis (AF), and the relatively small nucleus pulposus (NP), which is more centrally located within the AF, and has a lower capacity to swell.4 The roughly circular crosssection of the thoracic disk allows the force of torsion to be evenly distributed around its circumference, making it better able to withstand these kinds of forces.5 In the thoracic spine, the segmental nerve roots are mainly situated behind the inferior–posterior aspect of the upper vertebral body rather than behind the disk, which reduces the possibility of root compression in impairments of the thoracic disk, especially as the NP is small in the thorax. Because

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The Thoracic Spine

The thoracic vertebral body (Fig. 27-1) is roughly as wide as it is long so that its anteroposterior and mediolateral dimensions are of equal length.2 The anterior surface of the body is convex from side to side, whereas the posterior surface is deeply concave.2 The first thoracic vertebra is atypical and has a large, nonbifid spinous process, the superior aspect of which tends to lie in the same transverse plane as the zygapophyseal joints of T1 and T2. On the anterior aspect of the transverse process, there is a deep and concave facet which articulates with the convex facet of the first rib to form the costotransverse joint. The height, end-plate cross-sectional area, and bone mass of the vertebral bodies increase cranially to caudally, particularly in the lower levels. Progressive wedging of the thoracic vertebral bodies occurs with increasing age in the majority of individuals, with disk space narrowing at multiple levels occurring from the third decade of life.3 The vertebral bodies of most of the thoracic spine differ from those of the cervical and lumbar vertebrae because of the presence of a demifacet on each of their lateral aspects for articulation with the ribs (the costovertebral joint; see later discussion).

the intervertebral foramina are quite large at these levels, osseous contact with the nerve roots is seldom encountered in the thoracic spine, and, as the dermatomes in this region have a fair amount of overlap, they cannot be relied upon to determine the specific nerve root involved. In contrast to the cervical and lumbar regions, where the spinal canal is triangular/oval in cross-section and offers a large lateral excursion to the nerve roots, the midthoracic spinal canal is small and circular (Fig. 27-1), becoming triangular at the upper and lower levels. At the levels of T4–9, the canal is at its narrowest. The spinal canal is also restricted in its size by the pedicles, remaining within the confines of the vertebra and not diverging as they do in the cervical spine. This would tend to predispose the spinal cord to compression more than in the cervical spine, were it not for the smaller cord size and more oval shape of the thoracic canal. Despite this, central disk protrusions are more common in the thoracic region than in other regions of the spine. Complicating matters is the fact that this is an area of poor vascular supply, receiving its blood from only one radicular artery. This renders the thoracic spinal cord extremely vulnerable to damage by extra dural masses or by an overzealous manipulation.

ANATOMY

curvature from one of kyphosis to one of lordosis vary quite widely according to posture and age.

Transverse Processes The transverse processes of the thoracic spine are oriented posteriorly (i.e., they point backward) and are located directly between the inferior articulating process and the superior articulating process of the zygapophyseal joints of each level (Fig. 27-1). This anatomical feature makes the transverse processes useful as palpation points, when performing mobility testing in the midthorax. The transverse processes of the first 10 thoracic vertebrae differ from those of the cervical and lumbar spines because of the presence of a costal facet on the transverse process, which articulates with the corresponding rib to form the costotransverse joint (see later discussion). At the T11 and T12 levels, the costotransverse joint is absent because ribs 11 and 12 do not articulate with the transverse processes but rather with the vertebral body.

Spinous Processes Two short and thick laminae come together to form the spinous process (Fig. 27-1). The spinous processes of the thoracic region are long, slender, and triangular shaped in cross-section. Although all of the thoracic spinous processes point obliquely downward, the degree of obliquity varies. The first three spinous processes and the last three are almost horizontal, whereas those of the midthorax are long and steeply inclined. T7 has the greatest spinous process angulation. As elsewhere in the spine, the thoracic vertebrae are designed to endure and distribute the compressive forces produced by weight bearing, most of which is borne by the vertebral bodies. The thoracic vertebrae are classified as typical or atypical, with reference to their morphology. The typical thoracic vertebrae are found at T2–9, although T9 may be atypical in that its inferior costal facet is frequently absent. The atypical thoracic vertebrae are T1, T10, T11, and T12.

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The first vertebra (T1) resembles C7. The centrum of T1 demonstrates a larger transverse than the anteroposterior dimension of the vertebral body, being almost twice as wide as its length, and the spinous process is usually at least as long as that of C7. There are two ovoid facets on either side of the T1 vertebral body for articulation with the head of the first rib. The inferior aspect of the vertebral body of T1 is flat and contains a small facet at each posterolateral corner for articulation with the head of the second rib. Approximately 32 structures attach to the first rib and body of T1. Because of the ring-like structure of the ribs, and their attachments both anteriorly and posteriorly, the thoracic spine and ribs can be viewed as a cage-like structure forming a series of concentric rings. Any movement occurring at the various joints of each ring (costovertebral, costotransverse, sternocostal, and zygapophyseal joints) has the potential to influence motions at the other joints within the ring, or at the neighboring segments. The third vertebra is the smallest of the thoracic vertebra. The T9 vertebra may have no demifacets below, or it may have two demifacets on either side (in which case, the T10 vertebra will have demifacets only at the superior aspect). The T10 vertebra has one full rib facet located partly on the body of the vertebra and partly on the tubercle. It does not articulate with the 11th rib and so does not possess any inferior demifacets, and occasionally there is no facet for the rib at the costotransverse joint. The T11 and T12 segments form the thoracolumbar junction. The T11 vertebra has complete costal facets, but no facets on the transverse processes for the rib tubercle. The T12 vertebra only articulates with its own ribs and does not possess inferior demifacets.

Ligaments The common spinal ligaments are present at the thoracic vertebrae (Fig. 27-2), and they perform much the same function as they do elsewhere in the spine. However, the anterior longitudinal ligament in this region is narrower but thicker compared with elsewhere in the spine, whereas the posterior longitudinal ligament is wider here at the level of the IVD, but narrower at the vertebral body than in the lumbar region.2

Zygapophyseal Joints The zygapophyseal joints of the upper thoracic spine show some morphological features of the cervical region, and similarly the joints of the lower thoracic spine progressively approximate those of the upper lumbar region.6 The middle segments of the thoracic spine are designed for less mobility, as the thoracic cage articulations limit sagittal plane motion while accommodating axial displacements.6

CLINICAL PEARL

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The articulating facets of the thoracic zygapophysial joints are quite different from those of the cervical and lumbar spines because they are oriented in a more coronal direction, with the angle of inclination changing, depending on the segmental level:

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The upper segments are inclined at 45–60 degrees to the horizontal in a similar fashion as to those of the cervical spine. ▶▶ The middle segments are inclined at 90 degrees to the horizontal in the typical thoracic form. ▶▶ The lower segments are inclined as in the lumbar spine. Zygapophysial tropism (the moving toward or away from a stimulus) occurs most frequently at T11–12. The inferior articular facets of T12 are invariably lumbar in orientation and concavity, with the orientation changing by 90 degrees at either T11 or T12, allowing pure axial rotation to occur.3 ▶▶

The superior and inferior facets of the zygapophyseal joints arise from the upper and lower parts of the pedicle of the thoracic vertebra. The superior facet lies superiorly with the articular surface on the posterior aspect, whereas the inferior facet lies inferiorly with the articular surface on the anterior (ventral) aspect. The degree of superoinferior and mediolateral orientation is slight. The superior facet arises from near the lamina–pedicle junction and faces posteriorly, superiorly, and laterally. The inferior articulating facet arises from the laminae to face anteriorly, inferiorly, and medially, lying posterior to the superior facet of the vertebra below. The facet surfaces are concave anteriorly and convex posteriorly, bringing the axis of rotation through the centrum rather than through the spinous process, as in the lumbar vertebrae. This results in the biomechanical center of rotation coinciding with the actual center of rotation formed by body weight.

Ribs The bony thoracic cage is formed by 12 pairs of ribs, the sternum, the clavicle, and the vertebrae of the thoracic spine (Fig. 27-1). The first rib is the shortest of the 12, and the broadest at its anterior end. The primary function of the rib cage is to protect the heart and lungs. All of the ribs of the cage are different from each other in size, width, and curvature, although they share some common characteristics. The rib length increases further inferiorly until the seventh rib, after which they become progressively shorter. Ribs one to seven are named true ribs because their cartilage attaches directly to the sternum. The remaining ribs are false ribs, so named because their distal attachment is to the costochondral cartilage of their superior neighbor.

Typical Ribs Ribs three to nine are typical ribs. The typical rib is characterized by a posterior end, which is composed of a head, neck, and tubercle. The head of the typical rib is characterized as two articular facets, a superior costal facet and an inferior costal facet. a. The superior facet attaches to the costal semilunar demifacet of the vertebra above its level. b. The inferior facet attaches to the costal semicircular demifacet of the vertebra of the same level.

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Clavicle

Deltoid m.

Coracoid process Manubrium

2

ANATOMY

Subclavius m.

Pectoralis minor m.

Pectoralis major m.

External intercostal membrane

Body of sternum

4

6

Costal cartilages Latissimus dorsi m. Costochondral joint External oblique m.

The Thoracic Spine

Serratus anterior m.

Xiphoid process

A Rib 1

Intercostal n., a, and v. External intercostal membrane

Internal intercostal mm. External intercostal mm.

Intercostal mm.: External Internal Innermost

Sternum

Subcostal mm.

B

Sternum Transverse thoracis m.

External intercostal m.: Membrane Muscle

Innermost intercostal m. Internal intercostal m.: Muscle Membrane

Subcostal m.

C Thoracic vertebra FIGURE 27-2  Muscles of the thoracic spine. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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ANATOMY THE SPINE AND TMJ

The head of the typical rib projects upward in a very similar manner to that of the uncinate process in the cervical spine and, in fact, develops in much the same way during childhood, appearing to play a similar mechanical role.2 The head consists of a slightly enlarged posterior end, which is divided by a horizontal ridge. The ridge serves as an attachment for the intra-articular ligament. The intraarticular ligament, which travels between the head of the rib and the IVD, bisects the joint into superior and inferior portions. Each of these portions normally contains a demifacet for articulation with the synovial costovertebral joints. The tubercle of the typical rib lies on the outer surface, where the neck joins the shaft and is more prominent in the upper parts than in the lower. The articular portion of the tubercle presents an oval facet for articulation at the costotransverse joint (Fig. 27-1). The convex shaft of the rib is connected to the neck at the rib angle. The upper border of the shaft is round and blunt, whereas the inferior aspect is thin and sharp.2 The anterior end of the shaft has a small depression at the tip for articulation at the costochondral joint.

Atypical Ribs The 1st, 9th, 10th, 11th, and 12th ribs are considered atypical since they only articulate with their own vertebra via one full facet, and the lower two do not articulate with the costochondrium anteriorly.2 The atypical first rib is small but massively built. Being the most curved and the most inferiorly orientated rib, it slopes sharply downward from its vertebral articulation to the manubrium. The head is small and rounded and articulates only with the T1 vertebra. The first costal cartilage is the shortest and this, together with the fibrous sternochondral joint (Fig. 27-1), contributes to the overall stability of the first ring of the rib cage. The first rib attaches to the manubrium just under the sternoclavicular joint, and the second rib articulates with the sternum at the manubriosternal junction. The atypical second rib is longer and is not as flat as the first rib. The atypical 10th rib has only a single facet on its head, because of its lack of articulation with the vertebra above. The 11th and 12th ribs do not present tubercles and have only a single articular facet on their heads. The 11th and 12th ribs remain unattached anteriorly but end with a small piece of cartilage.

Attachment and Orientation of the Ribs

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The attachment of the ribs to the sternum is variable (Fig. 27-1). The upper five, six, or seven ribs have their own cartilaginous connection (see “Sternocostal Joint” section).2 The cartilage of the eighth rib ends by blending with the seventh. The same situation pertains for the ninth and the tenth ribs, thus giving rise to a common band of cartilage and connective tissue. The strong ligamentous attendance, and the presence of the two joints (costovertebral and costotransverse) at each level, severely limits the amount of movement permitted here to slight gliding and spinning motions, with morphology determining the function of each rib.

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The orientation of the ribs increases from being horizontal at the upper levels to being more downwardly oblique in the inferior levels of the thoracic spine (a point worth remembering when performing palpation).

CLINICAL PEARL The cervical rib is a rare anatomic variant estimated to occur in approximately 0.5–1% of the population and bilaterally in 66–80% of these cases.7 Diagnosis is most often incidental, as a result of routine chest radiographs or in patients developing thoracic outlet syndrome (see Chapter 25).

Costovertebral Joint The thoracic vertebrae are connected to their adjacent vertebrae by the bilateral hyalinated, and synovial, costovertebral joints, and their surrounding ligaments (see Fig. 27-1). The costovertebral articulation also forms an intimate relationship between the head of the rib and the lateral side of the vertebral body (see Fig. 27-1). The 1st, 11th, and 12th ribs articulate fully with their own vertebrae via a single costal facet, without any contact with the IVD, while the remaining ribs articulate with both their own vertebra and the vertebra above, as well as to the IVD. This could potentially predispose the 1st, 11th, and 12th costovertebral joints to early arthritic changes, as a result of more mechanical stress compared to the 2nd to the 10th ribs.6 The radiate ligament connects the anterior aspect of the rib head to the bodies of two adjacent vertebrae and their intervening disk in a fan-like arrangement. Each of the three bands of the radiate ligament has different attachments: 1. The superior part runs from the head of the rib to the body of the superior vertebra. 2. The inferior part runs to the body of the inferior vertebra. 3. The intermediate part runs to the intervening disk. The costovertebral joint and rib cage confer stability on the thoracic spine. As the ossification of the head of the rib is not developed at the superior costovertebral joint until about age 13, younger individuals, such as gymnasts, can demonstrate a vast amount of thoracic rotation and side bending.

Costotransverse Joint This is a synovial joint located between an articular facet on the posterior aspect of the rib tubercle and an articular facet on the anterior aspect of the transverse process, which is supported by a thin fibrous capsule (see Fig. 27-1). In the lower two thoracic vertebral segments, this articulation does not exist. The neck of the rib lies along the entire length of the posterior aspect of the transverse process. The short and deep costotransverse ligament runs posteriorly from the posterior aspect of the rib neck to the anterior aspect of its transverse process, filling the costotransverse foramen that is formed between the rib neck and its adjacent transverse process. The ligament has two divisions:

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CLINICAL PEARL Working together, the costotransverse and the costovertebral joints help provide stability to the thoracic spine.

Sternum The sternum consists of three parts: the manubrium, the body, and the xiphoid process. The manubrium (Fig. 27-1) is broad and thick superiorly and narrower and thinner inferiorly, where it articulates with the body of the sternum. The articulation between the manubrium and the sternum is usually a symphysis, with the ends of the bones being lined with hyaline cartilage. This manubriosternal symphysis remains separate throughout life although ossification can occur. On either side of the suprasternal notch are articulating facets for the clavicles, and below these are the facets for the first rib. On the immediate inferolateral aspects of the manubrium are two more small facets for the cartilage of the second rib. The body of the sternum is made up of the fused elements of four sternal bodies, and the vestiges of these are marked by three horizontal ridges. The upper end of the body articulates with the manubrium at the sternal angle. A facet at the superior end of the body laterally provides a joint surface common with the manubrium for the second costal cartilage. On each lateral border of the sternum are four other notches that articulate with the costal cartilages of the third through sixth ribs. The third rib has the deepest fossa on the sternum, indicating that it may serve as the axis for rotation and side bending during arm elevation. T7 articulates with both the sternum and the xiphoid. The xiphisternum, or xiphoid process (see Fig. 27-1), is the smallest part of the sternum. It begins life in a cartilaginous state, but, in adulthood, the upper part ossifies.

Sternocostal Joint The first, sixth, and seventh costal cartilages are each linked to the sternum by a synchondrosis. The second to fifth ribs are each connected to the sternum through a synovial joint, whereby the cartilage of the corresponding rib articulates with a socket-like cavity in the sternum.

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Muscles of Forced Expiration

Primary

Accessory

Abdominal muscles Internal and external oblique ▶ Rectus abdominis ▶ Transversus abdominis Internal intercostals (posterior) Transversus thoracis Transverse intercostals (intima)

Latissimus dorsi Serratus posterior inferior Quadratus lumborum Iliocostalis lumborum      

▶

Data from Kendall HO, Kendall FP, Boynton DA. Posture and Pain. Baltimore, MD: Lippincott Williams and Wilkins; 1952.

In all of these joints, the periosteum of the sternum and the perichondrium of the costal cartilage are continuous. A thin fibrous capsule, present in the upper seven joints, attaches to the circumference of the articular surfaces, blending with the sternocostal ligaments. The surfaces of the joints are covered with fibrocartilage and are supported by capsular, radiate sternocostal, or xiphicostal and intra-articular ligaments. The joint is capable of about 2 degrees of motion from full inspiration to full expiration and allows the full excursion of the sternum in these activities.

The Thoracic Spine

Very little posteroanterior or anteromedial–posterolateral translation is available at this joint.

TABLE 27-1

ANATOMY

1. The superior costotransverse ligament, also known as the interosseous ligament, or ligament of the neck of the rib, is formed in two layers. The anterior layer, which is continuous with the internal intercostal membrane laterally, runs from the neck of the rib up and laterally to the inferior aspect of the transverse process above. The posterior layer runs up and medially from the posterior aspect of the rib neck to the transverse process above. 2. The lateral costotransverse ligament runs from the tip of the transverse process laterally to the tubercle of its own rib. It is short, thick, and strong but is often damaged by direct blows to the chest (e.g., punch, kick, etc.).

Muscles A large number of muscles arise from and insert on the thoracic spine and ribs (Fig. 27-2). The muscles of this region can be divided into those that are involved in spinal or extremity motion, and those that are involved in respiration (Tables 27-1 and 27-2).

Spinal and Extremity Muscles Spinal Muscles  Iliocostalis Thoracis. The iliocostalis thoracis consists of several muscle straps that link the thoracic vertebrae and sacrum with the lower six or seven ribs. The muscle straps have a number of tendons, varying in different individuals, which insert in all angles in the lower six ribs. The function of the muscle is to extend the spine when working bilaterally and to side bend the spine ipsilaterally when working alone. TABLE 27-2

Muscles of Inspiration

Primary

Accessory

Diaphragm

Scaleni

Levator costarum

Sternocleidomastoid

External intercostals

Trapezius

Internal intercostals (anterior)

Serratus anterior and posterior and superior and inferior Pectoralis major and minor Latissimus dorsi Subclavius

     

Data from Kendall HO, Kendall FP, Boynton DA. Posture and Pain. Baltimore, MD: Lippincott Williams and Wilkins; 1952.

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ANATOMY THE SPINE AND TMJ

The iliocostalis consists of three subdivisions—iliocostalis lumborum, iliocostalis thoracis, and iliocostalis cervicis— which are a part of the external portion of the long erector spinae muscle group. The muscle receives its nerve supply by the posterior (dorsal) rami of the thoracic nerves. Longissimus Thoracis. The longissimus thoracis muscles originate with the intercostalis muscles from the transverse processes of the lower thoracic vertebrae. They insert into all of the ribs and into the ends of the transverse processes of the upper lumbar vertebrae. The function of the muscle is to extend the spine when working bilaterally and to side bend the spine ipsilaterally when working alone. The muscle is innervated by the posterior (dorsal) rami of the thoracic nerves.

thoracic region, they are single-bellied muscles and exist only from T10–11 to T12–L1. The function of the muscle is to side bend the spine ipsilaterally. The muscle is innervated by the posterior (dorsal) rami of the thoracic spinal nerves.

Spinalis Thoracis. The spinalis thoracis muscle (spinalis dorsi) originates from the spinous processes of the upper lumbar and two lower thoracic vertebrae. It inserts in the spinous processes of the middle and upper thoracic vertebrae. The function of the muscle is to extend the spine. The muscle is innervated by the posterior (dorsal) rami of the thoracic nerves. Semispinalis Thoracis. The semispinalis thoracis consists of long straps of muscle that stretch along and surround the vertebrae of the spine. The muscle can have between four and eight upper ends, which originate from the transverse processes of the T6–10. These straps of muscle insert in the spinous processes of the first four thoracic and fifth and sixth cervical vertebra. The function of the muscle is to extend the spine when working bilaterally and to rotate the spine contralaterally when working alone. The semispinalis thoracis is innervated by the posterior (dorsal) rami of the thoracic nerves.

Respiratory Muscles

Multifidus.  The multifidus is a deep back muscle that runs along the entire spine and lies deep to the erector spinae muscles. It originates from the sacrum, sacroiliac ligament, mammillary processes of the lumbar vertebrae, transverse processes of the thoracic vertebrae, and the articular processes of the last four cervical vertebrae. The multifidus consists of numerous bundles of fibers that cross over two to five vertebrae at a time and insert into the entire length of the spinous process above. The function of the muscle is to extend the spine when working bilaterally and to rotate the spine minimally contralaterally when working alone. The thoracic multifidus is innervated by the posterior (dorsal) rami of the thoracic spinal nerves. Rotatores Thoracis (Longus and Brevis). The rotatores muscles are deep spinal muscles that lie beneath the multifidus muscles. The rotatores brevis muscle lies just deep to the rotatores longus muscle. The rotatores muscles are the best developed in the thoracic region. There are a total of 11 small, quadrilateral rotatores muscles on each side of the spine. Each muscle arises from the transverse process of the vertebra and extends inward to the vertebra above. The rotatores muscles help rotate the appropriate thoracic segment. They are innervated by posterior (dorsal) rami of the thoracic spinal nerves. Intertransversarii.  The intratransversals are small muscles located between the transverse process of the vertebrae. In the

The other spinal muscles of the thoracic region act primarily on the cervical spine. These include the trapezius, levator scapulae, and anterior, posterior, and middle scalenes (see Chapter 25). Extremity Muscles.  The muscles of the thoracic region that act primarily on the extremities include the pectoralis major, latissimus dorsi, and serratus anterior (see Chapter 16).

The respiratory system is essentially a robust, multimuscle pump (Fig. 27-3). Connections to the respiratory mechanism have been found to exert a strong influence on such areas as the shoulder and pelvic girdles, as well as the head and neck. The primary task of the respiratory muscles is to displace the chest wall and, therefore, move gas in and out of the lungs to maintain arterial blood gas and pH homeostasis. The importance of normal respiratory muscle function can be appreciated by considering that respiratory muscle failure caused by fatigue, injury, or disease could result in an inability to maintain blood gas and pH levels within an acceptable range, which would have lethal consequences. Restoration of the respiratory mechanism is, thus, an essential element of thoracic intervention. The actions of various respiratory muscles, which are broadly classified as inspiratory or expiratory, based on their mechanical actions, are highly redundant and provide several means by which air can be effectively displaced under a host of physiologic and pathophysiologic conditions. At rest, movement of air into and out of the lungs is the result of the recruitment of several muscles, the expiratory phase of breathing at rest is also associated with active muscle participation. In a resting man, the tidal volume is the result of the coordinated recruitment of the diaphragm, the parasternal intercostal, and the scalene muscles (Tables 27-1 and 27-2). Although some have argued that the performance of the respiratory muscles does not limit exercise tolerance in normal healthy adults, heavy, or prolonged exercise has been shown to impair respiratory muscle performance in humans. Thus, an interest in the adaptability of respiratory muscles to endurance-type exercise has grown significantly during the last decade. The primary muscles of respiration include the diaphragm, the sternocostal, and the intercostals. The secondary muscles of respiration are the anterior/medial scalenes, serratus posterior, pectoralis major and minor, and, with the head fixed, the sternocleidomastoid.2 Diaphragm.  Anatomically, the diaphragm muscle may be divided into sternal, costal, and lumbar parts: ▶▶

The sternal fibers originate from two slips at the back of the xiphoid process.

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ANATOMY

Thoracic inlet Common carotid a. Internal jugular v.

Left subclavian a. and v. Rib 1 Rib 2

Right brachiocephalic v. Left brachiocephalic v.

Manubrium of sternum

The Thoracic Spine

Aortic arch

Superior vena cava

Pulmonary trunk

Right pulmonary vv.

Left pulmonary vv.

Left lung

Right lung

Heart

Body of sternum Xiphoid process of sternum

Rib 6

Boundary of parietal pleura

Lung

A

Visceral pleura Pleural cavity Thoracic outlet

Parietal pleura

B Parietal cervical pleura

Costomediastinal recess

Pleural reflection

Pleural cavity Pleural cavity Parietal mediastinal Visceral pleura pleura

Parietal costal pleura Visceral pleura

Costodiaphragmatic recess

C

Parietal mediastinal pleura

Parietal costal pleura Diaphragmatic pleura Pleural reflection

D

FIGURE 27-3  Components of the respiratory system. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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ANATOMY

The costal fibers originate from the lower six ribs and their costal cartilages. ▶▶ The lumbar fibers originate from the crura of the lumbar vertebra, and the medial and lateral arcuate ligaments. ▶▶

CLINICAL PEARL

THE SPINE AND TMJ

Patients with bilateral diaphragm paralysis or severe weakness present a striking clinical picture, with orthopnea as the major symptom. Lesser degrees of diaphragm weakness, however, are hard to detect and need specific testing. The diaphragm is attached around the thoracoabdominal junction circumferentially. From these attachments, the fibers arch toward each other centrally to form a large tendon. Contraction of the diaphragm pulls the large, central tendon inferiorly, producing diaphragmatic inspiration (see later discussion). The diaphragm has a phrenic C3–4 motor innervation and sensory supply by the lower six intercostal nerves. Intercostals.  Between the ribs are the intercostal spaces, which are deeper both in front and between the upper ribs. Between the ribs lie the internal and external intercostal muscles, with the neurovascular bundle lying beneath each rib. The intercostal muscles, together with the sternalis (or sternocostalis or transversalis thoracis), phylogenically form from the hypomeric muscles. These muscles correspond to their abdominal counterparts, with the sternalis being homologous to the rectus abdominis, and the intercostals homologous to the external oblique.2 External Intercostals. The external intercostal muscles (Fig. 27-2), of which there are 11, are laid in a direction that is superoposterior to inferoanterior (run inferiorly and medially in the front of the thorax and inferiorly and laterally in the back). Because of the oblique course of the fibers, and the fact that leverage is greatest on the lower of the two ribs, the muscle pulls the lower rib toward the upper rib, which results in inspiration. The external intercostals attach to the lower border of one rib and the upper border of the rib below, extending from the tubercle to the costal cartilage. Posteriorly, the muscle is continuous with the posterior fibers of the superior costotransverse ligament. The action of the external intercostals is believed to be entirely inspiratory, although the muscles also counteract the force of the diaphragm, preventing the collapse of the ribs. Innervation of this muscle is supplied by the adjacent intercostal nerve. Internal Intercostals.  The internal intercostals (see Fig. 27-2), which also number 11, have their fibers in an inferoposterior to a superoanterior direction. The internal intercostals are found deep to the external intercostals and run obliquely, and perpendicular, to the externals. The posterior fibers pull the upper rib down, but only during enforced expiration. The internal intercostals extend from the posterior rib angles to the sternum, where they end posteriorly. They are continuous

with the internal membrane, which then becomes continuous with the anterior part of the superior costotransverse ligament. Innervation of this muscle group is supplied by the adjacent intercostal nerve. Transverse Intercostals (Intima). The deepest of the intercostals, the transverse intercostals are attached to the internal aspects of two contiguous ribs. They become progressively more significant and developed, further down the thorax. This muscle is used during forced expiration. Transversus Thoracis. The transversus thoracis is a triangular-shaped sheet muscle, which originates from the posterior (dorsal) surface of the sternum and covers the inner surfaces of both the sternum and the second to eighth sternal costal cartilages. The apex of the muscle points cranially, with muscle slips running inferolaterally and eventually inserting on the sternal ribs quite close to the costochondral junctions. Morphologically, the transversus thoracis is similar to the anterior (ventral) part of the transversus abdominis. Its function is to draw the costal cartilages down. The muscle is innervated by the adjacent intercostal nerves. Levator Costae.  These consist of 12 strong short muscles that turn obliquely (inferolaterally), parallel with the external intercostals, from the tip of the transverse process to the angle of the rib, extending from C7 to T11. These muscles, which are innervated by the lateral branch of the posterior (dorsal) ramus of the thoracic nerve, function to raise the rib, but their importance in respiration is argued. The levator costae may also be segmentally involved in rotation and side bending of the thoracic vertebra. Serratus Posterior Superior.  The serratus posterior superior runs from the lower part of the ligamentum nuchae, the spinous processes of C7 and T1–3, and their supraspinous ligaments, to the inferior border of the second through fifth ribs, lateral to the rib angle. The muscle receives its nerve supply from the second through fifth intercostal nerves. Its function is unclear, but it is thought to elevate the ribs.2 Serratus Posterior Inferior.  This muscle arises from the spines and supraspinous ligaments of the two lower thoracic and the two or three upper lumbar vertebrae. It attaches to the inferior border of the lower four ribs, lateral to the rib angle. The muscle receives its nerve supply from the anterior (ventral) rami of the 9th through 12th thoracic nerves. Its function is unclear, but it is thought to pull the ribs downward and backward.

Vascular Supply The blood supply to this region is provided mainly by the posterior (dorsal) branches of the posterior intercostal arteries (Fig. 27-4) while the venous drainage occurs through the anterior and posterior venous plexuses. The spinal cord region between T4 and T9 is poorly vascularized.2

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Right superior intercostal v.

Left brachiocephalic v.

Subclavian a. Aorta

Posterior intercostal a.

Posterior intercostal v.

Internal thoracic v. Anterior cutaneous branches

Anterior intercostal v.

Anterior intercostal a.

Internal thoracic a.

Anterior cutaneous branches

Hemiazygos v.

A

B

FIGURE 27-4  Vasculature of the thoracic region. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

Neurology Thoracic pain is commonly referred from the cervical spine and both the abdominal and thoracic viscera. Conversely the thoracic spine can refer symptoms to the posterior shoulder region, rib cage, anterolateral abdominal wall, and iliac crest region. The spinal canal in this region is narrow, with only a small epidural space between the cord and its osseous environment. Innervation of the thoracic spinal canal is by the sinuvertebral nerve, which arises from the nerve root and reenters the epidural space. The thoracic spinal cord is unusually susceptible to injury because it occupies a greater percentage of the total crosssectional area of its surrounding spinal canal than do the cervical or lumbar sections of the spinal cord, and the thoracic cord is tightly packed in the canal and easily injured by displaced fragments of bone or disk material. Furthermore, the blood supply of the midthoracic spinal cord is tenuous, and seemingly trivial injuries can disrupt the blood supply to a substantial portion of the thoracic cord and result in devastating neurologic deficits. In the thoracic region, there is great variability in the topography of the nerves and the structures that they serve. Typically, the spinal root arises from the lateral end of the spinal nerve but, in 25% of cases, the spinal root is made up of two parts that arise from the superior border of the spinal nerve.2 The thoracic spinal nerves are segmented into posterior (dorsal) primary and anterior (ventral) primary divisions (see Chapter 3). As elsewhere, the dermatomes of this region are considered to represent the cutaneous region innervated by one spinal nerve through both of its rami. The peripheral nerves, which travel through the thoracic spine and chest wall, include the posterior (dorsal) scapular, thoracodorsal, and long thoracic nerves (see Chapter 3).

The Thoracic Spine

Azygos v.

BIOMECHANICS

Right brachiocephalic v.

Left superior intercostal v.

BIOMECHANICS Knowledge of the regional biomechanics of the thoracic spine and rib cage assists the clinician in the interpretation of active movement and motion palpation examination in relation to the patient’s symptoms.8 The thoracic spinal segments possess the potential for a distinctive array of movements. Although normative ranges of spinal motion have been reported for the lumbar spine, no such reliable data exist for the thoracic region.9 It is widely recognized that the mechanical behavior of the spine is influenced by load. Axial load has been shown to increase motion segment stiffness and decrease mobility. In addition, due to the modifying influence of the cage-like structure of the ribs, which provide a significant degree of stability, and the kyphotic shape of the curve, the biomechanics of the thoracic spine is considerably different from those of the lumbar and cervical regions.

Flexion Flexion of the thoracic spine in weight bearing is initiated by the abdominal muscles and, in the absence of resistance, is continued by gravity, with the spinal erector muscles eccentrically controlling the descent. Flexion may also occur during bilateral scapular protraction. There are about 4–5 degrees of flexion available at the upper thoracic levels, 6–8 degrees in the middle layers, and 9–15 degrees in the lower levels, giving an overall total range for thoracic flexion of 20–45 degrees.3 End-range flexion is resisted by the posterior half of the annulus and by the impaction of the zygapophyseal joints. According to Lee,3 flexion of the cervicothoracic region consists of an anterior rotation of the head of the rib and a 1305

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BIOMECHANICS THE SPINE AND TMJ

superoanterior glide of the zygapophyseal joints, whereas extension and arm elevation in this region consists of a posterior sagittal rotation and posterior translation of the superior vertebra. This latter action pushes the superior aspect of the head of the rib posteriorly at the costovertebral joint, producing a posterior rotation of the rib (the anterior aspect travels superiorly, while the posterior aspect travels inferiorly).3 In the remainder of the thorax, flexion results from the superior facets (i.e., the inferior articular processes of the superior vertebra of the segment) gliding superiorly and anteriorly3 (Table 27-3). This motion at the zygapophyseal joint is accompanied by an anterior translation of the superior vertebra, and a slight distraction of the centrum. It seems likely that the anterior vertebral translation produces a similar motion in the ribs, with a superior glide occurring at the costotransverse joint. During this motion, the anterior aspects of the ribs approximate each other, while the posterior aspects separate.

TABLE 27-3 Motions

Extension Extension of the thoracic spine is produced principally by the lumbar extensors and results in an inferior glide of the superior facet of the zygapophyseal joint (see Table 27-3). One to two degrees of extension is available at each thoracic segment, giving an overall average of 15–20 degrees of thoracic extension for the entire thoracic spine.3 Extension of the thoracic spine is restrained by the relative stiffness of the anterior IVD; the anterior longitudinal ligament; bony contact of the posterior elements, including the inferior facet onto the lamina below; and the spinous processes. Given the location of the axis of rotation of extension, which is close to the moving segment, more translation than rotation occurs during extension. The joint motions occurring with extension are essentially the opposite of those of flexion. The translation of the vertebra occurs in a posterior direction, with an accompanying

Biomechanics of the Thorax Z Joint

Rib Motion

Costotransverse Joint

Anterior rotation Posterior rotation NA NA Elevation Depression

NA NA NA NA NA NA

Varies (very mobile) anteroposterior rotation Varies (very mobile) anteroposterior rotation Ipsilateral—anterior rotation

Superior–inferior glide (varies)

Contralateral—posterior rotation Ipsilateral—posterior rotation

Contralateral—inferior glide Ipsilateral—inferior glide

Contralateral—anterior rotation Posterior rotation bilaterally Anterior rotation bilaterally

Contralateral—superior glide Inferior glide Superior glide

Vertebrochonral (T8–10) Flexion Superoanterior glide Extension Inferoposterior glide Latexion Varies             Rotexion Ipsilateral—inferior glide   Contralateral—superior glide

Anterior rotation Posterior rotation NA       NA  

Inspiration Expiration

NA NA

SMP glide ILA glide Apex in line with trochanter  Ipsilateral—SMP  Contralateral—ILA If not, the reverse occurs Ipsilateral—ILA, then anteromedial Contralateral—SMP, then posterolateral glide ILA glide SMP glide

Vertebromanubrial (T1–2) Flexion Superoanterior glide Extension Inferoposterior glide Latexion Ipsilateral coupling Rotexion Ipsilateral coupling Inspiration NA Expiration NA Vertebrosternal (T3–7) Flexion Superoanterior glide Extension

Posteroinferior glide

Latexion

Ipsilateral side bend and contralateral rotation   Ipsilateral side bend and ipsilateral rotation   NA NA

  Rotexion   Inspiration Expiration

NA NA

Superior–inferior glide (varies) Ipsilateral—superior glide

ILA, inferior lateral anterior; NA, not applicable; SMP, superior medial posterior.

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Thoracic spine extension motion is considered important for normal shoulder girdle function, and an impairment of this movement may contribute to the development of subacromial impingement and shoulder pain.10 Theoretically, facilitating extension motion in the thoracic spine may increase the acromiohumeral distance and range of arm elevation, and delay the onset of pain, in this population of patients. Indeed, short- and long-term benefits of thoracic spine manipulation have been described for the management of shoulder impingement disorders.11,12

Side Bending Side bending of the thoracic spine is initiated by the ipsilateral abdominals and erector muscles and is then continued by gravity. A total of 25–45 degrees of side bending is available in the thoracic spine, at an average of about 3–4 degrees to each side per segment, with the lower segments averaging slightly more, at 7–9 degrees, each.3 At the zygapophyseal joints, the primary motion involves the ipsilateral superior facet gliding inferiorly and the contralateral gliding superiorly (see Table 27-3). In effect, the ipsilateral zygapophyseal joint extends while the contralateral flexes. Side bending is restrained by the compression of the IVD and approximation of the ribs. Side bending in the upper thoracic spine is associated with ipsilateral rotation and ipsilateral translation. According to Lee,3 the coupling that occurs in the rest of the thoracic spine depends on which of the two coupling motions initiates the movement. If side bending initiates the movement, it is called latexion, and the biomechanics consists of side bending, contralateral rotation, and ipsilateral translation. The mechanism of this coupling, or actually tripling, is not certain, and one must guard against strong conclusions. The postulated mechanism is as follows: with side bending, a contralateral convex curve is produced. This causes the ribs on the convex side of the curve to separate and those on the concave side to approximate.3 Trunk side bending is essentially halted, by soft-tissue tension or rib approximation, or both, and the ribs

Rotation The axis of rotation for the thoracic spine varies according to the vertebral level. The axis of rotation lies within the vertebral body in the midthoracic joints, but anterior to the vertebral body in the upper and lower joints. Almost pure rotation can occur in the midthoracic region, whereas, in the upper and lower segments, rotation can be associated with side bending to either side (see Table 27-3). Axial rotation (rotexion) is produced either by the abdominal muscles and other trunk rotators or by the unilateral elevation of the arm. Pure axial rotation (twisting) can only occur at two points in the spine: at the thoracolumbar and cervicothoracic junctions. A total of 35–50 degrees of rotation is available in the thoracic spine.3 Segmental axial rotation in the thoracic spine averages 7 degrees in the upper thoracic area, approximately 5 degrees in the middle thoracic spine, and 2–3 degrees in the last two or three segments.

The Thoracic Spine

CLINICAL PEARL

become fixed. Furthermore side bending is modified by the fixed ribs.3 The ipsilateral articular facet of the transverse process glides inferiorly on its rib, resulting in a relative anterior rotation of the neck of the rib, while the contralateral transverse process glides superiorly, producing a posterior rotation of the rib neck.3 The effect of these bilateral rib rotations is to force the superior vertebra into rotation away from the direction of side bending.

BIOMECHANICS

slight compression of the centra. The posterior translation that occurs with extension is controlled by the posteriorly directed lamellae of the annulus, and by the capsule of the zygapophyseal joint. The transitional region between the thoracic and lumbar spines can produce an inflexion point that may serve to reduce the bending forces in the sagittal plane. However, stiffness in this area also may result in the thoracic spine pivoting over the thoracolumbar region, thereby increasing the risk of compression fracture (see Chapter 5). In addition to those motions occurring at the zygapophyseal joints and the vertebral body during thoracic extension, the motion also occurs at the rib articulations. The ribs rotate posteriorly, with the posterior aspects approximating and the anterior aspects separating, and an inferior glide occurs at the costotransverse joint.3

Respiration The ribs function as levers, with the fulcrum represented by the rib angle, the effort arm represented by the neck, and the load arm represented by the shaft. Because of the relatively small size of the rib neck, a small movement at the rib neck will produce a large degree of movement in the shaft. The shapes of the articular facets of the upper six ribs would suggest that the upward and downward gliding movements that occur would produce spinning of the neck of the rib. In fact, the main movement in the upper six ribs during respiration and other movements is one of rotations of the neck of the rib, with only small amounts of superior and inferior motion. In the seventh through tenth ribs, the principal movement is upward, backward, and medially during inspiration, with the reverse occurring during expiration.3 Because the anterior end of the ribs is lower than the posterior, when the ribs elevate, they rise upward, while the rib neck drops down. In the upper ribs, this results in an anterior elevation (pump handle) and in the middle and lower ribs (excluding the free ribs), a lateral elevation (bucket handle), with the former movement increasing the anteroposterior diameter of the thoracic cavity and the latter increasing the transverse diameter (Fig. 27-5). Both kinds of rib motion are produced by the action of the diaphragm. The seventh through tenth ribs act to increase the abdominal cavity free space to afford space for the descending diaphragm. As the ends of these ribs are elevated, they push up on each other, lifting each successive rib upward and finally lifting the sternum. The two lower ribs are depressed 1307

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EXAMINATION

Vertebral column

Vertebra

Sternum

Rib

THE SPINE AND TMJ

Rib

Sternum

FIGURE 27-5  Bucket and pump handle rib motions. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

by the quadratus lumborum to provide a stable base of action for the diaphragm. Quiet respiration involves very little zygapophyseal joint motion.

Inspiration During inspiration, the diaphragm descends and pulls the central tendon inferiorly through the fixed 12th ribs and L1–3 (Fig. 27-6). When the maximum extensibility (distention) of the abdominal wall is reached, the central tendon becomes stationary. Further contraction of the diaphragm produces an elevation and posterior rotation of the lower six ribs, with torsion of the anterior costal cartilage, and an anterosuperior thrust of the sternum (and eventually the inferior aspect of the manubrium). During inspiration in the normal population, because the second rib is longer than the first, the superior aspect of the manubrium is forced to tilt posteriorly as its inferior edge is moved anteriorly. As the top of the manubrium tilts back, the clavicle rolls anteriorly. Because the lower ribs are longer, the inferior sternum moves further anteriorly than the superior section during inspiration. The manubriosternal junction acts as the hinge for this motion. If this joint stiffens or ossifies, respiratory function will suffer. In addition, if the central tendon stiffens, inspiration will have to be accomplished, with the ribs moving laterally. Forced inspiration produces an increase in the activity level of the diaphragm, intercostals, scaleni, and quadratus lumborum. In addition, new activity occurs in the sternocleidomastoid, trapezius, both pectorals and serratus anterior. During inspiration, the ribs move with the sternum in an upward and forward direction, increasing the anteroposterior diameter of the chest while posteriorly rotating. The tubercles and costotransverse joints of 3 T1–7 glide inferiorly; T8–10 glide in an anterolateral and inferior direction; and ▶▶ T11 and T12 remain stationary, except for slight caliper motion increasing the lateral dimension. ▶▶ ▶▶

Expiration Quiet expiration occurs passively (Fig. 27-6). During forced expiration, there is activity in a number of muscles (Table 27-1). During expiration, the ribs rotate anteriorly and the tubercles and costotransverse joints of 3 T1–7 glide superiorly; ▶▶ T8–10 glide in a posteromedial and superior direction; and ▶▶ T11 and T12 remain stationary, except for slight caliper motion decreasing the lateral dimension. ▶▶

It may be possible to detect a subluxation of the costotransverse joints by palpating the ipsilateral transverse process and rib during inspiration and thoracic side bending.3 For example, a superior subluxation of the right rib may produce the following: ▶▶ ▶▶

A decreased inferior glide of the rib. A decreased thoracic motion in the directions of left side bending and right rotation.

The findings for other rib dysfunctions are outlined in Table 27-4.

EXAMINATION Differential diagnosis of thoracic pain can be difficult. This is due to the complicated biomechanics and function of the region, the proximity to vital organs, and the many articulations. Pain arising from inflammation of the axial spine can mimic a variety of serious conditions, including cardiac/pulmonary pathology, renal colic, fracture, a tumor, or numerous visceral and retroperitoneal abnormalities, including abdominal aortic aneurysm.13 The thoracic spine is less commonly implicated in musculoskeletal pain syndromes than the lumbar and cervical spines, and when it does occur, there is some disagreement as

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Diaphragm contracts

Diaphragm relaxes

Expiratory mm. contract (e.g., external intercostal mm.)

Expiratory mm. relax (abdominal mm. contract)

The Thoracic Spine

Exhalation

EXAMINATION

Inhalation

A

B

FIGURE 27-6  Biomechanics of respiration. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

to whether the ribs or the intervertebral joints are the major sources of the biomechanical dysfunction. Complicating matters is the fact that pain arising from the thoracic spinal joints has considerable overlap and can refer symptoms to distal regions (groin, pubis, and lower abdominal wall) (refer to Chapter 5). Apart from musculoskeletal lesions, the thoracic

TABLE 27-4

spine is also a common source of systemic pain, and the phenomenon of referred pain poses more diagnostic difficulties in the thoracic spine than in any other region of the vertebral column (Fig. 27-7). The algorithm outlined in Fig. 27-8 can serve as a guide to the examination of the thoracic spine and ribs.

Rib Dysfunctions

Dysfunction

Rib Angle

Intercostal Space

Anterior Rib

Thoracic Findings

Anterior subluxation

Less prominent

Tender

NA

More prominent

Posterior subluxation

More prominent

Tender

NA

Less prominent

External rib torsion

Prominent and tender superior border

Wide above and narrow below

ERS, ipsilateral at the level above

NA

Internal rib torsion

Prominent and tender inferior border

Narrow above and wide below

FRS, contralateral at the level above

NA

ERS, extended, rotated, and side flexed; FRS, flexed, rotated, and side flexed; NA, not applicable. Adapted with permission from Flynn TW. The Thoracic Spine and Rib Cage: Musculoskeletal Evaluation and Treatment. Boston, MA: Butterworth-Heinemann; 1996.

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EXAMINATION

Medical Causes of Thoracic Pain

Acute

Nonacute

Nonpleuritic

Cardiac

Pulmonary

Gastrointestinal

Chest wall

Pulmonary embolus Pericarditis Pleurisy Tracheobronchial pain

Myocardial infarction Aortic dissection Pericarditis Pulmonary embolus Cholecystitis Esophageal disorders Renal diseases

Angina pectoris Pericarditis Mitral valve prolapse

Pleuritis Pulmonary embolus

Esophageal disorders Peptic ulcer disease Cholecystitis

Herpes zoster Intercostal neuralgia Nerve entrapment

THE SPINE AND TMJ

Pleuritic

FIGURE 27-7  Medical causes of thoracic symptoms.

DIFFERENTIATION TESTS FOR BIOMECHANICAL DYSFUNCTION Tests include: Apley's scratch test Manubrium motion testing P-A rib springing—with and without stabilization Breathing/chest expansion

Thoracic spine dysfunction

Costal

AROM tests (around appropriate axis)

Refer to specific joint exam

Reduced motion

Normal motion

Assess end feel

Combined motions Latexion Rotexion

Abnormal for joint Springy, boggy, spasm empty

Normal for joint Capsular, elastic

Further investigation required

Assess glides

Reduced

Normal

Mobilize

Muscle energy

Reduced

Normal

Assess glides

Suspect hypermobility

Normal

Reduced

Normal

Mobilize

Suspect hypermobility Stress tests

Negative

Positive

Hypermobility

Instability

Stabilization exercises

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FIGURE 27-8  Thoracic spine examination algorithm.

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The history should include the chief complaints and a pain drawing. Referred chest pain patterns are outlined in Table 27-5. In addition to those questions listed under section History in Chapter 4, the following questions should be asked by the clinician:

TABLE 27-5

Chest Pain Patterns

Origin of Pain

Site of Referred Pain

Type of Disorder

Substernal or retrosternal

Neck, jaw, back, left shoulder and arm, and abdomen

Angina

Substernal, anterior chest

Neck, jaw, back, and bilateral arms

Myocardial infarction

Substernal or above the sternum

Next, upper back, upper trapezius, supraclavicular area, Pericarditis left arm, and costal margin

Anterior chest (thoracic aneurysm); abdomen (abdominal aneurysm)

Posterior thoracic, chest, neck, shoulders, interscapular, Dissecting aortic aneurysm or lumbar region

Variable

Variable, depending on structures involved

Costochondritis (inflammation of the costal cartilage): sternum and rib margins

Abdominal oblique trigger points: pain referred up into Musculoskeletal  the chest area

Upper rectus abdominis trigger points (left side), Pectoralis trigger points: pain referred down medial pectoralis, serratus anterior, and sternalis muscles: bilateral arms along ulnar nerve distribution (fourth precordial pain and fifth fingers)

Musculoskeletal

Musculoskeletal 

Precordium region (upper central abdomen and diaphragm)

Sternum, axillary lines, and either side of vertebrae; Neurological lateral and anterior chest wall; occasionally to one or both arms

Substernal, epigastric, and upper abdominal quadrants

Around chest area, shoulders, and upper back region

Gastrointestinal

Within breast tissue; may be localized in pectoral and supraclavicular regions

Chest area, axilla, midback, and neck and posterior shoulder girdle

Breast pain

Commonly substernal and anterior chest region

No referred pain

Anxiety

Data from Donato EB. Physical examination procedures to screen for serious disorders of the head, neck, chest, and upper quarter. In: Wilmarth MA, ed. Medical Screening for the Physical Therapist. Orthopaedic Section Independent Study Course 14.1.1. La Crosse, WI: Orthopaedic Section, APTA, Inc.; 2003:1–43; Goodman CC, Boissonnault WG. Pathology: Implications for the Physical Therapist. Philadelphia, PA: WB Saunders; 1998.

Dutton_Ch27_p1295-p1334.indd 1311

The Thoracic Spine

Was there a mechanism of injury? Any information regarding the onset is important. For example, most rib injuries are commonly caused by direct trauma. If there was no mechanism of injury, a disease process such as scoliosis could be indicated. Costovertebral and costotransverse joint hypomobility and active trigger points are possible sources of upper thoracic pain.14 ▶▶ Do the symptoms occur with breathing? Symptoms reproduced with respiration could indicate a rib dysfunction or pleuritic pain. If the symptoms are aggravated on exertion, the clinician should focus on the relationship of specific movements or activities. Any information regarding the onset, as well as aggravating factors, is important, especially if the pain appears only during certain positions or movements. Deep breathing or arm elevation tends to aggravate a rib dysfunction. ▶▶ Are the symptoms provoked or alleviated with movement or posture? This type of history indicates a musculoskeletal dysfunction. The pain of a mechanical origin tends to ▶▶

worsen throughout the day but is relieved with rest. Aggravating factors for the thoracic spine often encompass one or a combination of the following activities13: ■■ Thoracic movement, especially rotation and extension. ■■ Upper limb movements, especially into elevation or sustained upper limb activity. ■■ Sustained postural load, usually sitting. Chronic problems in this area tend to result from postural dysfunctions. ■■ Cervical motion. ■■ Repetitive lower limb activities. ■■ Pulling and pushing activities typically worsen thoracic symptoms. Aggravation of localized pain by coughing, sneezing, or deep inspiration tends to implicate the costovertebral joint.15 ▶▶ Is the pain deep, superficial, aching, burning, or stabbing? The patient is asked to describe the quality of the pain. Thoracic nerve root pain is often sharp, stabbing, and severe, although it can also have a burning quality. Nerve pain usually is referred in a sloping band along an intercostal space. Vascular pain and visceral pain often are described as being poorly localized and achy. A sudden onset of pain related to trauma could indicate a fracture, muscle strain, or ligament sprain.

EXAMINATION

History

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EXAMINATION



CLINICAL PEARL Pain from a musculoskeletal lesion in this area can vary from a dull ache to a feeling of local fatigue and cramping. Musculoskeletal pain is usually sharp and well localized, whereas muscle or tendon pain is typically dull and aching. Bone pain usually feels very deep and boring.

 edical Screening Questionnaire for the M Thoracic Spine and Rib Cage Region

 

Yes

No

The administration of the Oswestry Low Back Disability Questionnaire (Table 5-2), Neck Disability Index (Table 5-3), and McGill Pain Questionnaire (Chapter 4) may be helpful in determining the quality of pain and its effect on function.

Do you have a history of heart problems? Have you recently taken a nitroglycerin tablet? Do you take medication for hypertension? Have you been or are you now a smoker? Have you had a recent surgery? Have you recently been bedridden? Have you recently noticed that it is difficult for you to breathe, laugh, sneeze, or cough? Have you recently had a fever, infection, or other illness? Have you recently received a blow to the chest, such as during a fall or motor vehicle accident? Are your symptoms relieved after eating? Does eating fatty food increase your symptoms? Do you currently have a kidney stone, or have you had one in the past? Do you experience severe back or flank pain that comes on suddenly?

Systems Review

Reproduced with permission from Wilmarth MA. Medical Screening for the Physical Therapist. Orthopaedic Section Independent Study Course 14.1.1. La Crosse, WI: Orthopaedic Section, APTA, Inc.; 2003.

Where is the pain located? The patient should be asked to point to the area of pain. If the patient has difficulty localizing the pain, the clinician should suspect referred pain as the source. If the symptoms appear to be referred to the upper or lower extremities, or the head and neck, further investigation is required. ▶▶ Are the symptoms related to digestion? Some visceral conditions, such as ulcers, can be referred to T4–6 posteriorly. ▶▶

THE SPINE AND TMJ

Thoracic pain may originate from just about all of the viscera (Table 27-6; see also Chapter 5). Both visceral and somatic afferent nerves transmit pain messages from a peripheral stimulus and converge on the same projection neurons in the posterior (dorsal) horn. Visceral pain tends to be vague and dull and may be accompanied by nausea and sweating (see Chapter 5). To help differentiate between visceral pain



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TABLE 27-7

TABLE 27-6

 ymptoms and Possible Causes of S Thoracic Pain

Indication

Possible Condition

Severe bilateral root pain in elderly

Neoplasm (most common areas for metastasis are lung, breast, prostate, and kidney)

Wedging/compression fracture

Osteoporotic (estrogen deficiency) or neoplastic fracture

Onset–offset of pain unrelated to trunk movements

Ankylosing spondylitis, visceral

Decreased active motion: contralateral side flexion painful, with both rotations full

Neoplasm

Severe chest wall pain without articular pain

Visceral

Spinal cord signs and symptoms

Spinal cord pressure or ischemia

Pain onset related to eating or diet

Visceral

Dutton_Ch27_p1295-p1334.indd 1312

and musculoskeletal pain, the clinician should focus on the relationship of specific movements or activities. A medical screening questionnaire for the thoracic spine and rib cage region is provided in Table 27-7. The thoracolumbar outflow of the autonomic nervous system (see Chapter 3) has its location here. Systemic illnesses, such as rheumatoid arthritis and malignancy, and conditions causing referred pain must be included in the differential diagnosis. Nonmusculoskeletal causes of thoracic pain (Table 27-8) include the following16: Dissecting aortic aneurysm. ▶▶ Myocardial infarction. ▶▶ Intercostal neuralgia. ▶▶ Pleural irritation. When the tissues of an irritated pleura are stretched, chest pain can result. This pain can be increased by breathing, as well as by trunk movements, a situation that could lead the clinician to believe that the problem is musculoskeletal. ▶▶ Tumor. ▶▶ Acute thoracic disk herniation. ▶▶ Unstable or stable angina pectoris. ▶▶ Pericarditis. ▶▶ Pneumothorax. ▶▶ Pneumonia. ▶▶ Cholecystitis. ▶▶ Peptic ulcer. ▶▶ Pyelonephritis. ▶▶ Nephrolithiasis (kidney stones). ▶▶

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Red Flags for the Thoracic Spine and Rib Cage

Condition

Red Flags

Myocardial infarction    

Chest pain Pallor, sweating, dyspnea, nausea, or palpitations Presence of risk factors: previous history of coronary heart disease, hypertension, smoking, diabetes, and elevated blood serum cholesterol (>240 mg/dL) Men aged over 40 years and women aged over 50 years Symptoms lasting greater than 30 minutes and not relieved with sublingual nitroglycerin

   

Pericarditis    

Sharp or stabbing chest pain that may be referred to the lateral neck or either shoulder Increased pain with left side lying Relieved with forward lean while sitting (supporting arms on knees or a table)

Pulmonary embolus  

Chest, shoulder, or upper abdominal pain Dyspnea

Pleurisy  

Severe, sharp knife-like pain with inspiration History of a recent or coexisting respiratory disorder (e.g., infection, pneumonia, tumor, or tuberculosis)

Pneumothorax      

Chest pain that is intensified with inspiration, ventilation, or expanding rib cage Recent bout of coughing or strenuous exercise or trauma Hyperresonance upon percussion Decreased breath sounds

Pneumonia    

Pleuritic pain that may be referred to shoulder Fever, chills, headache, malaise, or nausea Productive cough

Cholecystitis    

Colicky pain in the right upper abdominal quadrant with accompanying right scapula pain Symptoms may worsen with ingestion of fatty foods Symptoms unaffected by activity or rest

Peptic ulcer      

Dull, gnawing pain, or burning sensation in the epigastrium, midback, or supraclavicular regions Symptoms relieved with food Localized tenderness at the right epigastrium Constipation, bleeding, vomiting, tarry colored stools, and coffee ground emeses

Pyelonephritis    

Recent or coexisting urinary tract infection Enlarged prostate Kidney stone or past kidney stone

Nephrolithiasis (kidney stones) 

Sudden, severe back, or flank pain Chills and fever Nausea or vomiting Renal colic Symptoms of urinary tract infection Reside in hot and humid environment Past episode(s) of kidney stone(s)

         

The Thoracic Spine

Stable angina pectoris Chest pain or pressure that occurs with predictable levels of exertion (if not, suspect unstable angina pectoris)   Symptoms are also predictably alleviated with the rest or sublingual nitroglycerin (if not, suspect unstable angina pectoris)

EXAMINATION

TABLE 27-8

Data from DuVall RE, Godges J. Introduction to physical therapy differential diagnosis: the clinical utility of subjective examination. In: Wilmarth MA, ed. Medical Screening for the Physical Therapist. Orthopaedic Section Independent Study Course 14.1.1. La Crosse, WI: Orthopaedic Section, APTA, Inc.; 2004:1–32; Canto JG, Shlipak MG, Rogers WJ, et al. Prevalence, clinical characteristics, and mortality among patients with myocardial infarction presenting without chest pain. JAMA. 2000;283:3223–3229; Culic V, Eterovic D, Miric D, et al. Symptom presentation of acute myocardial infarction: influence of sex, age, and risk factors. Am Heart J. 2002;144:1012–1017; Henderson JM. Ruling out danger: differential diagnosis of thoracic spine. Phys Sports Med. 1992;20:124–131; Wiener SL. Differential Diagnosis of Acute Pain by Body Region. New York, NY: McGraw-Hill; 1993:532, 542, 616, 645, 678, 680; Liu KJ, Atten MJ, Donahue PE. Cholestasis in patients with acquired immunodeficiency syndrome: a surgeon’s perspective. Am Surg. 1997;63:519–524; Wells K. Nephrolisthiasis with unusual initial symptoms. J Manipulative Physiol Ther. 2000;23:196–201.

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EXAMINATION THE SPINE AND TMJ

Questions should be asked with regard to bowel and bladder function; upper and lower extremity numbness, tingling, or weakness; and visual or balance disorders. These symptoms may indicate compromise to the spinal cord, cauda equina, or central nervous system. Questions must also be asked about unexplained weight loss, fever, chills, and night pain. These symptoms often are associated with cancer or systemic disease, although night pain may just be because the patient has an increased, and fixed, kyphosis and needs a softer bed to accommodate the deformity. Yellow flags are indicators of psychosocial factors associated with poor recovery from injury, which makes them important to identify.13

Tests and Measures Observation The patient should be suitably disrobed to expose as much of this region as is necessary. As a quick orientation to the relationship of the bony structures (Fig. 27-1), the clinician should confirm the following findings: The spine of the scapula is level with the spinous process of T3. ▶▶ The inferior angle of the scapula is in line with the spinous processes of T7–9. ▶▶ The medial border of the scapula is parallel with the spinal column and about 5 cm lateral to the spinous processes. ▶▶ The iliac crests are level and symmetric. One crest higher than the other could suggest a leg-length discrepancy, an iliac rotation, or both. ▶▶ The shoulder heights are level. A normal variant is that individuals carry their dominant shoulder slightly lower than the nondominant side. ▶▶

The clinician also should evaluate the following: The smoothness of the thoracic curve.  By running the palm of the hand down the midline of the patient’s thoracic spine, the clinician can determine the smoothness of the curvature. Any areas of flatness could suggest a vertebral dysfunction such as an opening restriction (extended, rotated, and side flexed [ERS] lesion), whereas areas of relative increased curvature suggest a closing restriction (flexed, rotated, and side flexed [FRS] lesion); refer to Chapter 22. ▶▶ The degree of thoracic kyphosis.  As elsewhere in the spine, posture has an important influence on the available range of motion of the neighboring joints. Conversely, changes in the lumbar posture, such as excessive lordosis, and changes in the cervical spine, such as those rendered by a forward head position, can affect the thoracic spine. An increased lumbar lordosis increases the stresses applied to the thoracolumbar junction, whereas a forward head increases the stresses at the cervicothoracic junction. ▶▶

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The thoracic spine adopts a natural kyphotic curve, which is an increased convexity of the thoracic vertebrae. Varying

Dutton_Ch27_p1295-p1334.indd 1314

degrees of kyphosis can occur in the thoracic spine. For example, the thoracic kyphosis typically increases with age, and in women more than men.17 The appearance of increased kyphosis in the young is typically postural, but could be the result of Scheuermann disease, or ankylosing spondylitis (see Chapter 5).18 The degree of curvature of the spine also has been found to be diurnal, with a slight flattening of the thoracic kyphosis occurring overnight. The common kyphotic deformities include the following: Dowager hump.  This deformity is characterized by a severely kyphotic upper posterior (dorsal) region, which results from multiple anterior wedge compression fractures in several vertebrae of the middle to upper thoracic spine (see Chapter 5), usually caused by postmenopausal osteoporosis or long-term corticosteroid therapy. ▶▶ Hump back.  This deformity is a localized, sharp, posterior angulation, called gibbus, produced by an anterior wedging of one of the two thoracic vertebrae as a result of infection (tuberculosis), fracture, or a congenital bony anomaly of the spine.19 ▶▶

Round back.  This deformity is characterized by decreased pelvic inclination and excessive kyphosis. ▶▶ Flat back.  This deformity is characterized by decreased pelvic inclination, increased kyphosis, and a mobile thoracic spine. ▶▶ Pelvic heights.  A significant leg-length discrepancy (greater than 1/2 in) can alter the lateral curvature of the spine, resulting in compensation. ▶▶ The amount of lateral curvature of the thoracic spine.  When observing the thoracic spine, it is important to note any lateral curvature (see Chapter 6). ▶▶ Chest wall shape.  On the anterior aspect of the thoracic region, the clinician should look for evidence of deformity. ▶▶ Barrel chest.  In this deformity, a forward and upward projecting sternum increases the anteroposterior diameter. The barrel chest results in respiratory difficulty, stretching of the intercostal and anterior chest muscles, and adaptive shortening of the scapular adductor muscles. ▶▶ Pigeon chest.  In this deformity, a forward and downward projecting sternum increases the anteroposterior diameter. The pigeon chest results in a lengthening of the upper abdominal muscles and an adaptive shortening of the upper intercostal muscles. ▶▶ Funnel chest.  In this deformity, a posterior-projecting sternum occurs secondary to an outgrowth of the ribs. The funnel chest results in adaptive shortening of the upper abdominals, shoulder adductors, pectoralis minor, and intercostal muscles, and in lengthening of the thoracic extensors and middle and upper trapezius. ▶▶ The motion of the ribs during quiet breathing.  During inspiration the thorax widens as the ribs elevate, and the middle portion of the lower ribs moves more laterally during the elevation. ▶▶

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TABLE 27-9

 nterior and Posterior Palpation Points of A the Thoracic Region

Anterior Aspect

Posterior Aspect

Suprasternal notch

Spinous and associated transverse processes

Manubriosternal angle T2—level with base of spine of scapula Spinal gutter (rotatores)

Infrasternal angle

Erector spinae

Sternochondral junctions

Rib angles

Costal cartilage

Rib shafts and rib joint line of costotransverse joint C6—locate largest spinous process at base of neck and have patient extend neck; first spinous process to move anteriorly under your finger is C6

▶▶

Any lesions, swellings, or scars on the back and chest.  This is a common area for the characteristic lesion pattern of herpes zoster (shingles), which follows the course of the affected nerve (see Chapter 5).

Gait The analysis of the patient’s gait pattern can provide valuable information as to whether the condition originates in the spine or lower extremities, resulting in an impact on the muscles that affect gait (see Chapter 6). For example, a decreased arm swing during gait can indicate stiffness of the thoracic segments.

Palpation The spinous processes of the thoracic vertebrae are readily palpated (see Fig. 27-1) because they are not covered by muscle or thick connective tissue. Due to their depth relative to the more superficial structures of the spine, palpation of the thoracic transverse processes is more difficult. The landmarks outlined in Table 27-9 may be helpful to determine the segmental level involved. The spinous processes are long and slender and have varying degrees of caudal obliquity, which changes slightly throughout the kyphotic curvature of the thorax, increasing in caudal angulation to the level of T7 and then decreasing in caudal angulation below T9. Traditionally, palpation of this area has utilized the “rule of threes.”

The rule of threes has been widely accepted in orthopaedic and manual therapy texts, but until recently, never validated with research. Based on a pilot study to investigate the validity of the rule of threes of the thoracic spine, Geelhoed et al.,20 using five cadaver specimens, determined that the rule of threes was not an accurate predictor of the location of the transverse processes of the thoracic spine. The limitations of the study were the small sample size, the fact that measurements were only performed in the horizontal plane (prone position), and the fact that cadavers were used instead of live subjects, which could affect IVD height and spinal alignment. In a separate study, Geelhoed et al.21 have proposed a new model for predicting the location of the transverse processes of the thoracic spine. This proposed method states that the location of the transverse processes of a thoracic vertebra can be found lateral to the most prominent aspect of the spinous process of the vertebra one level above.21

T1-T4, T9 Transverse process up 1 interspinous space T5-T8 Transverse process up 2 interspinous spaces

CLINICAL PEARL The areas of spinous process obliquity may be divided into four regions by the so-called rule of three (an alternate version is illustrated in Fig. 27-9): ▶▶ The upper three spinous processes (T1–3). The tips of these spinous processes are level with the vertebral body of the same level.

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The Thoracic Spine

Xiphoid process

The second group of three spinous processes (T4–6). The tips of these spinous processes are in a plane that is half way between its own transverse process and those of the inferior vertebra (level with the IVD of the inferior level). This can be estimated at about three fingerbreadths. ▶▶ The third group of three spinous processes (T7–9). The tips of these spinous processes are level with the transverse processes of the vertebral body of the level below. ▶▶ The last three vertebrae (T10–12) reverse the obliquity of the spinous processes: ■■ T10 is level with the vertebral body of the vertebra below (same as T7–9). ■■ T11 is level with the disk of the inferior vertebra (same as T6). ■■ T12 is level with its own vertebral body (same as T3). ▶▶

EXAMINATION



T9-T11 Transverse process at base of spinous process

FIGURE 27-9  The rule of threes.

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EXAMINATION THE SPINE AND TMJ

Surface landmarks can be used to locate the ribs. The first rib is located 45 degrees medially to the junction of the posterior scalene and trapezius. Palpation of the first rib during respiration can detect the presence of asymmetry. Palpation of the first rib can also be performed during testing of the active motions of cervical rotation and side bending in patients with suspected brachialgia (see Chapter 25). The fifth rib passes directly under, or slightly inferior to, the male mammary nipples. To palpate the rib angles of the interscapular ribs, the shoulders are positioned in horizontal adduction. The rib angles of 3–10 can then be felt about 2–5 cm lateral to the spinous processes. When palpating anteriorly, on the sternum, a rib dysfunction will be highlighted by the presence of asymmetry and should be compared with the posterior findings. A prominent rib angle on the back and a depression of that rib at the sternum indicate a posterior subluxation, the reverse occurring in an anterior subluxation, whereas a rib that is prominent both anteriorly and posteriorly indicates a single rib torsion. The transverse processes are roughly level with their own body. The costal cartilages of the second rib articulate with the junction between the sternum and manubrium (Fig. 27-1). Palpation of the soft tissues of the region is important. The clinician should note the presence of any tenderness, temperature changes, and muscle spasm. A comparison should be made between the firmness and tenderness of the paravertebral muscles and their relationship from side to side.

Active Motion Testing

1316

Active range-of-motion tests are used to determine the osteokinematic function of two adjacent thoracic vertebrae during active motions, to identify which joints are dysfunctional, as well as the specific direction of motion loss.22 Active range of motion initially is performed globally, looking for abnormalities, such as asymmetric limitations of motion. A specific examination is then performed on any region that appears to have either excessive or reduced motion. If the history indicated that the patient’s symptoms were altered with repetitive motions or sustained positions, these movements and postures should be included. Various techniques are used to assess each area of the thoracic spine. Movement restriction of the upper thoracic spine may be secondary to pain or a result of adaptive shortening of connective tissue or muscle.23 Because of the relationship that the first two ribs share with the zygapophyseal joints as part of the manubrial ring, associated movement dysfunction of these ribs is common. Physiologic movement in the thoracic spine decreases with age. Midthoracic hypomobilities are the most common thoracic presentation, with the movement restrictions being more common in the sagittal and frontal planes, particularly extension, and side bending.23 Most of the trunk rotation below the level of C2 occurs in the thoracic spine. The clinician should look for capsular or noncapsular patterns of restriction, pain, or painful weakness (possible fracture or neoplasm). The capsular pattern of the thoracic spine appears to be a symmetric limitation of rotation and side bending, extension loss, and least loss of flexion. Joint capsular lesions demonstrate a capsular pattern as an equal and grossly severe limitation of movement in every direction.19

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With an asymmetric impairment, such as trauma, the capsular pattern appears to be an asymmetric limitation of rotation and side bending, extension loss, and a lesser loss of flexion. Overpressure applied at the end of the available range of motion is used to take the joint from its physiologic barrier to its anatomic barrier. During overpressure, an increase in resistance to motion should be felt. The end-feels should be noted. If the normal elastic end-feel of thoracic rotation is replaced by a stiffer one, it may indicate the presence of osteoporosis or ankylosing spondylitis (see Chapter 5). ▶▶ During forward flexion, nonstructural scoliosis disappears, whereas structural scoliosis does not. ▶▶ If side bending is more seriously affected than rotation, neoplastic disease of the viscera or chest wall may be present. ▶▶ If, during side bending, the ipsilateral paraspinal muscles demonstrate a contracture (Forestier bowstring sign), ankylosing spondylitis may be present. ▶▶ Side bending away from the painful side, which is the only painful and limited movement, almost always indicates a severe extra-articular impairment, such as a pulmonary or abdominal tumor or a spinal neurofibroma. The functional examination normally confirms the patient history. ▶▶

A marked restriction of motion in a noncapsular pattern with one or more spasmodic end-feels could indicate a thoracic disk herniation. ▶▶ Anterior or lateral pain with resisted thoracic rotation could indicate a muscle tear. Localized pain with resisted testing could indicate a rib fracture. ▶▶

Because of the length of the spine in this region, it is important to ensure that all parts of the thoracic spine are involved in the range-of-motion testing. Motion in the thoracic spine requires a synchronous movement between the intervertebral and zygapophyseal joints and the rib articulations. Thus, the presence of joint dysfunction or degeneration, or structural changes in the spinal curvature, will influence the amount of available range of motion, and the pattern of these coupled motions.24

CLINICAL PEARL It is important to remember that maximum arm elevation requires motion in the upper thoracic segments. The inclinometer techniques recommended by the American Medical Association are used to measure thoracic motion objectively.25 Flexion.  Two inclinometers are used to measure thoracic flexion and both are aligned in the sagittal plane. The center of the first inclinometer is placed over the T1 spinous process. The center of the second one is placed over the T12 spinous process. The patient is asked to slump forward as though trying to place the forehead on the knees, and both inclinometer angles are recorded. The thoracic flexion angle is calculated

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EXAMINATION The Thoracic Spine

FIGURE 27-10  Thoracic spine flexion.

FIGURE 27-11  Thoracic spine extension.

by subtracting the T12 from the T1 inclinometer angle. The patient should be able to flex approximately 20–45 degrees. The clinician observes for any paravertebral fullness during flexion, which might indicate hypertonus from a facilitated segment. The thoracic spine during flexion should curve forward in a smooth and even manner (Fig. 27-10). There should be no evidence of segmental rotation or side bending. To decrease pelvic and hip movements, McKenzie advocates examining thoracic flexion with the patient seated.26 Extension.  The clinician places one hand and arm across the upper chest region of the patient and the other hand over the spinous processes of the lower thoracic spine. The patient is guided into a backward slump (Fig. 27-11). Overpressure is applied by the arm across the front of the patient while avoiding any anterior translation occurring at the lumbar spine. Clinical guidelines for measurements of thoracic extension recommend that range of motion be defined with reference to the magnitude of the kyphosis measured in standing. However, to date, the relationship between the magnitude of the thoracic kyphosis and the amount of thoracic extension movement has not been reported.9 Thoracic extension may be measured using the same technique and inclinometer positions as described for flexion. The thoracic extension angle is calculated by subtracting the T12 from the T1 inclinometer angle. Alternatively, the thoracic extension can be measured using a tape measure. The distance between two points (the C7 and T12 spinous processes) is measured. During thoracic extension, the thoracic curve should curve backward or straighten. As with flexion, there should be no evidence of segmental rotation or side bending. Rotation.  The patient is seated and is asked to turn to each side at the waist. Overpressure is applied through both

shoulders (Fig. 27-12). This motion tests the ability of the ribs and the superior vertebrae to translate in the direction opposite to the rotation—a motion that is essential if complete rotation and side bending is to occur. A total of 35– 50 degrees of rotation is available in the thoracic spine.9 Rotation is a primary movement of the thoracic spine and a key component of functional activities. Side Bending.  A total of 25–45 degrees of side bending is available in the thoracic spine.9 Using a hand placed against the patient’s side, the patient is asked to side bend over the clinician’s hand. Overpressure is applied through the contralateral shoulder to avoid compression (Fig. 27-13). Side bending can be measured objectively using a tape measure. Two ink marks are placed on the skin of the lateral trunk. The upper mark is made at a point where a horizontal line through the xiphisternum crosses the coronal line. The lower mark is made at the

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FIGURE 27-12  Thoracic spine rotation.

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EXAMINATION

The motions of the ribs are palpated during breathing. If a rib stops moving in relation to the other ribs on the same side during inspiration, it is classified as a depressed rib. If a rib stops moving in relation to the other ribs during expiration, it is classified as an elevated rib.

Resisted Testing

THE SPINE AND TMJ

Resistance applied at the point of overpressure can give the clinician an indication of the integrity of the musculotendinous units of this area. Assessment of the trunk, hip, and axial scapular muscle system will be determined by the behavior of the symptoms and observation of altered movement patterns. For example, axioscapular-girdle control should be assessed when the behavior of thoracic symptoms involved upper limb or postural activities, and hip muscle control will be important to assess when the patient reports symptoms with functional activities involving standing and repetitive lower limb movement.13 The muscles of the thoracic spine can be assessed by applying resistance at the end range of thoracic flexion, extension, rotation, and side bending, while the clinician looks for pain, weakness, or painful weakness. Pain that is exacerbated with motion, but not with resisted isometric contraction, suggests a ligamentous lesion. FIGURE 27-13  Thoracic spine side bending.

highest point on the iliac crest. The distance between the two marks is measured in centimeters, with the patient standing erect, and again after full ipsilateral side bending. The second measurement is subtracted from the first, and the remainder is taken as an index of lateral spinal mobility.

CLINICAL PEARL A finding of painful and limited side bending away from the painful side, with both rotations free from pain, should always create a suspicion of serious lesions.

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Inspiration and Expiration.  Using a tape measure, the clinician measures the amount of rib expansion that occurs with a deep breath. The respiratory excursion is measured at three levels, using a tape measure placed circumferentially around the chest at the level of the axilla, the xiphoid level, and the 10th rib level. Comparisons are made between the measurements taken at the position of maximum expiration and the measurement taken at full inspiration. The normal difference between inspiration and expiration is 3–7.5 cm (1–3 in). Ankylosing spondylitis (see Chapter 5) is a disease that can include ossification of the anterior longitudinal ligament, the thoracic disk, and the thoracic zygapophyseal joints. Findings of ankylosing spondylitis are common in the thoracic region, making chest expansion measurements a requirement in this region. Decreased expansion can highlight the presence of ankylosing spondylitis but may also be the result of diaphragm palsy (C4), intercostal weakness, pulmonary (pleura) problems, old age, a rib fracture, or a chronic lung condition.

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Respiration Optimal respiration involves both abdominal and lower rib cage expansion. The most common component lost in patients with thoracic dysfunction is a lateral costal expansion.27 When lateral/posterior lateral expansion is absent, excessive excursion occurs in the abdomen (making it difficult to attain a functional transversus abdominis contraction) or in the upper chest (associated with excessive accessory respiratory muscle activity).27 Three common types of abnormal breathing patterns are recognized: Apical. This is characterized by movement in the upper chest during breathing. ▶▶ Lateral costal expansion. This is characterized by movement in the lateral lower rib cage during breathing. ▶▶ Upper and lower abdominal. This is characterized by an expansion of the abdomen during breathing. ▶▶

In the ideal scenario, most of the movement on inspiration should occur in the lower lateral rib cage with a concurrent movement of the upper abdomen.27 Respiration is first assessed through observation over several inspiration/ expiration cycles as the clinician looks for where most of the movement occurs during breathing. Following observation, the clinician places both hands on the lateral aspect of the low rib cage and monitors movement during inspiration/expiration, checking for the amount and symmetry of movement between the left and right sides.

Static Postural Testing A complete postural assessment is described in Chapter 6. Thoracic pain of a postural origin is difficult to provoke with active motion and resistive testing. Thus, McKenzie and May26 recommend placing the patient in a position for approximately 3 minutes to load the structures sufficiently to provoke postural pain.

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The patient bends forward so that the joint complex is flexed, and an evaluation is made as to the position of the T6 vertebra relative to T7 by noting which transverse process is the most posterior. A posterior left transverse process of T6 relative to T7 is indicative of a left-rotated position of the T6–7 complex in flexion. ▶▶ The patient bends backward so that the joint complex is extended, and an evaluation is made as to the position of the T6 vertebra in relation to T7 by noting which transverse process is the most posterior. A posterior left transverse process of T6 relative to T7 is indicative of a left-rotated position of the T6–7 joint complex in extension. ▶▶

The Thoracic Spine

The next stage in the examination process depends on the clinician’s background. For clinicians who are heavily influenced by the muscle energy techniques of the osteopaths, position testing is used to determine the segment on which to focus. Other clinicians omit the position tests and proceed to the combined motion and passive physiologic tests. Position Testing: Spinal. The vertebrae may be tested for positional symmetry. If an ERS or FRS is present, passive mobility testing will definitively diagnose the movement impairment. The upper thoracic joints (C7–T4) can be assessed using the cervical techniques described in Chapter 25. The following techniques can be used for the T4–12 levels. Example: T6–7.  The patient is positioned in sitting, with the clinician standing behind. Using one thumb, the clinician palpates the transverse process of the T6 vertebrae. Using the other thumb, the clinician palpates the transverse process of the T7 vertebrae (Fig. 27-14). The joint is tested in the following manner:

Combined Motion Testing.  As normal function involves complex and combined motions of the thoracic spine, combined motion testing can also be used. The motions tested include forward flexion with side bending, extension with side bending, side bending with flexion, and side bending with extension. The results from these motions are combined with the findings from the history and the single plane motions to categorize the symptomatic responses. This information can guide the clinician when determining which motions to use in the intervention. Passive Physiologic Mobility Testing.  The upper thoracic zygapophyseal joints (C7–T4) can be assessed using the cervical techniques described in Chapter 25. The following techniques can be used for the T4–12 levels. Flexion of the Zygapophyseal Joints.  The patient is seated at the end of the table, with arms together and hands resting on the back of the head. The clinician stands by the side of the patient and reaches around the front of the patient with one arm and hand. The clinician can apply a slight pressure with the sternum against the patient’s shoulder so that the patient is gently squeezed. Using the other hand to monitor intersegmental motion between the spinous processes (Fig. 27-15), the clinician flexes the thoracic spine (Fig. 27-15). The quantity and quality of motion are noted and compared with the levels above and below. Extension of the Zygapophyseal Joints. The patient is seated with the arms together and both hands behind the head. The clinician stands to the side of the patient. While palpating the interspinous spaces or the transverse processes of the level to be tested with one hand, the clinician wraps the other arm around the front of the patient and rests that hand on the patient’s contralateral elbow

EXAMINATION

Differing Philosophies

Once a segment has been localized by one of the preceding techniques, the arthrokinematics of the segment can be tested using the following passive mobility tests, which incorporate specific symmetric or asymmetric motions. Care in the interpretation of the passive mobility tests is important, because local tenderness in the thoracic region is common, especially over the spinous processes as a result of the proximity of the posterior (dorsal) rami over the apex of these bony prominences.9

FIGURE 27-14  Position testing for T6–7.

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FIGURE 27-15  Passive mobility testing for flexion.

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EXAMINATION THE SPINE AND TMJ FIGURE 27-16  Passive mobility testing for extension.

(Fig. 27-16). Crouching slightly, the clinician then places his or her anterior shoulder region close to the lateral aspect of the patient’s shoulder. Using the other hand to monitor intersegmental motion between the spinous processes, the clinician extends the thoracic spine (Fig. 27-16). The quantity and quality of motion are noted and compared with the levels above and below. Combined Motions of the Zygapophyseal Joints.  The patient is seated with one hand on top of one of the shoulders and the other hand under the opposite axilla. The clinician stands to the side of the patient. While palpating the interspinous spaces or the transverse processes of each level with one hand, the clinician wraps the other arm around the front of the patient, across or under the patient’s crossed arms, resting his or her hand on the patient’s contralateral hand. Crouching slightly, the clinician then places the anterior shoulder region against the lateral aspect of the patient’s shoulder. Side bending and rotation of the patient’s thoracic spine is then performed away from the clinician (Fig. 27-17), as the clinician lifts with his or her body. The palpating hand palpates the concave side of the curve.

Passive Articular Mobility Testing of the Midthoracic Spine

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Under normal circumstances, if the active motions and passive mobility motions of a joint are found to be restricted, the arthrokinematics of the restricted motion(s) are assessed to determine if the hypomobility is articular or extra-articular (myofascial). However, given the number of joints at each segmental level and the proximity of many of them, it is unlikely that passive articular mobility testing in this region will yield any useful information.

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FIGURE 27-17 Passive mobility testing for side bending and rotation away from clinician.

Neurologic Tests A neurologic deficit is very difficult to detect in the thoracic spine. Several tests have been devised to help assess the integrity of the neurologic system in this area. The Slump Test.  This neurodynamic mobility test can be used as a general assessment (see Chapter 11). Sensory Testing.  Sensation should be tested over the abdomen. The area just below the xiphoid process is innervated by T8, the umbilicus by T10, and the lower abdominal region, level with the anterior superior iliac spines, by T12. Too much overlap exists above T8 to make sensation testing reliable. Pathological Reflexes.  Because of the proximity and vulnerability of the spinal cord in this region, long tract signs (Babinski, Oppenheim, clonus, and muscle stretch [deep tendon] reflexes) should be routinely assessed. Lhermitte’s Symptom.  This impairment usually is considered to be a lesion to the cervical spinal cord (see Chapter 3), and it is associated with demyelination, prolapsed cervical disk, neck trauma, or subacute combined degeneration of the cord. Because the thoracic cord is immobilized by the denticulate ligaments, flexion will produce only limited stretching of the cord and thus less excursion. Lhermitte’s symptom, characterized by an electric shock-like sensation into the spinal cord and limbs during neck flexion, may be present in the thoracic spine with compression of the thoracic cord. Brown–Séquard Syndrome.  This syndrome is characterized by ipsilateral flaccid segmental palsy, ipsilateral spastic palsy below the impairment, and ipsilateral anesthesia, loss of proprioception, and loss of appreciation of the vibration of a tuning fork (dysesthesia). Contralateral discrimination

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EXAMINATION

of pain sensation and thermoanesthesia may be present and are both noted below the impairment. If a neurologic impairment is suspected, the clinician must first exclude a neoplastic process, infectious process, or fracture, and then consider a disk protrusion. A nondiskal disorder of the thoracic spine could include a neurofibroma; some of the signs to help confirm its presence are that the patient reports preferring to sleep sitting up; the pain, which slowly increases over a period of months, is felt mainly at night and is uninfluenced by activities; ▶▶ the patient reports a band-shaped area of numbness that is related to one dermatome; and ▶▶ the patient reports the presence of pins and needles sensations in one or both feet or reports any other sign of cord compression. ▶▶ ▶▶

Special Tests Very few special tests exist for this region, and even fewer have undergone diagnostic accuracy studies to determine reliability, sensitivity, and specificity. Rib Spring Test.  The patient is positioned prone, and the clinician stands on one side of the patient. Reaching over the patient, the clinician spreads the length of the thumb and index finger over the right rib in question and applies a posteroanterior force (Fig. 27-18). This is the equivalent of a left rotation of the thoracic spine. The clinician then repeats the posteroanterior force on the rib, except this time, the rotation of the thoracic spine is blocked by the clinician placing the ulnar border of the other hand over a group of left transverse processes. Pain produced with this maneuver implicates the rib because the thoracic spine is stabilized. Thoracic Spring Test.  The patient is positioned as previously. Spring testing in a posteroanterior direction is applied using the thumbs, with the elbows locked over the spinous processes of the thoracic spine (Fig. 27-19). These spring tests are provocative for pain but may also be used for a gross assessment of mobility. Reflex Hammer Test.  The patient is sitting, and the clinician uses a reflex hammer to tap over each spinous process (Fig. 27-20). If tenderness is encountered, especially in a patient with a history of trauma to the area, a fracture must be ruled out. Deep Breathing and Flexion. This test can be used for patients who complain of pain with thoracic flexion.

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The Thoracic Spine

Brown–Séquard syndrome symptoms may also occur with an idiopathic spinal cord herniation. This syndrome is caused by damage to the lateral funiculus of the spinal cord. The spinal cord frequently is shifted ventrolaterally and sometimes rotated toward the side of tethering, which might cause unilateral damage of the lateral funiculus. For the diagnosis of spinal cord herniation, magnetic resonance imaging (MRI) and computed tomography (CT) myelography are essential. An MRI myelogram can show acute, angular, anterior (ventral) deviation of the spinal cord in the sagittal plane. CT myelograms can detect anterior (ventral) or ventrolateral shifts of the spinal cord and, sometimes, an extradural cyst in the anterior (ventral) epidural space.

FIGURE 27-18  Rib spring test.

The patient is seated with the thoracic spine positioned in neutral. The patient is asked to inhale fully and then to flex the thoracic spine until the pain is felt. At this point, the patient maintains the position of flexion and slowly exhales. If further flexion can be achieved after exhalation, the source of the pain is likely to be the ribs rather than the thoracic spine.28

FIGURE 27-19  Thoracic spring test.

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THE SPINE AND TMJ

FIGURE 27-20  Reflex hammer test.

The Sitting Arm Lift Test.29  The sitting arm lift (SAL) test is based on the principles of the active straight leg raise (see Chapter 29), a validated test of failed load transfer in the pelvic girdle associated with pregnancy-related pelvic girdle pain. The patient is positioned in relaxed sitting with the hand resting on the thighs. The clinician asks the patient to lift one arm (usually the pain-free side is tested first if ipsilateral symptoms are present), with the arm straight, into elevation and then to lower the arm (Fig. 27-21). Next, the patient is asked to lift the other arm and lower it and the clinician notes whether symptoms are produced, and also observes which arm looks as if it requires more effort to lift, especially from the initiation of movement to the first 70–90 degrees of elevation. Then, the patient is asked “does one arm feel heavier to lift on the other, or different to lift than the other?” If one arm is reported to be heavier or required more effort to lift, the test result is positive for loss of neuromuscular control and

FIGURE 27-22  The prone arm lift (PAL) test.

indicates a load transfer problem. To determine the affected level or levels, the clinician then palpates the osteokinematic motion of each thoracic ring as the patient performs active elevation through flexion with the heavier arm. A positive test result is indicated when a thoracic ring/rings is/are felt to translate along any axis or rotate in any plane, or any component of the ring (vertebra or rib) translates or rotates along any axis or plane. The Prone Arm Lift Test.29  The prone arm lift (PAL) test is a modification of the SAL test as it is performed in a higher load position (prone). The patient is positioned in prone with both arms overhead in approximately 120 degrees of flexion and the upper arms supported on the bed (the head of the bed needs to be dropped down). The clinician instructs the patient to lift one arm and then lower it (Fig. 27-22). The movement is then repeated on the other side. The arm that tests positive for loss of neuromuscular control is the arm that is heavier to lift. As with the SAL test, the same techniques can be used to assess the osteokinematic motions. It is particularly important to assess this ability in patients who require this position functionally (e.g., overhead workers).

INTERVENTION STRATEGIES

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FIGURE 27-21  The sitting arm lift (SAL) test.

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Interventions for thoracic and rib dysfunctions require a multifaceted and eclectic approach because of the complexity of this area. Once the causes for referral of symptoms have been ruled out, dysfunctions of the thoracic spine and rib cage may be categorized as somatic or biomechanical. Clearly, specific management of thoracic musculoskeletal symptoms is dependent upon accurate diagnostics allowing a targeted approach.

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Acute Phase In the acute phase of rehabilitation for the thoracic spine, the intervention goals are to ▶▶

decrease pain, inflammation, and muscle spasm;

promote healing of tissues; increase pain-free range of vertebral and costal motion; ▶▶ regain soft-tissue extensibility; ▶▶ regain neuromuscular control; ▶▶ initiate postural education; ▶▶ promote correct breathing; ▶▶ educate the patient about activities to avoid and positions of comfort; and ▶▶ allow progression to the functional phase. ▶▶ ▶▶

Pain relief may be accomplished initially by the use of modalities such as cryotherapy and electrical stimulation, gentle exercises, and occasionally the temporary use of a spinal brace. Thermal modalities—especially ultrasound, with its ability to penetrate deeply—may be used after 48–72 hours. Ultrasound is the most common clinically used deepheating modality to promote tissue healing. Electrical stimulation can be used in the thoracic region to create a muscle contraction through nerve or muscle stimulation. The purpose of this muscle contraction and stimulation is to create a muscle pump to aid in the healing process. Electrical stimulation of muscles for the correction of scoliosis has not been found to be effective in preventing scoliosis progression. ▶▶ decrease pain through the stimulation of sensory nerves (TENS); and ▶▶ provide muscle reeducation and facilitation through both motor and sensory stimulation. ▶▶

Once the pain and inflammation are controlled, the intervention can progress toward the restoration of full strength, range of motion, and normal posture. Range-of-motion exercises are initiated at the earliest opportunity. These are performed during the early stages in the pain-free ranges. Submaximal isometric exercises are then performed throughout

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the pain-free ranges. These exercises are progressed as the range of motion and strength increase. Manual techniques during this phase may include myofascial release, grade I and II joint mobilizations, massage, gentle stretching, and muscle energy techniques.

Functional Phase The duration of this phase can vary tremendously and depends on several factors: Severity of the injury. Healing capacity of the patient. ▶▶ How the condition was managed during the acute phase. ▶▶ The level of patient involvement in the rehabilitation program. ▶▶ ▶▶

The goals of this phase are the following: To achieve a significant reduction or to complete resolution of the patient’s pain. ▶▶ To restore full and pain-free vertebral and costal range of motion. During this phase, the patient learns to initiate and execute functional activities without pain and while dynamically stabilizing the spine in an automatic manner. ▶▶

The Thoracic Spine

The intervention approaches for the upper thoracic spine are similar to that of the cervical spine (see Chapter 25), whereas the approach for the lower thoracic spine is similar to that of the lumbar spine (see Chapter 28). The approach to the midthoracic region is variable and depends on the cause. This region is prone to both postural and biomechanical dysfunctions. The evidence supporting the use of mobilization and high-velocity thrust techniques in the thoracic spine continues to increase.30–32 The overall goal of treatment should be to optimize load transfer and the sharing of forces throughout the thorax, the spine, and the entire body, which requires restoration of mobility to restricted areas, restoration of muscle control, and the capacity to stabilize poorly controlled areas.1 The techniques to increase joint mobility and soft-tissue extensibility are described later, under “Therapeutic Techniques” section.

Full integration of the entire upper and lower kinetic chains. The exercises prescribed must challenge and enhance muscle performance while minimizing loading of the thoracic spine and ribs to reduce the risk of injury exacerbation. Interindividual differences in injury status or training goals may allow for a continuum of required muscle stress and acceptable loading of the spine. ▶▶ Complete restoration of respiratory function. ▶▶ Restoration of thoracic and upper quadrant strength and neuromuscular control. The stabilization of this region must include postural stabilization retraining of the entire spine, including the stabilization progressions outlined in Chapters 25 and 28, to (1) gain dynamic motion control of spine forces, (2) eliminate repetitive injury to the motion segments, (3) facilitate improved thoracic erector spinae endurance and strength, (4) encourage healing of the injured segment, and (5) restore normal lumbopelvic and cervical postural and movement patterns. ▶▶

PRACTICE PATTERN 4B: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, AND RANGE OF MOTION ASSOCIATED WITH IMPAIRED POSTURE Postural Dysfunction Postural dysfunctions of the thoracic spine are relatively common. Postural pain is not typically reproducible with the typical physical examination, and the diagnosis is based solely on the history of pain following sustained positions or postures. Occasionally, patients with this type of pain may report that their pain is aggravated by stress, or fatigue.

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Abnormal Pelvic Tilting.  Good mobility of the pelvis in all directions is important for the thoracic spine. Two postural deviations are associated with pelvic tilting:

THE SPINE AND TMJ

1. Posterior pelvic tilting in the sitting position produces an increase in lumbar and thoracic spine flexion and a forward head posture (FHP). This posture is thought to result in a posterior shifting of the thoracic disk, which in turn places stress on the posterior longitudinal ligament and the dura mater. This stress can produce both local and nonsegmental referrals of pain. This condition can be treated by having the patient sit on a wedge that tilts the pelvis anteriorly. 2. Anterior pelvic tilting in the standing position causes the trunk to lean backward and results in overstretching of the rectus abdominis and a pulling forward of the shoulders, shortening of the posterior neck muscles, and increased extension of the atlanto-occipital joint. This condition can be treated by having the patient perform posterior pelvic tilts while standing, or by standing with one foot in front of the other.

Precordial Catch Syndrome This is a benign cause of chest pain in children and adolescents that remains underrecognized.33,34 It is characterized by sharp, stabbing pain in the precordial and left parasternal region that does not radiate. This pain usually lasts a few seconds and may occur at rest or with mild-to-moderate exercise. When occurring at rest, it is often associated with being seated in a slouched position and may be relieved by stretching into a more upright position. It affects males and females equally but is uncommon after the age of 35 years. The etiology of this condition is unknown, but it may originate from the pleura. After excluding other causes, management consists of explanation, reassurance, postural education, and exercises to correct any muscle imbalances.

CLINICAL PEARL Patients with any form of postural dysfunction often benefit from the movement therapies of the Alexander technique, Feldenkrais method, Trager psychophysical integration, Pilates, and Tai Chi Chuan (see Chapter 10).

PRACTICE PATTERN 4D: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, AND RANGE OF MOTION ASSOCIATED WITH LIGAMENT OR OTHER CONNECTIVE TISSUE DISORDERS Thoracic Disk Pathology

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Herniated disks have been found at every level of the thoracic spine, although they are more common in the lower thoracic spine.35,36 At the cervical and lumbar levels, the thoracic spinal nerves emerge from the cord as a large anterior (ventral) and a smaller posterior (dorsal) ramus, which unite to form a short spinal

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nerve root. There are no plexuses in this area, and the spinal nerves form the intercostal nerves.2 The intraspinal course of the upper thoracic nerve root is almost horizontal (as in the cervical spine). Therefore, the nerve can only be compressed by its corresponding disk. More inferiorly in the spine, though, the course of the nerve root becomes more oblique, and the lowest thoracic nerve roots can be compressed by disk impairments of two consecutive levels (T12 root by 11th or 12th disk).2 The major etiological factor in most cases of thoracic disk herniation appears to be degenerative changes in the disk.35,36,37McKenzie argues that the derangement syndrome can be divided into posterior and anterior disk derangements because of the distinct clinical presentations. The McKenzie classification system is outlined in Chapter 22. Anterior derangement is rare in the thoracic spine. The following derangement patterns are seen in the thoracic spine37: Derangement 1.  This type of derangement typically produces central or symmetric pain between T1 and T12. These derangements are rapidly reversible. ▶▶ Derangement 2.  This type of derangement, which is rare and the results of acute trauma or serious pathology, produces an acute kyphosis. ▶▶

▶▶

Derangement 3.  This type of derangement typically produces unilateral or asymmetric pain across the thoracic region, with or without radiation around the chest wall. These derangements are rapidly reversible.

CLINICAL PEARL The clinical manifestations of thoracic disk herniation are extremely variable and vague. This often results in long delays between presentation and diagnosis. Midline back pain and compressive myelopathy symptoms progressing over months or years are the predominant clinical features of a thoracic disk herniation, although some thoracic disk herniations are asymptomatic.35 Unusual features of thoracic disk herniation include Lhermitte’s symptom precipitated by rotation of the thoracic spine, neurogenic claudication with positional dependent weakness, and flaccid paraplegia.13 T1 and T2 Levels. Disk herniations at these levels are extremely rare. This rarity may be due to the protection afforded by the presence of the first and second ribs. Compression of the nerve at the T1 and T2 segmental levels may result in numbness, tingling, and weakness of the hand, and pain in arm and medial forearm. T2 and T3 Levels.  A disk herniation at these levels is the rarest type. Symptoms produced by this herniation include pain referred toward the clavicle, to the scapular spine, and down the inner side of the upper arm. T3–8 Levels.  Compression of the nerves at these lower levels may result in symptoms that are experienced at the side, or front of the trunk.19 Compression of the dura in the thoracic spine results in unilaterally referred pain, which is extrasegmental. A T6-level compression of the dura can cause pain up to the base of the neck and down to the waist, whereas a dural compression at T12 can refer pain up to T6 and down to the sacrum.19

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Thoracic disk herniations requiring surgical management are uncommon and account for less than 2% of all operations performed on herniated IVDs.35 Electrodiagnosis of Thoracic Disk Lesions.  Electrodiagnostic studies are important in identifying physiologic abnormalities of the nerve root in the cervical, thoracic, and lumbar spine, and they have been shown to be a useful diagnostic test in the diagnosis of radiculopathy correlating well with findings on myelography and surgery. There are two parts to the electromyogram: nerve conduction studies and needle electrode examination. The nerve conduction studies are performed by placing surface electrodes over a muscle belly or sensory area and stimulating the nerve, supplying either the muscle or the sensory area from fixed points along the nerve. From this, the amplitude, distal latency, and conduction velocity can be measured. The amplitude reflects the number of intact axons, whereas the distal latency and conduction velocity are more of a reflection of the degree of myelination. Traction: Mechanical or Manual for Thoracic Disk Lesions.  Manual or mechanical traction has long been a preferred intervention throughout the spine with the intent of improving range of motion, and to treat both zygapophyseal joint impairments as well as disk herniation. The efficacy of traction has not been scientifically proven in a randomized controlled trial, but it is commonly used and thought to be of benefit in reducing radicular pain. For traction to be effective, the imparted force must be sufficient to overcome soft tissue resistance prior to the relaxation of the involved musculature. Traction can be applied continuously, or intermittently, and with the patient positioned in sitting or lying. Intermittent traction produces twice as much separation as sustained. The duration of traction recommended varies from 20 to 30 minutes. Performed manually, traction can be very time consuming and, in the lumbar and thoracic spines, requires a good deal of strength—approximately 2 times a patient’s body weight is needed to develop significant distraction of the vertebral bodies. However, a greater degree of specificity can be obtained using manual traction, especially if it is performed using spinal locking techniques to localize the distraction to a specific level. Pain relief, or a centralization of symptoms,

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with manual traction may also be an indication for the use of mechanical traction. Vertebral axial decompression, a newer method to cause a distraction, probably represents a higher-tech version of traction, although there is no evidence in the current peerreviewed literature to support this type of intervention. From clinical experience, it would appear that traction yields better results if at least one of the spinal motions is full and pain free. However, a one-session trial of short duration is worthwhile, even if all of the motions are restricted. Spinal traction is contraindicated in the following conditions: acute lumbago; instability; ▶▶ respiratory or cardiac insufficiency; ▶▶ respiratory irritation; ▶▶ painful reactions; ▶▶ a large extrusion; ▶▶ medial disk herniation; and ▶▶ altered mental state; this includes the inability of the patient to relax. ▶▶ ▶▶

The Thoracic Spine

T9–11 Levels.  Lower thoracic disk herniations have been associated with pain radiating to the buttock in some cases, confusing the diagnosis with that of a lumbosacral root compression. How a herniated disk at a low thoracic level could appear to be a lumbosacral radiculopathy may be best explained by the anatomic arrangement of the spinal cord and vertebral bodies. In adults, the conus medullaris ends between the 12th thoracic and 3rd lumbar vertebrae, and the lumbar enlargement of the spinal cord is usually located at the lower thoracic level. Therefore, a lower thoracic disk herniation could compress the lumbosacral spinal nerves after their exit from the lumbar enlargement of the spinal cord and thus produce symptoms of compressive lumbosacral radiculopathy; thus, a herniation into an already tight canal may produce bilateral symptoms and sphincter disturbance, as in patients with a conus medullaris impairment.

Electrotherapeutic and Physical Modalities of Thoracic Disk Lesions. Modalities such as electrical stimulation appear to be helpful in reducing the associated muscle pain and spasm but should be limited to the initial pain-control phase of the intervention. Once there is control of pain and inflammation, the patient’s intervention should be progressed to restore full range of motion and flexibility of the spine, trunk, and extremity muscles.

Zygapophyseal Joint Dysfunction Apart from the upper and lower segments of this region, little is known about the extent or patterns of thoracic zygapophyseal joint degeneration. However, these joints have been found to be potential sources of local and referred pain. The pathomechanics describing mechanical dysfunction in this region are largely based on expert opinion and the principles of anatomy and biomechanics. Given the controversy surrounding the nature of coupled motions in the thoracic spine, and the number of structures involved in executing motion at these levels, the clinician is advised to diagnose dysfunction in this region based on restrictions of motion, rather than on specific structures. Restriction of motion can have many causes in this region, including zygapophyseal joint hypomobility, soft-tissue contracture, and costovertebral–costotransverse joint hypomobility. Differentiation of these structures, to find the specific cause of dysfunction, requires a great deal of expertise. For the sake of simplicity, and because the spinous and transverse processes are more easily palpated in this region, the osteopathic approach to diagnosing a positional dysfunction using position testing is recommended. As elsewhere in the spine, dysfunctions can be either symmetric or asymmetric. Symmetric impairments are more common in the thoracic region than in the lumbar,

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THE SPINE AND TMJ

particularly in the upper and cervicothoracic spine as a result of fixed postural impairments. These, of course, will not be apparent on position testing and must be sought after when the position tests are negative. If no asymmetry is found on position testing, then the segment of interest should be separately passively flexed, extended, and rotated in all directions. Layer palpation is used to determine which lesion is present. The position of the superior vertebra and the posteroanterior relationship of the transverse processes to the coronal body plane are noted and compared with the level above and below, in thoracic flexion and then extension (see “Position Testing: Spinal” section earlier).

Rib Dysfunction The costovertebral joint may be involved in inflammatory or degenerative joint disease. Complaints of symptoms in these joints are common in conditions such as ankylosing spondylitis as a result of synovitis. The clinical features of severe arthropathy of the costovertebral joint include pain with deep breathing, trunk rotation, sneezing, or coughing. CT scans are helpful in confirming the diagnosis. Inflammation of the costovertebral joint commonly causes localized pain about 3–4 cm from the midline, where the rib articulates with the transverse process and the vertebral body. According to the osteopathic doctrine, rib dysfunctions are described as structural, torsional, or respiratory. Structural.  Structural rib dysfunctions are true joint subluxations that occur secondary to trauma. These dysfunctions are extremely painful and significantly reduce motion of the ribs during inspiration and expiration. The most important landmarks for structural rib dysfunctions are the rib angle and the anterior rib. Ribs can sublux anteriorly or posteriorly (see Table 27-4). The first rib can sublux superiorly. ▶▶ Torsional.  As their name suggests, these rib dysfunctions are twisting injuries, in which the rib is held in a position of internal or external rotation. These dysfunctions affect the thoracic spine motions as well as the motions of respiration (see Table 27-4). ▶▶ Respiratory.  Respiratory rib dysfunctions usually are related to poor posture and result in a restriction of either inspiration or expiration. ▶▶

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The first rib can sublux anteriorly, posteriorly, or, more commonly, superiorly. If the motion is perceived as abnormal, passive movement testing should be performed. The arthrokinematic is tested with the patient seated and the clinician standing behind. Using the medial aspect of the metacarpophalangeal (MCP) joint of the index finger, the clinician applies an anterior–inferior–medial glide of the rib to assess the inspiration glide, while a posterior–superior– lateral glide is applied to assess the expiration glide. The end-feel is assessed. If it is abrupt and hard (pathomechanical) in both glide directions as compared with the same rib on the other side, then the problem is a subluxation. If it is stiff (hard capsular) in both directions as compared with the same rib on the other side, then a pericapsular restriction is present. If both glides are normal, then the problem is likely to be myofascial.

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Unilateral restriction of anterior rotation of the first rib.  This dysfunction is seen when the scalene muscles are hypertonic or adaptively shortened and hold the anterior aspect of the first rib superiorly or when the superior glide of the first rib is restricted at the costotransverse joint. This dysfunction will restrict unilateral elevation of the arm (both arms may be involved). If the dysfunction is intraarticular, rotation and side bending of the head/neck will be limited to the side of the restricted rib (this motion requires a superior glide of the rib at the costotransverse joint). Full expiration will also reveal asymmetry of rib motion. If the restriction is intra-articular, the superior glide of the first rib at the costotransverse joint will be restricted. The presence or absence of pain depends upon the stage of the pathology (substrate, fibroblastic, and maturation) and the irritability of the surrounding tissue. The grade of the mobilization technique is directed by these factors. ▶▶ Unilateral restriction of posterior rotation of the first rib.  This dysfunction, also known as an expiratory or anterior sagittal lesion, is seen when the posterior aspect of the first rib is held superiorly or when the inferior glide of the first rib is restricted at the costotransverse joint. This dysfunction will restrict unilateral elevation of the arm on either side, rotation and side bending of the head/neck to the opposite side of the restricted rib, and full inspiration. If the restriction is intra-articular, the inferior glide of the first rib at the costotransverse joint will be restricted. The presence or absence of pain depends on the stage of the pathology (substrate, fibroblastic, and maturation) and the irritability of the surrounding tissue. The grade of the mobilization technique is directed by these factors. ▶▶

The intervention for costovertebral dysfunctions involves mobilization and manipulation techniques or local anesthetic injections, or both.

PRACTICE PATTERN 4E: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, AND RANGE OF MOTION ASSOCIATED WITH LOCALIZED INFLAMMATION Tietze Syndrome Tietze syndrome is a local inflammation of the costosternal cartilage, which most commonly affects the second and third costochondral junctions.38,39 Tietze syndrome may also affect any of the cartilaginous articulations of the chest wall, including the sternoclavicular joints. The clinical findings for this condition include a history of a gradual or sudden onset of pain in the involved region, which is increased with deep inspiration, coughing, or sneezing. Upon physical examination, there is often a localized swelling of the costosternal cartilage. This is a self-limiting condition, which can last from weeks to years. The intervention can involve local injections of corticosteroid and specific joint mobilizations to the costovertebral articulations.

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Muscle Strains

Contusions The severity of soft-tissue injury to the chest wall is dependent on the mechanism of injury and the degree of protection between the traumatic force and the chest wall. Chest injury is commonly produced by the restraining influence of the diagonal component of a seat belt. Seat belt injuries occur predominantly on the side of the belt and hence occur on different sides in drivers and passengers.41 These take the form of abrasions, ecchymoses, and friction burns, producing an imprint of the belt.41 Trauma to the female breast can be produced by a combination of compression and shearing stress produced by a seat belt, and subcutaneous rupture of breast tissue can occur. The presence of a persistent breast mass after trauma must always be taken seriously, as trauma may draw attention to an unsuspected carcinoma.41 Chest trauma can also result in disruption of a subcutaneously placed pacemaker generator or leads, long-term indwelling central venous catheter, or subcutaneous portions of arterial bypass grafts.41 Severe skeletal trauma to the chest wall can be associated with large chest wall hematomas or collections of air within the chest wall, which can communicate with the intrathoracic space.41 The conservative intervention for thoracic cage contusions depends on the severity of the injury and the tissues involved. Typically, the initial intervention for soft-tissue injury is cryotherapy with rest. Gentle pain-free active range-of-motion exercises are introduced as tolerated. Once the acute stage is over, thermal modalities are used, and the range-of-motion exercises progressed to strengthening exercises in all planes.

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PRACTICE PATTERN 4G: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, AND RANGE OF MOTION ASSOCIATED WITH FRACTURES Thoracic Vertebral Fractures Fractures of the thoracic spine are most often a result of hyperflexion or axial loading injuries and less commonly attributable to rotational stresses, side bending, horizontal shear, and hyperextension. The most common fractures seen in the thoracic spine are anterior wedge compression fractures and burst fractures (see Chapter 5). Most thoracic spine fractures secondary to osteoporosis occur between the 9th and 11th vertebral bodies. Only 12% of patients with fracture– dislocations of the thoracic spine are neurologically intact, and 62% of patients with thoracic spine fracture–dislocations have complete neurologic deficits.41

The Thoracic Spine

Muscle strains, which are common in this region, are characterized by localized pain and tenderness, which are exacerbated with isometric testing or passive stretching of the muscle. Rather than attempt to isolate muscles in this region, the clinician can determine the directions that alleviate the symptoms and those that do not. A gradual strengthening and gentle, passive stretching program into the painless directions is initially performed, before progressing as tolerated into the painful directions. Intercostal Muscles. Injuries to intercostal muscles are mainly caused by direct trauma or after unaccustomed or excessive muscular activity (e.g., lifting a heavy object or persistent coughing). On occasion, the onset of pain or symptoms may be of gradual onset with no obvious inciting event.40 Intercostal muscle injuries are more likely in activities in which upper body use is extreme, such as regular use of a pickaxe.40 The classic presentation is pain between the ribs that is worse on movement, deep inspiration, or coughing, and tender to palpation. The intervention for intercostals muscle strains includes antiinflammatory medications, the avoidance of exacerbating activities, and the treatment of any underlying pathology where appropriate.

Rib Fractures Fractured ribs can lacerate the pleura, lung, or abdominal organs. Fractures of the upper ribs, clavicle, and upper sternum can signal brachial plexus or vascular injury. Isolated fractures of the ribs, clavicle, or scapula seldom represent significant injuries in and of themselves, but they do reflect the magnitude of force imparted, particularly in older patients with noncompliant chest walls. Fractured rib ends can lacerate the pleura or lung, resulting in hemothorax or pneumothorax.41 There is a much greater incidence of rib fractures in older patients, whose ribs are relatively inelastic, compared with the incidence of rib fractures in children, whose ribs are more pliable and resilient.41 For this reason, a posttraumatic pneumothorax in older patients is almost always associated with one or more rib fractures, whereas children can sustain a pneumothorax or major internal thoracic injury after trauma without an associated rib fracture. Fractures of the first three ribs, in particular, indicate significant energy transfer, because they are well protected by the shoulder girdles and associated musculature.41 Double fractures of three or more adjacent ribs or contiguous combined rib and sternal or costochondral fractures, or single fractures of four or more contiguous ribs, can produce a focal area of chest wall instability. Paradoxical movement of a “flail” segment during the respiratory cycle can impair respiratory mechanics, promote atelectasis, and impair pulmonary drainage. The common findings for a rib fracture are described in Chapter 5. A key factor in the intervention of rib fractures is believed to be adequate pain control to allow early aggressive respiratory care and, hence, prevent the development of pulmonary complications. Early intervention includes assistance with coughing, intracostal nerve blocks, and muscle relaxants.

Scheuermann Disease Scheuermann disease, also known as Scheuermann kyphosis, juvenile kyphosis or juvenile discogenic disease, which is found in approximately 10% of the population and in males and females equally, is typically seen in pubescent athletes.42

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The thoracic spine is most commonly involved, although involvement can include the thoracolumbar/lumbar region as well.42 The disease involves a defect to the ring apophysis of the vertebral body and anterior wedging of the affected vertebrae, as a result of a flexion overload of the anterior vertebral body. The end plate can crack, thus making it possible for disk material to bulge into the vertebral body (Schmorl node). Clinical findings include evidence of a thoracic kyphosis and pain with thoracic extension and rotation. The intervention depends on the severity but typically involves postural education, a modification of the aggravating activity, exercise (seated rotation and extension in lying exercises), or bracing. The exercise program involves the stretching of the pectoralis major and minor muscles, and muscle-strengthening exercises for the thoracic spine extensors and the scapular adductors.

Scapular Fractures Fractures of the scapula are relatively rare due to the thick muscles lying both superficial and deep to the scapula and the energy-absorbing ability of the scapula to move on the chest wall. Because a large amount of force is required to fracture a scapula, these fractures are often associated with other major injuries, including pneumothorax, and injuries of the suprascapular nerve, axillary nerve, axillary artery, and subclavian artery.41 Scapular fractures may not be recognized on the initial chest radiograph as they are frequently radiographically obscure and are commonly associated with multiple other regional injuries, such as clavicular and rib fractures, subcutaneous air, pneumothorax, and pulmonary contusion.41 Sternal Fractures. The tremendous force necessary to cause a fracture of the sternum has led to the belief that the presence of a sternal fracture is a harbinger of severe associated injuries. The association of seat belt wearing with sternal fractures is well known. Sternal fractures, as such, do not generally cause problems either in healing or by direct damage to adjacent structures. Dislocation of the sternoclavicular joint, however, with posterior displacement of the inner end of the clavicle may cause compression of the trachea and the adjacent vessels, with significant clinical consequences.43,44

INTEGRATION OF PRACTICE PATTERNS 4B AND 4F: IMPAIRED JOINT MOBILITY, MOTOR FUNCTION, MUSCLE PERFORMANCE, RANGE OF MOTION SECONDARY TO IMPAIRED POSTURE, SYSTEMIC DYSFUNCTION (REFERRED PAIN SYNDROMES), SPINAL DISORDERS, AND MYOFASCIAL PAIN DYSFUNCTION Referred Pain

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Referred pain to this area is extremely common. Referred pain is characterized by a poorly localized pain that is nontender to palpation and does not change with movements or alterations of posture (see Table 27-6).

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T4 Syndrome The name of this syndrome is a bit of a misnomer because the syndrome can additionally affect any of the T2–7 levels although it always includes the T4 segment. The T4 syndrome has an unknown etiology, although it is believed to result from a sympathetic reaction to a hypomobile segment because the symptoms appear to resolve in response to manual therapy techniques to the thoracic segments.45 In the thorax, the sympathetic trunks lie on or just lateral to the costovertebral joints. These trunks may undergo mechanical deformation with abnormal posture (forward head, accentuated thoracic kyphosis, and protracted shoulder girdle), trauma, or pulling and reaching activities, producing pain and sympathetic epiphenomena. Neurovascular symptoms are not a feature of this syndrome though a differential diagnosis should consider such conditions.45,46 The upper extremity symptoms are glovelike in distribution and are not segmentally related. Nocturnal symptoms are common, usually occurring in the side lying or supine position. More women are affected by this condition than men, in a ratio of more than 3:1.45,46 Clinical findings include local tenderness of bony points, positive slump test, positive upper limb tension tests, depression or prominence of one or more spinous processes, and local thickening and stiffness of one segment, although gross cervical and thoracic motions are usually normal. The differential diagnosis includes carpal tunnel syndrome, thoracic outlet syndrome (see Chapter 25), cervical disk disease, vascular disease, and neurologic disease.45,46 There is no high-quality evidence published about T4 syndrome.47 The intervention for this condition typically involves mobilization and manipulation of the involved segment, followed by an exercise progression emphasizing upper thoracic flexibility and muscle strength.

Notalgia Paresthetica Notalgia paresthetica is a chronic neuropathic dysesthesia of unknown etiology characterized by a pruritus located on the medial border of the inferior scapula.48 The name of this condition comes from the Greek root meaning “pain in the back.” Clinically, this condition involves localized dysesthesia and hyperesthesia in the distribution of one of the cutaneous posterior (dorsal) rami of the upper thoracic area. Most studies attribute a thoracic polyradiculopathy due to spinal nerve compression as the primary etiology behind the pruritus, while others state the anatomical angle of sensory nerve fiber penetration through the surrounding muscle is the cause.48 Treatment remains disappointing and oral neurologic modulators, such as gabapentin, are reported to be the most efficacious therapy.48

THERAPEUTIC TECHNIQUES The selection of a manual technique is dependent on a number of factors, including the acuteness of the condition and the restriction to the movement that is encountered. Oftentimes, the same technique that was used to examine the segment can be used for the intervention, the difference being the intent of the clinician and the goal of the intervention.

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Techniques to Increase Joint Mobility Joint Mobilizations and High-Velocity Thrust Techniques Mobilization and high-velocity thrust techniques have traditionally been used routinely in this region to restore thoracic mobility; ▶▶ reduce stresses through both the fixation and the leverage components of the spine; ▶▶ reduce stresses through the hypermobile segments; and ▶▶ reduce the overall force needed by the clinician, thus giving greater control. ▶▶

considering using high-velocity thrust techniques in this region. These include the following: A number of studies have demonstrated that the meninges may be vulnerable to thoracic manipulative thrust techniques.53 ▶▶ The narrow dimensions of the midthoracic spinal canal. ▶▶ The poor blood supply to this region as compared to other areas of the spine. ▶▶ The potential fragility of the bones in this area due to such conditions as osteoporosis, and rheumatoid arthritis. ▶▶

It is, therefore, recommended that the clinician performs the slump test (see Chapter 11) and a premanipulative hold (see Chapter 10) prior to any technique. Long Sit Superior Distraction (T5–6).  The patient is positioned on the treatment table in the long sit position, with the buttocks on the edge of the back of the table and the hands on the back of the neck, fingers interlocked. The clinician stands behind the patient and places a small towel roll at the T6 level. The towel roll is held in place by the clinician’s chest (made easier if the clinician turns slightly so that the side of the chest is used). The clinician threads his or her arms under the patient’s armpits and places the heel of the palms under the patient’s forearms. The patient is asked to flex the neck. A stride stance (one foot in front of the other) is adopted by the clinician (Fig. 27-23), and, while keeping the elbows close together, the clinician gently rocks the patient backward and forward. After two or three rocks, the traction force is applied, as the clinician shifts his or her body weight from the forward leg to the back, while lifting the patient and pushing the patient’s forearms toward the ceiling.

The Thoracic Spine

For example, if stretching of the mechanical barrier rather than pain relief is the immediate objective of the intervention, a mobilization technique is carried out at the end of the available range. The antagonist muscle must be relaxed to achieve this, and this is most easily accomplished using a hold–relax technique. After this has been gained (and sometimes before and after), there is some minor pain to be dealt with, using grade IV oscillations, after which the joint capsule can be stretched, using either grade IV++ or prolonged stretch techniques. The prolonged stretch or the strong oscillations are continued for as long as the clinician can maintain good control. At the point where control is about to be lost, several isometric contractions to the agonists and the antagonists are demanded of the patient’s muscles in the new range, to give the central nervous system information about the newly acquired range. To complete the reeducation, concentric and eccentric retraining is carried out throughout the whole range of the joint. Active exercises are continued at home and at work on a regular and frequent basis to reinforce the reeducation.

CLINICAL PEARL Cleland et al.49 developed a clinical prediction rule (CPR) to identify a subgroup of patients with neck pain who were considered more likely to benefit from a high-velocity thrust technique of the thoracic spine. However, more recent evidence has questioned its validity.50 A recent study that included 24 consecutive patients51 tested two different forms of high-velocity thrust techniques to the thoracic spine based on this CPR. The study found that patients who were treated with a combination of cervical spine high-velocity thrust techniques and exercises showed significantly greater improvement in pain and disability compared to those treated with thoracic spine high-velocity techniques and exercises. A number of studies have demonstrated clinical success with high-velocity thrust techniques to the thoracic spine.30–32,51,52 However, it must be remembered that the isolation of a particular segment in the thoracic spine is extremely difficult, if not impossible because of the number of articulations that exist at each segmental level. In addition, there are a number of concerns that the clinician must be aware of prior to

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FIGURE 27-23  Long sit superior distraction thrust technique.

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FIGURE 27-24  Shoulder sweep exercise.

FIGURE 27-26  Thoracic spine extension over Swiss ball.

Exercises to Increase Soft-Tissue Extensibility

attempts to lie supine on the ball and then places the hands on the ball (Fig. 27-26). The patient is then instructed to move the top of the head toward the floor, in an attempt to fully extend the thoracic spine. This position is held for 8– 10 seconds, after which the patient relaxes. The exercise is repeated 8–10 times. This exercise can be made more challenging by moving the hands from beside the body, out to the sides (Fig. 27-27) while maintaining the balance. If the patient is unable to maintain his or her balance on the Swiss ball, a foam roll may be used. The foam roll also allows the clinician to focus the extension exercise on a specific segment. Thoracic Spine Rotation.  The following Swiss ball exercises to improve thoracic rotation range of motion and strength are recommended for the athletic population, only.

Shoulder Sweep This exercise is used to mobilize the chest wall and to integrate upper extremity function with thoracic spine and rib cage motion.54 The patient is positioned supine on the floor or on a mat table, with the hips and knees flexed to about 90 degrees (Fig. 27-24). The patient is asked to reach sideways and place the back of the hand as far out to the side as is comfortable. While maintaining contact with the floor, the patient moves the hand above the head and to the other side of the body, making a large circle around his or her body (see Fig. 27-24). Manual assistance applied to the scapula or rib cage can be used as can deep breathing, in order to move into the restricted ranges. Thoracic Spine Flexion.  The patient kneels in front of a Swiss ball. The patient positions themselves over the Swiss ball so that weight is applied through the feet and the forearms (Fig. 27-25). While applying some body weight through the forearms, the patient arches the thoracic spine as far as is comfortable. This position is held for 8–10 seconds, after which the patient relaxes. The exercise is repeated 8–10 times. Thoracic Spine Extension.  It is advised that the clinician monitors this exercise in case the patient loses his or her balance. The patient sits on a Swiss ball, with the feet on the ground. Once the patient has good sitting balance, he or she

FIGURE 27-25  Thoracic spine flexion over Swiss ball.

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FIGURE 27-27  Thoracic spine extension over Swiss ball—arms out to the side.

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FIGURE 27-30  Thoracic side bending over Swiss ball.

The patient kneels with his or her back facing the Swiss ball. Using one leg at a time, the patient reaches back with the foot and places it on top of the Swiss ball. Once both feet are on the ball, the legs are straightened, and the weight of the body is primarily borne by the arms. Using the dorsum of the feet and the anterior legs, the patient induces a rotation of the thoracic region by twisting at the waist (Fig. 27-28), while maintaining balance through the arms. This position is held for 8– 10 seconds, after which the patient relaxes. The exercise is repeated 8–10 times. By alternatively moving the legs into hip flexion and extension, rotation of the thoracic spine can be achieved, while maintaining balance with the arms (see Fig. 27-28). For the nonathletic population, thoracic rotation exercises can be performed using a firmer base of support. The patient kneels in front of a wobble board and places both hands on the board. Once good balance is achieved, the patient is asked to raise one arm out to the side as high as is comfortable, while keeping both knees on the floor. This position is held for 8–10 seconds, after which the patient relaxes. The exercise is repeated 8–10 times. Thoracic rotation exercises can also be performed in the supine position. The patient lies supine with both knees bent and feet placed on the floor. The arms are abducted to approximately 90 degrees (Fig. 27-29). Keeping the trunk against the

floor, the patient lowers the thighs to one side and then the other (see Fig. 27-29), as far as is comfortable. This position is held for 8–10 seconds, after which the patient relaxes. The exercise is repeated 8–10 times.

Myofascial Stretch into Extension. The patient is positioned supine, and the clinician stands at the head of the bed. The patient elevates both arms over the head and reaches around the back of the clinician’s thighs. By having the patient hold a towel in this position, the clinician can place both of his or her hands under the patient’s rib cage and pull the rib cage in an anterior and cranial direction, thereby encouraging thoracic extension (Fig. 27-31). A belt wrapped around the patient at the correct level can make this technique more specific.

FIGURE 27-29  Hook lying rotations with arms abducted.

FIGURE 27-31  Supine myofascial stretch into extension.

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The Thoracic Spine

FIGURE 27-28  Thoracic spine rotation with trunk on Swiss ball.

Thoracic Spine Side Bending.  The patient kneels to the side of a Swiss ball. The patient is asked to lean sideways over the ball and, with the arm closest to the ball, to attempt to touch the floor on the other side of the ball (Fig. 27-30) without losing balance. This position is held for 8–10 seconds, after which the patient relaxes. The exercise is repeated 8–10 times.

Rib Techniques for the Midlower Thoracic Spine

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CASE STUDY RIGHT ANTERIOR CHEST PAIN

THE SPINE AND TMJ

HISTORY

Questions

A 25-year-old man presented at the clinic complaining of pain in his right anterior chest. About 1 month previously, the patient had experienced a sudden and sharp pain in his right posterior chest at the midscapular level during a tug of war game at his company’s picnic. The posterior chest pain subsided very quickly and did not bother him for the rest of the game. However, the next morning, pain was felt in the anterior aspect of the chest. This anterior chest pain eased off over the next few days with rest, but recurred as soon as the patient returned to weight lifting.

1. Given the mechanism of injury, what structure(s) could be at fault? 2. Should the report of anterior chest pain concern the clinician in this case? 3. What is your working hypothesis at this stage? List the various diagnoses that could present with anterior chest pain, and the tests you would use to rule out each one. 4. Why do you think the pain shift from posterior thoracic to anterior thoracic? 5. Does this presentation/history warrant a scan? Why or why not?

CASE STUDY BILATERAL AND CENTRAL UPPER THORACIC PAIN HISTORY A 30-year-old housewife presents at the clinic with a 3-day history of constant central and bilateral upper thoracic pain that is deep and dull and can be felt in the front of the chest when the pain is aggravated. The pain is reported to be worse with flexion motions but is improved with lying on a hard surface. Further questioning revealed that the patient had a history of minor back pain but was otherwise in good health and had no report of bowel or bladder impairment.

Questions

2. Should the report of anterior chest pain concern the clinician in this case? 3. Why was the statement about “no reports of bowel or bladder impairment” pertinent? 4. What is your working hypothesis at this stage? List the various diagnoses that could manifest with central and bilateral upper thoracic pain and the tests you would use to rule out each one. 5. Does this presentation/history warrant a scanning examination? Why or why not?

1. What structure(s) could be at fault with central and bilateral upper thoracic pain as the major complaint?

CASE STUDY NECK SPRAIN HISTORY A 42-year-old right-handed woman was referred by her primary-care physician with a diagnosis of neck sprain. The patient reported a 10-year history of intermittent neck pain (right greater than left), which had worsened over the past 6 months. More recently, the patient reported developing right shoulder (right upper trapezius) and arm pain, as

well as infrequent (about twice a week) paresthesia in the right arm and hand involving the fourth and fifth digits. The patient described the pain as a sharp stabbing pain at the right side of the neck and a dull aching pain in the right upper trapezius region. She indicated that the neck pain was independent of the upper trapezius pain. At the time of the evaluation, the neck and upper trapezius pain were a

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attacks, dysarthria, dysphagia, tinnitus, and night pain unrelated to position.

Questions 1. List the structure(s) that could be at fault with these complaints. 2. Does this sound like a neuromusculoskeletal condition? 3. Are there any other questions you would ask this patient? 4. What is your working hypothesis at this stage? List the various diagnoses that could manifest with central and bilateral upper thoracic pain and the tests you would use to rule out each one. 5. Does this presentation/history warrant a scanning examination? Why or why not?

The Thoracic Spine

3/10 and 4/10, respectively. The symptoms improved when she positioned herself supine or left side lying with a pillow under the head. The upper trapezius pain was reduced when she side bent the head toward the side of pain and worsened as the day progressed, especially when she was at work and performing elevated arm activities. She reported that the paresthesias of the ulnar aspect of a right forearm, as well as digits 4 and 5, appeared more often during the afternoon and occasionally at night. When inquiring about the irritability of the condition, the patient reported that between a few hours and 1 day were required for the pain to decrease after it was provoked. The patient worked as a faculty member at a local college, which involved spending prolonged periods of time on the computer and extensive reading. The patient’s past medical history was negative for dizziness, diplopia, unexpected weight change, drop

CASE STUDY INTERSCAPULAR PAIN HISTORY

Questions

A 21-year-old woman presented with a 1-week history of left-sided interscapular pain that started at work. The patient worked as a computer operator. The pain was reported to be aggravated by lying prone, deep breathing in, and standing or sitting erect. Further questioning revealed that the patient had a history of this pain over the past few months but that it had not been as intense as it was currently. The patient was otherwise in good health and had no reports of bowel or bladder impairment.

1. List the structures that can produce interscapular pain. 2. Given the fact that this patient works at a computer, what could be the cause of her pain? 3. What is your working hypothesis at this stage? List the various diagnoses that could manifest with interscapular pain and the tests you would use to rule out each one. 4. Does this presentation/history warrant a scan? Why or why not?

REFERENCES 1. Lee D, Lee L-J. Integrated, multimodal approach to the thoracic spine and ribs. In: Magee DJ, Zachazewski JE, Quillen WS, eds. Pathology and Intervention in Musculoskeletal Rehabilitation. St. Louis, MO: Saunders; 2009:306–337. 2. Standring S, Gray H. Gray’s Anatomy: The Anatomical Basis of Clinical Practice. 41st ed. London, England: Elsevier; 2015. 3. Lee DG. The Thorax—and Integrated Approach. Delta, B.C., Canada: D.O.P.C.; 2003. 4. Mercer S. Comparative anatomy of the spinal disc. In: Boyling JD, Jull GA, eds. Grieve’s Modern Manual Therapy: The Vertebral Column. Philadelphia, PA: Churchill Livingstone; 2004:9–16. 5. Lundon K, Bolton K. Structure and function of the lumbar intervertebral disk in health, aging, and pathological conditions. J Orthop Sports Phys Ther. 2001;31:291–306. 6. Singer KP, Boyle JJW, Fazey P. Comparative anatomy of the zygapophysial joints. In: Boyling JD, Jull GA, eds. Grieve’s Modern Manual Therapy: The vertebral column. Philadelphia. PA: Churchill Livingstone; 2004:17–29. 7. Tubbs RS, Tyler-Kabara EC, Salter EG, Sheetz J, Zehren SJ, Oakes WJ. Additional vascular compression of the brachial plexus in a cadaver with a cervical rib: case illustration. Surg Radiol Anat. 2006;28(1):112–113.

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8. Edmondston SJ. Clinical biomechanics of the thoracic spine including the rib cage. In: Boyling JD, Jull GA, eds. Grieve’s Modern Manual Therapy: The Vertebral Column. Philadelphia, PA: Churchill Livingstone; 2004:55–65. 9. Edmondston SJ, Waller R, Vallin P, Holthe A, Noebauer A, King E. Thoracic spine extension mobility in young adults: influence of subject position and spinal curvature. J Orthop Sports Phys Ther. 2011;41: 266–273. 10. Theisen C, van Wagensveld A, Timmesfeld N, et al. Co-occurrence of outlet impingement syndrome of the shoulder and restricted range of motion in the thoracic spine—a prospective study with ultrasoundbased motion analysis. BMC Musculoskelet Disord. 2010; 11:135. 11. Boyles RE, Ritland BM, Miracle BM, et al. The short-term effects of thoracic spine thrust manipulation on patients with shoulder impingement syndrome. Man Ther. 2009;14:375–380. 12. Tate AR, McClure PW, Young IA, Salvatori R, Michener LA. Comprehensive impairment-based exercise and manual therapy intervention for patients with subacromial impingement syndrome: a case series. J Orthop Sports Phys Ther. 2010;40:474–493. 13. Scott Q. Clinical examination and targeted management of thoracic musculoskeletal pain. In: Jull G, Moore A, Falla D, Lewis J, McCarthy C, Sterling M, eds. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. London, England: Elsevier; 2015:444–449.

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14. Fruth SJ. Differential diagnosis and treatment in a patient with posterior upper thoracic pain. Phys Ther. 2006;86:254–268. 15. Le T, Biundo J, Aprill C, Deiparine E. Costovertebral joint erosion in ankylosing spondylitis. Am J Phys Med Rehabil. 2001;80:62–64. 16. Goodman CC, Snyder TK. Introduction to screening for referral in physical therapy. In: Goodman CC, Snyder TK. Differential Diagnosis in Physical Therapy. Philadelphia, PA: Saunders; 2012:1–30. 17. Kaczmarek W, Pucher A, Nowicki J. Correction of thoracic kyphosis and lumbar lordosis in the treatment of idiopathic scoliosis treatment with Cotrel-Dubousset instrumentation. Ortop Traumatol Rehabil. 2005;7(2):163–169. 18. Sucato DJ, Agrawal S, O’Brien MF, Lowe TG, Richards SB, Lenke L. Restoration of thoracic kyphosis after operative treatment of adolescent idiopathic scoliosis: a multicenter comparison of three surgical approaches. Spine (Phila Pa 1976); 2008;33(24):2630–2636. 19. Bland JH. Diagnosis of thoracic pain syndromes. In: Giles LGF, Singer KP, eds. Clinical Anatomy and Management of the Thoracic Spine. Oxford: Butterworth-Heinemann; 2000:145–156. 20. Geelhoed MA, Viti JA, Brewer PA. A pilot study to investigate the validity of the rule of threes of the thoracic spine. J Man Manip Ther. 2005;13:91–93. 21. Geelhoed MA, McGaugh J, Brewer PA, Murphy D. A new model to facilitate palpation of the level of the transverse processes of the thoracic spine. J Orthop Sports Phys Ther. 2006;36:876–881. 22. Lawrence DJ, Bakkum B. Chiropractic management of thoracic spine pain of mechanical origin. In: Giles LGF, Singer KP, eds. Clinical Anatomy and Management of Thoracic Pain. Oxford: ButterworthHeinemann; 2000:244–256. 23. Singer KP, Edmondston SJ. Introduction: the enigma of the thoracic spine. In: Giles LGF, Singer KP, eds. Clinical Anatomy and Management of Thoracic Spine Pain. Oxford: Butterworth-Heinemann; 2000. 24. McCarthy C, et al. Aging and the musculoskeletal system. In: Jull G, Moore, A, Falla, D, Lewis, J, McCarthy C, Sterling, M. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. London, England: Elsevier; 2015:126–135. 25. American Medical Association. The Spine and Pelvis. In: Cocchiarella L, Andersson GBJ, eds. Guides to the Evaluation of Permanent Impairment. 5th ed. Chicago: American Medical Association; 2001. 26. McKenzie RA, May S. The Cervical and Thoracic Spine: Mechanical Diagnosis and Therapy. Waikanae, NZ: Spinal Publications; 2006. 27. Lee DG. Restoring force closure/motor control of the thorax. In: Lee DG, ed. The Thorax—and Integrated Approach. Delta, B.C., Canada: D.O.P.C.; 2003:104–135. 28. Evjenth O, Gloeck C. Symptom Localization in the Spine and Extremity Joints. Minneapolis, MN: OPTP; 2000. 29. Mens JM, Huis In ‘t Veld YH, Pool-Goudzwaard A. The active straight leg raise test in lumbopelvic pain during pregnancy. Man Ther. 2012;17:364–368. 30. Griswold D, Learman K, Kolber MJ, O’Halloran B, Cleland JA. Pragmatically applied cervical and thoracic nonthrust manipulation versus thrust manipulation for patients with mechanical neck pain: a multicenter randomized clinical trial. J Orthop Sports Phys Ther. 2018;48:137–145. 31. Hartstein AJ, Lievre AJ, Grimes JK, Hale SA. Immediate effects of thoracic spine thrust manipulation on neurodynamic mobility. J Manipulative Physiol Ther. 2018;41:332–341. 32. Sueki D, Almaria S, Bender M, McConnell B. The immediate and 1-week effects of mid-thoracic thrust manipulation on lower extremity passive range of motion. Physiother Theory Pract. 2018:1–11. 33. Gumbiner CH. Precordial catch syndrome. South Med J. 2003;96:38–41.

34. Hayes D, Jr., Younger BR, Mansour HM, Strawbridge H. Precordial catch syndrome in elite swimmers with asthma. Pediatr Emerg Care. 2016;32:104–106. 35. Carr DA, Volkov AA, Rhoiney DL, et al. Management of thoracic disc herniations via posterior unilateral modified transfacet pedicle-sparing decompression with segmental instrumentation and interbody fusion. Global Spine J. 2017;7:506–513. 36. Ruetten S, Hahn P, Oezdemir S, Baraliakos X, Godolias G, Komp M. Operation of soft or calcified thoracic disc herniations in the fullendoscopic uniportal extraforaminal technique. Pain Physician. 2018;21:E331–E340. 37. McKenzie R, May S. Mechanical diagnosis. In: McKenzie R, May S, eds. The Human Extremities: Mechanical Diagnosis and Therapy. Waikanae, New Zealand: Spinal Publications New Zealand Ltd; 2000:79–88. 38. Kaplan T, Gunal N, Gulbahar G, et al. Painful chest wall swellings: tietze syndrome or chest wall tumor? Thorac Cardiovasc Surg. 2016;64:239–244. 39. Senturk E, Sahin E, Serter S. Prolotherapy: an effective therapy for tietze syndrome. J Back Musculoskelet Rehabil. 2017;30:975–978. 40. Gregory PL, Biswas AC, Batt ME. Musculoskeletal problems of the chest wall in athletes. Sports Med. 2002;32:235–250. 41. Collins J. Chest wall trauma. J Thorac Imaging. 2000;15:112–119. 42. Mansfield JT, Bennett M. Scheuermann Disease. Treasure Island, FL: StatPearls; 2018. 43. Liang HM, Chen QL, Zhang EY, Hu J. Sternal fractures and delayed cardiac tamponade due to a severe blunt chest trauma. Am J Emerg Med. 2016;34:758.e1–3. 44. Ulusan A, Karakurt O. Cardiac findings of sternal fractures due to thoracic trauma: a five-year retrospective study. Ulus Travma Acil Cerrahi Derg. 2018;24:249–254. 45. Conroy JL, Schneiders AG. The T4 syndrome. Man Ther. 2005;10: 292–296. 46. Hirai PM, Thomson OP. T4 syndrome—a distinct theoretical concept or elusive clinical entity? A case report. J Bodyw Mov Ther. 2016;20: 722–727. 47. Karas S, Pannone A. T4 syndrome: a scoping review of the literature. J Manipulative Physiol Ther. 2017;40:118–125. 48. Robbins BA, Ferrer-Bruker SJ. Notalgia Paresthetica. Treasure Island, FL: StatPearls; 2018. 49. Cleland JA, Childs JD, Fritz JM, Whitman JM, Eberhart SL. Development of a clinical prediction rule for guiding treatment of a subgroup of patients with neck pain: use of thoracic spine manipulation, exercise, and patient education. Phys Ther. 2007;87:9–23. 50. Cleland JA, Mintken PE, Carpenter K, et al. Examination of a clinical prediction rule to identify patients with neck pain likely to benefit from thoracic spine thrust manipulation and a general cervical range of motion exercise: multi-center randomized clinical trial. Phys Ther. 2010;90:1239–1250. 51. Puentedura EJ, Landers MR, Cleland JA, Mintken PE, Huijbregts P, Fernandez-de-Las-Penas C. Thoracic spine thrust manipulation versus cervical spine thrust manipulation in patients with acute neck pain: a randomized clinical trial. J Orthop Sports Phys Ther. 2011;41:208–220. 52. Costello M. Treatment of a patient with cervical radiculopathy using thoracic spine thrust manipulation, soft tissue mobilization, and exercise. J Man Manip Ther. 2008;16:129–135. 53. Suh SI, Koh SB, Choi EJ, et al. Intracranial hypotension induced by cervical spine chiropractic manipulation. Spine. 2005;30:E340–E342. 54. Flynn TW. Thoracic spine and chest wall. In: Wadsworth C, ed. Current Concepts of Orthopedic Physical Therapy—Home Study Course. La Crosse, WI: Orthopaedic Section, APTA; 2001.

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C H A P T E R 2 8

CHAPTER OBJECTIVES At the completion of this chapter, the reader will be able to: 1. Describe the vertebrae, ligaments, muscles, and blood and nerve supply that comprise the lumbar intervertebral segment. 2. Outline the coupled movements of the lumbar spine, the normal and abnormal joint barriers, and the reactions of the various structures to loading. 3. Perform a detailed examination of the lumbar musculoskeletal system, including history, observation, palpation of the articular and soft tissue structures, specific passive mobility and passive articular mobility tests for the intervertebral joints, and stability testing. 4. Evaluate the results of the examination and establish a diagnosis. 5. Describe the common pathologies and lesions of this region. 6. Describe intervention strategies based on clinical findings and established goals. 7. Design an intervention based on patient education, manual therapy, and therapeutic exercise. 8. Apply mobilization techniques for the lumbar spine, using the correct grade, direction, and duration, and explain the mechanical and physiologic effects. 9. Evaluate intervention effectiveness to progress or modify intervention. 10. Plan an effective home program, including spinal care, and instruct the patient in this program. 11. Help the patient to develop self-reliant intervention strategies.

OVERVIEW Over the past few decades, low back pain (LBP) has become increasingly problematic, placing significant burdens on health systems and social-care systems. Indeed, survey

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Lumbar Spine

studies show that the lifetime prevalence of LBP is greater than 80% in the adult population,1 making it one of the most common disorders encountered by physical therapists.2 The clinical course of LBP can be described as acute, subacute, recurrent, or chronic. Fortunately, LBP resolves in the majority of these patients within the first 6 weeks of onset.3 This had led to the assumption that most cases of LBP are benign in nature, despite the fact that between 5% and 30% of the proportion of individuals who have acute or subacute LBP episodes will develop chronic LBP,4 and it is this proportion of people who account for 75–90% of the cost associated with LBP.5 In addition, this population has been associated with a reduced quality of life, poor health, comorbidities, and high medical costs.5–7 Thus, establishing an effective approach for patients with LBP at high risk for chronicity that has a focus on addressing modifiable prognostic factors could have significant personal, financial, and societal benefits.8,9

ANATOMY The lumbar spine (Fig. 28-1) consists of five lumbar vertebrae, which, in general, increase in size from L1 to L5 to accommodate progressively increasing loads. Between each of the lumbar vertebrae are the intervertebral disks (IVDs).

VERTEBRAL BODY The anterior part of each vertebra is called the vertebral body. The pedicles, which project from the posterior aspect of the vertebral body, represent the only connection between the posterior joints of the segment and the vertebral bodies, both of which deliver tensile and bending forces. Noticeably, the muscles that act on a lumbar vertebra pull downward, transmitting the muscular action to the vertebral body. These resistive forces are transmitted to the vertebral body along the pedicles. The lamina (see Fig. 28-1) functions to absorb the various forces that are transmitted from the spinous and articular processes. The pars interarticularis connects the vertically oriented lamina and the horizontally extending pedicle. The two laminae meet and fuse with one another, forming an arch of bone aptly called the vertebral, or neural arch, which serves

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ANATOMY

Cauda equina nerve roots Posterior longitudinal ligament Facet joint

L3 vertebral body Pedicle (cut)

Dural tube Lamina (cut)

Superior articular process

THE SPINE AND TMJ

Ligamentum flavum

L3 nerve root Facet joint

Transverse process

L5 spinous process FIGURE 28-1  Structures of the lumbar spine.

as a bony tunnel for the spinal cord. Both the transverse and the spinous processes of the vertebral body provide areas for muscle attachments. The first sacral segment, the point at which the sacrum joins the lumbar spine, is usually included in discussions of the lumbar spine. In most cases, this is a fixed segment, but in some cases it may be mobile (lumbarization of S1). At other times, the fifth lumbar segment may be fused to the sacrum or ilium, resulting in a sacralization of that vertebra. It is unclear how these anomalies affect the biomechanics of the spine.

Intervertebral Disk Annulus Fibrosis

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In the lumbar spine, the superior and inferior surfaces of the vertebral bodies are comparatively large and flat, reflecting their load-transfer function. The lumbar disk is approximately cylindrical, its shape being determined by the integrity of the annulus fibrosis (AF). The AF consists of approximately 10–12 (often as many as 15–25) concentric sheets of predominantly type I collagen tissue, bound together by proteoglycan gel.10 The number of annular layers decreases with age, but there is a gradual thickening of the remaining layers.10 The fibers of the AF are oriented at approximately 65 degrees from vertical. The fibers of each successive sheet or lamella maintain the same inclination of 65 degrees, but in the opposite direction to the preceding lamella, resulting in every second sheet having the same orientation. Thus, only 50% of the fibers are under stress with rotational forces at any given time. This alteration in the direction of fibers in each lamella is vital in enabling the disk to resist torsional (twisting) forces.11 Although each lamella is thicker anteriorly than posteriorly, the lumbar disks are thinner and more tightly packed,

Dutton_Ch28_p1335-p1416.indd 1336

posteriorly than anteriorly.10 Consequently, the posterior part of the annulus will have thinner but stronger fibers, and it is capable of withstanding tension applied to this area during flexion activities and postures. However, because of the predominance of flexion activities in life, fatigue damage may occur in the posterior aspect of the disk, making it a common site of injury.12 The wedge-shaped appearance of the disk produced by the configuration of the lamellae contributes to the normal lordosis of this region.12 The outermost lamellae insert into the ring apophysis of the upper and lower vertebrae by mingling with the periosteal fibers (fibers of Sharpey). These fibers, attached to the bone, may be considered as ligaments and as such are designed primarily to limit motion between adjacent vertebrae.13 The inner portions of the lamellae are attached to the superior and inferior cartilaginous end plates, and form an envelope around the nucleus pulposus (NP).10

Nucleus Pulposus The lumbar IVDs of a healthy young adult contain an NP that is composed of a semifluid mass of mucoid material.

CLINICAL PEARL The overall consistency of the NP changes with increasing age, as the water content of the NP diminishes and subsequently becomes drier. At birth, the water content of the NP is approximately 80%. In the elderly, the water content is approximately 68%.13 Most of this water content change occurs in childhood and adolescence, with only approximately 6% occurring in adulthood.13

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The IVDs are able to distribute compressive stress evenly between adjacent vertebrae because the NP and inner AF act like a pressurized fluid, in which the pressure does not vary with location or direction.11

Vertebral End Plates Each vertebral end plate consists of a layer of hyaline and fibrocartilage approximately 0.6–1 mm thick,10 which covers the top or bottom aspects of the disk and separates the disk from the adjacent vertebral body. Peripherally, the end plate is surrounded by the ring apophysis. At birth, the end plate is part of the vertebral body growth plate, but with aging, the growth zone becomes thinner and disappears, leaving only a thickened articular plate. Nutrition of the disk comes via a diffusion of nutrients from the anastomosis over the AF and from the arterial plexi underlying the end plate. Although almost the entire AF is permeable to nutrients, only the center portions of the end plate are permeable. It is possible that a mechanical pump action produced by spine motion could aid with the diffusion of the nutrients. The two end plates of each disk, therefore, cover the NP in its entirety but fail to cover the entire extent of the AF.

CLINICAL PEARL Because of the attachment of the AF to the vertebral end plates on the periphery, the end plates are strongly bound to the IVD. In contrast, the vertebral end plates are only weakly attached to the vertebral bodies. Between the ages of 20 and 65 years, the end plate thins and the vascular foramina in the subchondral bone become occluded, resulting in decreased nutrition to the disk. At the same time, the underlying bone becomes weaker, and the end plate gradually bows into the vertebral body.

Nerve Root Canal The nerve root canal is located at the lateral aspect of the spinal canal (Fig. 28-1). The dural sac forms the medial wall of the canal, the internal aspect of the pedicle, and the lateral wall. The posterior border of the nerve root canal is formed by the ligamentum flavum (LF), superior articular process, and lamina. The anterior border of the canal is formed by the vertebral body and IVD.

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The entrance zone is medial and anterior to the superior articular process. ▶▶ The middle zone is located under the pars interarticularis of the lamina and below the pedicle. ▶▶ The exit zone is the area surrounding the intervertebral foramen. ▶▶

A decrease in the dimension of this canal results in a condition called lateral stenotic syndrome.

Innervation The outer half of the IVD, the posterior longitudinal ligament (PLL), and the dura are innervated by the sinuvertebral nerve, which is considered to arise from the anterior (ventral) ramus and the sympathetic trunk.10

Lumbar Spine

CLINICAL PEARL

The nerve root canal can be described according to its location10:

ANATOMY

The portion of the NP that is not water is made up of cells that are largely chondrocytes and a matrix consisting of proteoglycans, collagen fibers, other noncollagenous proteins, and elastin.10 With the exception of early youth, there is no clear boundary between the NP and AF. The biomechanical makeup of the NP is similar to that of the AF, except that the NP contains mostly type II collagen, as opposed to type I.10 The collagen interacts with the ground substance to form a concentration proportional to the viscoelastic requirements of the AF.

Alterations in Disk Structure Although the lumbar IVD appears destined for tissue regression and destruction, it remains unclear why similar agerelated changes remain asymptomatic in one individual yet cause severe LBP in others. The basic changes that influence the responses of the disk to aging appear to be biochemical and may concern the collagen content levels in the NP. Recently, advances in brain and spine imaging have begun to yield encouraging findings of a number of central and peripheral mechanisms thought to be important components of the generation and propagation of LBP.14–16 Among these hypothesized mechanisms is an increase in the diffusion of water within various soft tissues of the spine, occurring in response to treatment and movement, which may be linked to pain reduction.16 A recent study found that changes in the diffusion of water within the lumbar IVDs at the L1–2, L2–3, and L5–S1 levels appeared to be related to differences in withinsession pain reports following a single treatment of spinal manipulative therapy.16

CLINICAL PEARL In general, the IVD becomes drier, stiffer, less deformable, and less able to recover from creep with age. As the NP becomes more fibrous, its ability to handle compressive loading becomes more compromised, and more weight is taken by the AF.

Zygapophyseal Joint The articulations between two consecutive lumbar vertebrae form three joints. One joint is formed between the two vertebral bodies and the IVD. The other two joints are formed by the articulation of the superior articular process of one vertebra and the inferior articular processes of the vertebra above it. These latter joints are known as the zygapophyseal joints. In the intact lumbar vertebral column, the primary function of the zygapophyseal joint is to protect the motion segment from anterior shear forces, excessive rotation, and

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ANATOMY THE SPINE AND TMJ

flexion. Additional functions include the production of spinal motions including coupling movements. From an anteroposterior perspective, the zygapophyseal joints of the lumbar spine appear straight, but when viewed from above, they are seen to be curved into a J or C shape. Their orientation varies both with the level and with the individual subject. It is thought that this orientation serves to restrict maximally anterior and rotary movements, and that the C-shaped joints do better in preventing anterior displacement than the J-shaped joints, because of the curvature of the joint surfaces.11 Both shapes competently prevent rotation. The area of the zygapophyseal joints most involved in resisting anterior shear forces is the anteromedial part of the superior zygapophyseal joint.

Posterior longitudinal ligament Transverse process Ligamentum flavum

Intertransverse ligament Supraspinous ligament

CLINICAL PEARL

Interspinous ligament

At the thoracolumbar junction, the morphologic configuration of the zygapophysial joints is extremely variable. In general, there is a change from a relatively coronal orientation at T10–11 to a more sagittal orientation at L1–3, before returning to the more coronal orientation at L5 and S1. A fibrous capsule surrounds the joint on all of its aspects except the anterior aspect, which consists of the LF.10 Posteriorly, the capsule is reinforced by the deep fibers of the multifidus.10 Superiorly and inferiorly, the capsule is very loose. Superiorly, it bulges toward the base of the next superior transverse process, whereas, inferiorly, it does so over the back of the lamina. In both the superior and the inferior poles of the joint capsule, there is a very small hole that allows the passage of fat from within the capsule to the extracapsular space.10 Within the zygapophyseal joints, there are intra-articular meniscoids. It is thought that the function of these intraarticular meniscoids is to fill the joint cavity; ▶▶ increase the articular surface area without reducing flexibility; ▶▶ protect the articular surfaces, as they become exposed during extreme flexion and extension. ▶▶

Ligaments Anterior Longitudinal Ligament

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Anterior longitudinal ligament

The anterior longitudinal ligament (ALL) covers the anterior aspects of the vertebral bodies and IVD (Fig. 28-2). The ALL extends from the sacrum along the anterior aspect of the entire spinal column, becoming thinner as it ascends.10 The ALL is connected only indirectly with the anterior aspect of the IVD by loose areolar tissue.10 Some of the ligament fibers insert directly into the bone or periosteum of the centrum. Because of these attachments, and the pull on the bone from the ligament, it is proposed that the anterior aspect of the vertebral body becomes the site for osteophytes. The remaining ligament fibers cover two to five segments, attaching to the upper and lower ends of the vertebral body.

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FIGURE 28-2 Ligaments of the lumbar spine. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

The ALL of the lumbar spine is under tension in a neutral position of the spine and functions to prevent overextension of the spinal segments. In addition, the ALL functions as a minor assistant in limiting anterior translation and vertical separation of the vertebral body. The ALL receives its nerve supply from recurrent branches of the gray rami communicantes.10

Posterior Longitudinal Ligament The PLL is found throughout the spinal column, where it covers the posterior aspect of the centrum and IVD (see Fig. 28-2). Its deep fibers span two segments; from the superior border of the inferior vertebra to the inferior margin of the superior.10 These fibers integrate with the superficial annular fibers to attach to the posterior margins of the vertebral bodies.10 The more superficial fibers span up to five segments. In the lumbar spine, the ligament becomes constricted over the vertebral body and widens out over the IVD. It does not attach to the concavity of the body but is separated from it by a fat pad, which acts to block the venous drainage through the basivertebral vein during flexion, as the ligament presses it against the opening of the vein. Although the PLL is rather narrow and is not as substantial as the ALL, it is thought to be important in preventing IVD protrusion. The PLL is innervated by the sinuvertebral nerve.10

Ligamentum Flavum The LF connects two consecutive laminae (see Fig. 28-2). This is a bilateral ligament. The medial aspect of the ligament attaches superiorly to the lower anterior surface of the lamina and the inferior surface of the pedicle.10 The LF attaches inferiorly to the back of the lamina and the pedicle of the next inferior vertebra.10

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Interspinous Ligament

Supraspinous Ligament The supraspinous ligament (SSL) (see Fig. 28-2) is broad, thick, and cord like, but it is only well developed in the upper lumbar region.10 Because this ligament is the most superficial of the spinal ligaments and the farthest from the axis of flexion, it has a greater potential for sprains. The SSL is supplied by the medial branch of the posterior (dorsal) rami.10

Iliolumbar Ligament The iliolumbar ligament is one of the three vertebropelvic ligaments, the others being the sacrotuberous and the sacrospinous ligaments. While the structure of the ILL has been shown to vary among humans, it most commonly consists of two parts: an anterior (upper) band and a posterior (lower) band.10 The iliolumbar ligament functions to restrain flexion, extension, axial rotation, and side bending of L5 on S1.17,18 The innervation of the iliolumbar ligament has been described differently by various authors. The innervation of the iliolumbar ligament appears similar to the posterior lumbar ligaments.19

Multifidus The lumbar multifidus is the largest of the intrinsic back muscles to cross the lumbosacral junction and lies most medially in the spinal gutter (Fig. 28-3).10 The lumbar

Lumbar Spine

The interspinous ligament (see Fig. 28-2) lies deeply between two consecutive spinal processes. The ligament is important for stability, as it represents a major structure for the posterior column of the spine. Unlike the longitudinal ligaments, it is not a continuous fibrous band but, instead, consists of loose tissue that fills the gap between the bodies of the spinous processes.10 The interspinous ligament most likely functions to resist separation of the spinous processes during flexion. This ligament is supplied by the medial branch of the posterior (dorsal) rami.10

The muscle is active during inspiration, fixing the lowest rib to afford a stable base from which the diaphragm can act. The importance of this muscle from a rehabilitation viewpoint is its contribution as a lumbar spine stabilizer.11 Working unilaterally, it is typically involved with side bending of the lumbar spine, especially with eccentric control of contralateral side bending. The quadratus lumborum is an important, yet often underappreciated; lateral lumbar spine stabilizer.11 The quadratus lumborum is supplied by the anterior (ventral) rami of T12–L2.10

ANATOMY

Its lateral portion attaches to the articular process and forms the anterior capsule of the zygapophyseal joint. The LF is formed primarily from elastin (80%), with the remainder (20%) being collagen.10 Thus, it is an elastic ligament that is stretched during flexion and recovers its neutral length with the neutral position, or extension. The main function of the LF is to resist separation of the lamina during flexion.

Semispinalis capitis m. Splenius capitis m. Serratus posterior superior m. Levatores costarum mm. Erector spinae mm.: Iliocostalis m. longissimus m. Spinalis m.

Rotator thoracic longi mm.

Serratus posterior inferior m.

Multifidus m.

Muscles Quadratus Lumborum The quadratus lumborum muscle is large and rectangular, with fibers that pass medially upward. The fibers attach to the anterior inferior surface of the 12th rib; the anterior surface of the upper four transverse processes; ▶▶ the anterior band of the iliolumbar ligament; ▶▶ the iliac crest lateral to the attachment of the iliolumbar ligament. ▶▶

▶▶

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FIGURE 28-3 Multifidus and erector spinae. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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ANATOMY

multifidus originates in three groups, which arise from the same vertebra. 1. Laminar fibers arise from the inferoposterior edge of the lamina. 2. Basal fibers arise from the base of the spinous process. 3. Common tendon fibers arise from a common tendon attached to the inferior tip of the spinous process.

THE SPINE AND TMJ

The lumbar multifidus has a complicated insertion (Table 28-1). Over the past several decades, there has been much research regarding the lumbar multifidus, with particular reference to its relationship to LBP, and its importance in lumbar spine stabilization.20–22 In vitro biomechanical studies have shown that the lumbar multifidus is an important muscle for lumbar segmental stability through its ability to provide segmental stiffness and to control motion.20–22 Isolated multifidus strengthening has been shown to restore the muscle size at the segmental level of the dysfunction.23 Although not considered a primary lumbar rotator, the multifidus is consistently active during both ipsilateral and contralateral spinal rotation, and both multifidi are simultaneously active regardless of which way the spine is turning.24,25 The major function of the multifidus from a biomechanical perspective is one of arthrokinematic control. It is believed that the lumbar multifidus acts as an antagonist to flexion and opposes the flexing moment of the abdominals as they rotate the trunk.24,26 This synergistic function may be compromised with an injury to the multifidus. Using magnetic resonance imaging, the signal intensities of the multifidus during lumbar hyperextension have been found to be markedly diminished in patients with chronic LBP compared with normal patients.24,26 The lumbar multifidus has the distinction of being innervated segmentally by the medial branch of the posterior (dorsal) ramus of the same level or the level below the originating spinous process.10

TABLE 28-1

Multifidus Attachments

Laminar

Basal

Common Tendon

L1; MP L3

MP L4

MP L5, S1, and PSIS

L2; MP L4

MP L5

MP S1 and anterolateral aspect of PSIS

L3; MP L5

MP S1

Inferior to PSIS and lateral sacrum

L4; MP S1

As common tendon

Sacrum, lateral to foramina

L5; common

As common tendon

Sacrum, medial to tendon foramina

MP, mammillary process; PSIS, posterior-superior iliac spine.

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Data from Meadows J, Pettman E. Manual Therapy: NAIOMT Level II & III Course Notes. Denver, CO: North American Institute of Manual Therapy, Inc., 1995; Bogduk N, Twomey LT. Anatomy and biomechanics of the lumbar spine. In: Bogduk N, Twomey LT, eds. Clinical Anatomy of the Lumbar Spine and Sacrum. 3rd ed. Edinburgh: Churchill Livingstone, 1997:2–53, 81–152, 171–176.

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Erector Spinae The erector spinae is a composite muscle consisting of the iliocostalis lumborum and the thoracic longissimus (Fig. 28-3). Both of these muscles are subdivided into the lumbar and thoracic longissimus and iliocostalis. The nerve supply to the erector spinae muscles is by the medial branch of the posterior (dorsal) ramus of the thoracic and lumbar spinal nerves. Longissimus Thoracis Pars Lumborum.  This is a fascicular muscle that arises from the accessory processes of the lumbar vertebrae to insert into the posterior-superior iliac spine (PSIS) and the iliac crest lateral to it. The upper four tendons converge to form the lumbar aponeurosis that inserts laterally to the L5 fascicle. The longissimus thoracis pars lumborum muscles have both a vertical and a horizontal vector. The vertical vector is much the larger of the two and can produce extension or side bending, depending on whether it is functioning bilaterally or unilaterally.11 Iliocostalis Lumborum Pars Lumborum.  There are four overlying fascicles arising from the tip of the upper four transverse processes and the adjoining middle layer of the thoracolumbar fascia (TLF). The fibers insert onto the iliac crest, with the lower and deeper fibers attaching lateral to the PSIS.10 There is no muscular fiber from L5, but it is believed that this is represented by the iliolumbar ligament, which is completely muscular in children, becoming collagenous by approximately 30 years of age. Longissimus Thoracis Pars Thoracis.  This muscle group consists of 11–12 pairs of muscles, which extend from the transverse processes of T2 and their ribs, and run inferomedially to attach to the spinous processes of L3–5 and the sacral spinous processes, as well as the PSIS. The orientation and various attachments of this muscle group allow it to act indirectly on the lumbar spine. The main action of the muscle appears to be the extension of the thoracic spine on that of the lumbar. Iliocostalis Lumborum Pars Thoracis.  The thoracic iliocostalis serves as the thoracic part of the iliocostalis lumborum and not the iliocostalis thoracic. This muscle completely spans the lumbar spine and is in an excellent position to extend and side bend the spine, as well as to increase the lumbar lordosis.

Abdominal Muscles Rectus Abdominis.  The rectus abdominis (Fig. 28-4) originates from the cartilaginous ends of the fifth through seventh ribs and xiphoid and inserts on the superior aspect of the pubic bone.10 The linea alba (Fig. 28-4) is the anterior abdominal aponeurosis or rectus sheath in the midline. It is formed by the interlacing of the aponeurosis of the external oblique, internal oblique (IO), and transversus abdominis (TrA) muscles from both sides. It is broader superiorly, where the recti are separated at a considerable interval, and narrower inferiorly, where the recti are closely packed (Fig. 28-4).

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ANATOMY

Pectoralis major m.

Serratus anterior m.

Linea alba

External oblique m. (cut) External oblique m.

Internal oblique m. (cut) Transversus abdominis m.

Umbilicus

Lumbar Spine

Rectus abdominis m. (covered by rectus sheath) Rectus abdominis m. (anterior layer of the rectus sheath removed)

Tendinous intersection Anterior superior iliac spine Inguinal ligament

Pyramidalis m.

Inguinal canal

A Rectus abdominis m. Linea alba

External oblique m.

Extraperitoneal fascia

Internal oblique m.

Parietal peritoneum Transversalis fascia

B

Superficial fascia: Camper’s fascia Scarpa’s fascia

Skin

Transversus abdominis m.

Aponeuroses Extraperitoneal fascia External oblique m.

Gut tube

Internal oblique m.

Visceral peritoneum

Peritoneal cavity

Transversus abdominis m.

C

Parietal peritoneum

Mesentery

Extraperitoneal fascia in the retroperitoneal space

FIGURE 28-4  Abdominal muscles. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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ANATOMY

CLINICAL PEARL A split between the two rectus abdominis to the extent that the linea alba may split under strain is known as diastasis recti (see Chapter 30).

THE SPINE AND TMJ

The rectus abdominis muscle functions to produce torque during flexion of the vertebral column, as it approximates the thorax and pelvis anteriorly. The muscle appears to serve a beneficial role in helping to stabilize the lumbar spine in the sagittal plane.23 Transversus Abdominis.  The TrA muscle (Fig. 28-4) originates from the lateral one-third of the inguinal ligament, the anterior two-thirds of the inner lip of the iliac crest, the lateral raphe of the TLF, and the internal aspects of the lower six costal cartilages, where it interdigitates with the diaphragm.27 Its upper and middle fibers run transversely around the trunk and blend with the fascial envelope of the rectus abdominis muscle, while the lower fibers blend with the insertion of the IO muscle on the pubic crest.28 A number of differences in the fiber orientation of the upper, middle, and lower regions of the TrA have been noted29: Upper fibers: these fibers, which include the fibers from the sixth costal cartilage to the inferior border of the rib cage, have been found to be oriented superomedially. ▶▶ Middle fibers: these fibers, which include the fibers from the inferior border of the rib cage to a line connecting the superior borders of the iliac crest, have been found to be oriented inferomedially. ▶▶ Lower fibers: these fibers, which include those from the iliac crest and the pubic symphysis, were found to be oriented more inferomedially than the middle fibers. ▶▶

Although much emphasis has traditionally been placed on the strengthening of the rectus abdominis during lumbar spine rehabilitation, attention has switched to the contraction of the hoop-like TrA that creates a rigid cylinder, resulting in enhanced stiffness of the lumbar spine and stabilization of the lumbar motion segment (see “Biomechanics” section).30 Since the midportion of the TrA attaches to the cross-hatch arrangement of the middle layer of the TLF (see later), contraction of the TrA has been thought to increase spinal stability and motor control via tensioning of the TLF in the middle and lower regions of the lumbar spine or by producing a mild stabilizing compressive force on the lumbar vertebrae.23,27 The TLF creates a pressurized visceral cavity anterior to the spine when the TrA contracts. This force is theorized to increase the stability of the lumbar spine during a variety of postures and movements.

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Internal Oblique.  The IO (see Fig. 28-4), which forms the middle layer of the lateral abdominal wall, is located between the TrA and the external oblique muscles. It has multiple attachments to the inguinal ligament, lateral raphe, iliac crest, pubic crest, TrA, and costal cartilages of the seventh through ninth costal cartilages. Because of these multiple attachment sites, the different fascicles of the muscle can have very different force vectors. The IO is active during a number of functions, including gait (most often close to initial contact31) and erect sitting

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and standing postures.32 Acting bilaterally, the IOs flex the vertebral column and assist in respiration. Acting in unison, the muscle, in conjunction with the external obliques, can produce rotation of the vertebral column, bringing the thorax backward (when the pelvis is fixed) or the pelvis forward (when the thorax is fixed).33 External Oblique.  The external oblique (see Fig. 28-4) originates from the lateral aspect of the fifth through 12th ribs, and through interdigitations with the serratus anterior and latissimus dorsi. The muscle travels obliquely, medially, and inferiorly to insert into the linea alba, inguinal ligament, anterior superior iliac spine (ASIS), iliac crest, and pubic tubercle. When acting bilaterally, the external obliques flex the vertebral column and tilt the pelvis posteriorly. Acting in unison, the muscle, in conjunction with the IOs, can produce side bending of the vertebral column, approximating the thorax and the iliac crest laterally.10

Psoas Major Although traditionally viewed as a muscle of the hip, the psoas major muscle combines with the iliacus muscle to directly attach the lumbar spine to the femur.10 The psoas major originates from the anterolateral aspects of the vertebral bodies; IVDs of T12–L5; ▶▶ transverse processes of L1–5; ▶▶ tendinous arch spanning the concavity of the sides of the vertebral bodies. ▶▶ ▶▶

The iliacus is attached superiorly to the iliac fossa and the inner lip of the iliac crest. Joining with the psoas major, the combined tendon passes over the superior lateral aspect of the pubic ramus and attaches to the lesser trochanter of the femur. Taken individually, the iliacus and psoas major serve different functions. The psoas major is electromyographically active in many different positions and movements of the lumbar spine, and its activity can add a stabilizing effect on the lumbar spine with compressive loading.11 With the foot fixed on the ground (closed chain), contraction of the psoas major increases the flexion of the lumbar–pelvic unit on the femur.34 ▶▶ With the foot fixed on the ground, contraction of the iliacus produces an anterior torsion of the ilium and extension of the lumbar zygapophyseal joints. If there is a decrease in the length of the iliopsoas as a result of adaptive shortening or increased efferent neural input to the muscle, the result is an anteriorly rotated pelvis and an increase in lordosis. ▶▶

From a clinical perspective, the iliacus and psoas major usually are considered together as the iliopsoas. Working bilaterally (insertion fixed), the iliopsoas can produce flexion of the trunk on the femur as in the sit-up from a supine position, or in bending over to touch one’s toes. The iliopsoas muscle also side bends the spine ipsilaterally.11 Working from a stable spine above (origin fixed), the iliopsoas muscle flexes the hip joint by flexing the femur on the trunk. The iliopsoas is innervated by the anterior (ventral) rami of L1 and L2.

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The TLF travels from the spinous process of T12 to the PSIS and iliac crest.10 The functions of the TLF are varied. The TLF11:

The nerve supply to the lumbar spine follows a general pattern. The outer half of the IVD is innervated by the sinuvertebral nerve and the gray rami communicantes, with the posterolateral aspect innervated by both the sinuvertebral nerve and the gray rami communicantes. The lateral aspect receives only sympathetic innervation.10 The zygapophyseal joints are innervated by the medial branches of the posterior (dorsal) rami.10 Each joint receives its nerve supply from the corresponding medial branch above and below the joint. For instance, the L4–5 joint receives its nerve supply from the medial branches of L3 and L4. The lateral branches cross the subjacent transverse process and pursue a sinuous course inferiorly, laterally, and posteriorly through the iliocostalis lumborum.10 They innervate that muscle, and eventually the L1–3 lateral branches pierce the posterior (dorsal) layer of TLF and become cutaneous, supplying the skin over the lateral buttock as far as the greater trochanter.10

provides muscle attachment for the TrA; stabilizes the spine against anterior shear and flexion moments; ▶▶ resists segmental flexion via tension generated by the TrA on the spinous process; ▶▶ assists in the transmission of extension forces during lifting activities. The posterior ligamentous system has been proposed as a model to explain some of the forces required for lifting. ▶▶ ▶▶

Lumbopelvic Fascia The lumbopelvic fascia connects the proximal structures of the trunk to the hip girdle. The TrA, obliques, erector spinae, and multifidus all have attachments with the lumbopelvic fascia and connect the latissimus dorsi superiorly to the gluteal muscles inferiorly. It has been theorized that the lumbar fascia has a specialized function as an elastic structure storing energy from isometric actions of the latissimus dorsi and contralateral gluteus maximus during ambulation.35 The latissimus dorsi and gluteus maximus are linked through this structure and provide a “pathway for uninterrupted mechanical transmission between pelvis and trunk” through four muscular “slings.”36,37 The anterior oblique system, which is comprised of the external oblique, contralateral IO, and contralateral adductors. This system contributes to the stability of the pubic symphysis and sacroiliac joint. ▶▶ The posterior oblique system, which is comprised of the latissimus dorsi, contralateral gluteus maximus, and TLF. This system contributes to the stability of the sacroiliac joint and is a significant contributor to load transference through the pelvic girdle during rotational activities and gait. The fibers of the latissimus dorsi and contralateral gluteus maximus are in line with each other, and perpendicular to the sacroiliac joint, providing external support. ▶▶ The deep longitudinal system, which is comprised of the erector spinae, sacrotuberous ligament, multifidus, biceps femoris, fibularis (peroneus) longus, and anterior tibialis. This system is engaged when the foot is in contact with the ground and serves to transmit energy from the upper trunk through the thoracic or lumbar fascia and erector spinae muscles to the biceps femoris and the lower extremity musculature. ▶▶ The lateral system, which is comprised of the gluteus medius and minimus, contralateral adductors, and contralateral quadratus lumborum. The muscles of this system provide essential frontal plane stability by indirectly facilitating pelvic girdle control during standing and ambulation. ▶▶

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Lumbar Spine

Nerve Supply of the Lumbar Segment

BIOMECHANICS

Thoracolumbar Fascia

Lumbar Spine Vascularization The blood supply to the lumbar spine is provided by the lumbar arteries (Fig. 28-5), and its venous drainage occurs via the lumbar veins (Fig. 28-5).

BIOMECHANICS Physiologic motions at the lumbar spine joints can occur in three cardinal planes: sagittal (flexion and extension), coronal (side bending), and transverse (rotation). Including accessory motions, six degrees of freedom are available at the lumbar spine. The amount of segmental motion at each vertebral level varies. Most of the flexion and extension of the lumbar spine occurs in the lower segmental levels, whereas most of the side bending of the lumbar spine occurs in the midlumbar area.27,38 Rotation, which occurs with side bending as a coupled motion, is minimal and occurs most at the lumbosacral junction.27,38 The amount of range available in the lumbar spine generally decreases with age.

Flexion The lumbar spine is well designed for flexion, which is its most commonly used motion in daily activities. Flexion of the lumbar spine from erect standing involves an unfolding or straightening of the lumbar lordosis, followed by, at most, a small reversal of the lordotic curve.39 During lumbar flexion in standing, which normally is initiated by the abdominal muscles, the entire lumbar spine leans forward, and there is a posterior sway of the pelvis as the hips flex.

CLINICAL PEARL Flexion of the lumbar spine can also occur with a posterior pelvic tilt. The posterior pelvic tilt can be performed voluntarily, or it may occur as a result of weak paraspinal extensor muscles or adaptively shortened hamstring and gluteal muscles.

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BIOMECHANICS

Left subclavian a.

THE SPINE AND TMJ

Internal thoracic a.

Intercostal a.

Internal thoracic a. and v.

Superior epigastric a.

Intercostal v., a., and n.

Aorta

Internal oblique m.

Lumbar a.

Rectus abdominis m. External oblique m. Transversus abdominis m. Inferior epigastric a. and v.

Inferior epigastric a.

Superficial circumflex iliac a.

Superficial circumflex iliac a. and v. Superficial epigastric a. and v.

Superficial epigastric a. Femoral a.

FIGURE 28-5  Vasculature of the spine. (Reproduced with permission from Morton DA, Foreman KB, Albertine KH. The Big Picture: Gross Anatomy. 2nd ed. New York, NY: McGraw-Hill Education; 2019.)

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Extension

Axial Rotation During axial rotation, which produces torsion of the IVD, those collagen fibers of the AF that are orientated in the same direction as the twist are stretched and resist the torsional force, while the others remain relaxed, thereby sharing the stress of twisting. Rotational movements of the lumbar spine do appear to produce the appropriate motor patterns for optimal trunk muscle cocontraction and spinal stability. The axis of rotation in the sagittal plane passes through the anterior aspect of the IVD and vertebral body.

Side Bending Side bending is a complex and highly variable movement involving lateral flexion and rotatory movements of the interbody joints and a variety of movements at the zygapophyseal joints.39 The means of how this is achieved has been the subject of debate for many years, and it is difficult to ascertain how an impaired segment would behave, compared with a healthy one. The general pattern of coupled motion is for side bending to be associated with contralateral axial rotation at the mid and upper lumbar levels but ipsilateral axial rotation at L5–S1.39 However, there is at present little evidence for strict rules of coupled motion that determine whether an individual has abnormal ranges or directions of coupling in the lumbar spine.39,40 Bending motions can occur in any direction, producing both a rocking motion and a translation shearing effect on the IVD. The NP tends to be compressed and the AF buckles in the direction of the rocking motion, and there is a

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Axial Loading (Compression) Axial compression or spinal loading occurs in weight bearing, whether in standing or sitting. It has been demonstrated experimentally that the AF, even without the NP, can withstand the same vertical forces that an intact disk can for short periods, provided that the lamellae do not buckle. However, if the compression is prolonged or if the lamellae are not held together, the sheets buckle and the system collapses on itself. The extent and magnitude of the compression depend on the amount of applied compressive force, the disk height, and the cross-sectional area of the disk. Variations in disk height can be divided into two categories: primary disk height variations and secondary disk height changes. Under normal circumstances, the NP acts like a sealed hydraulic system. The NP is deformable but relatively incompressible. Therefore, when a load is applied to it vertically, the nuclear pressure rises, absorbing and transmitting the compression forces to the vertebral end plates and the AF. The peripheral pressure increases the tension on the collagen fibers, which resist it until a balance is reached, at the point when the radial pressure is matched by the collagen tension.27 This equilibrium achieves two things:

Lumbar Spine

Extension movements of the lumbar spine produce a converse of those that occur in flexion. Theoretically, true extension of the lumbar spine is pathologic and depends on one’s definition: pure extension involves a posterior roll and glide of the vertebra and a posterior and inferior motion of the zygapophyseal joints, but not necessarily a change in the degree of lordosis. During lumbar extension, the inferior zygapophyseal joint of the superior vertebra moves downward, impacting with the lamina below and producing a buckling of the interspinous ligament between the two spinous processes. An anterior pelvic tilt increases the lumbar lordosis and results in an anterior motion of the vertebrae and their associated structures. Although the differing terminology between true extension and the extension created by increasing the lordosis is seemingly esoteric, there are clinical implications during the examination, when the clinician is assessing the ability of the patient to assume the extended position of the lumbar spine.

tendency for the AF to be stretched in the opposite direction, while the pressure on the posterior aspect of the NP is relieved.

BIOMECHANICS

At the segmental level, lumbar flexion produces a combination of an anterior roll and an anterior glide of the vertebral body, and a straightening, or minimal reversal, of the lordosis.27,38

1. Pressure is transferred from one end plate to another, thus relieving the load on the AF. 2. The NP braces the AF and prevents it from buckling under the sustained axial load.

Lumbar Stabilization Muscle activity is available and required in the lumbar spine throughout the ROM, except in specific situations, such as at the end of lumbar flexion ROM when a reflex reduction in paraspinal muscle activity occurs, the so-called “flexion relaxation phenomenon.”32,41,42 At the end of spinal ROM, the restraints to bending, rotation, and shear forces are provided largely by tension and compression on the spine’s passive structures. Mobilizer muscles, which tend to work over two joints or several segments, are superficial, and have narrow insertions with long tendons.43 The mobilizer muscles function to produce movement in the sagittal plane using concentric acceleration and are capable of generating a tremendous amount of force (see Chapter 22). The stabilizer muscles, as their name suggests, provide stabilization, and can be either local or global (see Chapter 22). The local muscle system is important for the provision of segmental control to the spine and provides an important stiffening effect on the lumbar spine, thereby enhancing its dynamic stability. The local stabilizers also function to maintain a continuous low-force activity at joints in all positions and directions and thus provide segmental joint support. Two prominent and similar theories for active lumbar stabilization are the bracing mechanisms, proposed by

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EXAMINATION

McGill,44 and the deep corset mechanism, proposed by Richardson et al.45 ▶▶

THE SPINE AND TMJ ▶▶

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Bracing mechanism: muscles act similar to guy wires when stabilizing the spine and that a loss of tension can result in unstable buckling of the spinal structures. The muscles of the trunk function via a complex interaction of agonist/antagonist spinal muscles, both segmentally and regionally to provide tension (active stiffness). According to this theory lightly pretensioning, or bracing, the abdominal muscles using an isometric contraction is a way to enhance the guy wire affect by taking up the slack prior to activities that may destabilize the spine.46 The external oblique, IO, and TrA overlay each other to create the abdominal wall and act through attachments to the abdominal and TLF to create a cylinder. As the intra-abdominal pressure increases, the three-dimensional force per unit area exerted on the spine also increases, potentially constraining spinal movement in all directions. Deep corset mechanism: Richardson et al.45 have proposed that a pressure corset is formed by the muscles of the lumbar spine. Under this proposal, the TrA forms the wall of the cylinder, and the muscles of the pelvic floor and diaphragm form the base and lid, respectively. Within this system, the intra-abdominal pressure group is maintained at a level that provides spinal support. Since the abdominal cavity has a finite volume, the intra-abdominal pressure (force/area) will increase if the abdominal cavity volume is reduced (contraction of the muscles in the pelvic floor, abdominal muscles and diaphragm, and the wearing of a lumbar corset) In addition, the increase in intra-abdominal pressure is thought to provide a mild distractive force to the spinal segments, due to separation of the pelvic floor and diaphragm. Because intra-abdominal pressure and fascial tension are important for the control of intervertebral motion, the muscles that surround the abdominal cavity, such as the diaphragm and the pelvic floor muscles (see Chapter 29), provide an additional contribution. These two muscle groups also have important respiratory and continence functions. Theoretically, reduced contribution of the diaphragm to spinal stability may occur during periods of increased respiratory demand. As the diaphragm descends during inspiration, intra-abdominal pressure increases provided that the musculature of the abdominal and pelvic floor maintains its respective tension.

Conflicting evidence exists on what strategy is the most effective in preventing back injury during lifting. Although lifting from a squat position, using the legs, with the lumbar spine maintained in lordosis is a commonly taught strategy, there is little evidence to support that this posture reduces compressive and shear forces acting on the spinal segments.47 Existing evidence suggests that compressive and shear forces acting on the lumbar spine are most influenced by load moment, lifting speed, and acceleration.48 A study by Kigma et al.47 showed that the width of an object and the height from which an object is lifted are more important determinants of

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forces acting on the lumbar spine than the strategy used to perform the lift. The study further suggests that squatting may be an effective technique to reduce compressive forces acting at L5–S1 when lifting narrow loads, such as those loads that can be placed between the feet, but straddling and stooping techniques are more effective at reducing compressive forces when lifting wider loads from the floor.47 Although current training programs for lifting focus on maintaining the load’s proximity to the body’s center of gravity (COG), minimizing trunk rotation, matching the load magnitude to the lifter’s capacity, and avoiding fatigue, it remains unclear the role that breath control may play in achieving lumbar segmental control during lifting tasks.49 An intriguing study by Hagins and Lamberg49 reported that individuals with LBP performed a lifting task with more inhaled lung volume than individuals without LBP. It would appear that lumbar stability is maintained in vivo by increasing the activity (stiffness) of the lumbar segmental muscles (local muscle system), and the degree of motor control to coordinate muscle recruitment between large trunk muscles (the global muscle system) during functional activities to ensure that mechanical stability is maintained.42 The scientific literature reports varying disruptions in patterns of recruitment and cocontraction within and between different muscles synergies such as pain, and a loss of strength, endurance, and muscle atrophy.42

EXAMINATION Given the numerous causes and types of LBP, it is imperative that any clinician examining and treating the lower back have a sound understanding and knowledge of the anatomy and biomechanics of this region. Although this knowledge is not the sole determinant of the approach to LBP, it does provide a solid framework on which to build successful management. There have also been moves toward the design of clinical prediction rules (CPRs) (see Chapter 5) on how best to treat patients with LBP (see “Intervention” section). LBP can arise from a number of local structures in the lumbar spine and a number of sources more distal (see Chapter 5). A number of local structures have been found to cause LBP when stimulated. Theoretically any innervated structure in this area can cause symptoms so the distributions and descriptions of referred symptoms must always be considered in relation to the neurologic supply of the lumbar segment. Idiopathic and nonspecific LBP have emerged as catchall terms in the diagnosis of low-back dysfunction. Indeed, up to 85% of patients cannot be given a definitive diagnosis because of weak associations among symptoms, pathologic changes, and imaging results. Muscle aches, muscle sprains, tendinitis, sacroiliac and low-back sprain, lumbago, mechanical LBP, and lumbar strain are just some of the diagnoses currently in clinical use. This difficulty in determining a specific diagnosis stems from a variety of reasons, including the fact that multiple structures in one or more segments may be involved. These structures include the interconnecting ligaments, the

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Radiating pain.  LBP radiating to a leg seems to be a more persistent and severe type of pain than nonspecific LBP. This type of pain is frequently referred to as sciatica, an arcane but encompassing term used to describe all forms of radiating leg pain, but the term is neither diagnostic nor epistemologically accurate due to a lack of consensus over a universally accepted definition, the absence of widely accepted diagnostic criteria, and a poor understanding of the underlying pathophysiology, as sciatica can have a number of causes (Table 28-2).55,56 The current definition of sciatica considers it a disease of the peripheral nervous system57 and the use of the term in this text follows this definition. Whatever the cause, sciatic pain causes more disability and longer absence from work than non-sciatic pain.58,59 ▶▶ Smoking.  It has been suggested that smoking accelerates degeneration by impairing the blood supply to the vertebral body and nutrition of the IVD.60 Smoking also ▶▶

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Some Causes of Sciatica

Nerve root compression  Tumor  Abscess  Arthritis   Vertebral collapse   Inflammatory synovitis Inflammatory disease of nerve   Toxins (alcohol and heavy metals)   Diabetes mellitus  Syphilis Data from Judge RD, Zuidema GD, Fitzgerald FT, eds. Clinical Diagnosis. 4th ed. Boston, MA: Little, Brown and Company; 1982.

increases coughing activity, which causes an increase in intradiscal pressure. Also, it has been hypothesized that the high serum proteolytic activity in the blood of cigarette smokers gains access to a previously degenerated neovascularized disk and accelerates the degenerative process. Increased proteolytic activity may also weaken the spinal ligaments, resulting in spinal instability.61 However, besides its direct harmful effects, and its link to other health risk factors as well as lifestyle and behavioral patterns, no substantive evidence appears to support smoking as a definitive cause of LBP. ▶▶ Obesity.  There are several hypotheses relating to a link between obesity and LBP due to the increased mechanical demands causing LBP through excessive wear and tear. A 2018 meta-analysis concluded that being overweight is a risk factor for LBP in men and women.62 ▶▶

Psychological factors.  Four explanations for the association between psychosocial work characteristics and musculoskeletal symptoms have been suggested63: (1) psychosocial work characteristics can directly influence the biomechanical load through changes in posture, movement, and exerted forces; (2) these factors may trigger physiologic mechanisms, such as increased muscle tension or increased hormonal excretion, that may, in the long term, lead to organic changes and the development or intensification of musculoskeletal symptoms or may influence pain perception and thus increase symptoms; (3) psychosocial factors may change the ability of an individual to cope with an illness, which, in turn, could influence the reporting of musculoskeletal symptoms; and (4) the association may well be confounded by the effect of physical factors at work. It seems plausible that psychosocial factors in private life also could affect musculoskeletal symptoms through the second and third mechanism.63 Studies have also found an effect of low workplace-social support and low job satisfaction. However, the effect found for low job satisfaction may be a result of insufficient adjustment for psychosocial work characteristics and physical load at work.63 Although psychological factors, like obesity, appear to have a meaningful effect on the duration of LBP, they do not cause LBP.

Lumbar Spine

Genetics.  A number of studies50–52 have suggested that genetic factors play an important role in the development of lumbar disk degeneration, but their role in the cause of clinical LBP is unclear. ▶▶ Age older than 40 or 50 years.  The relation between chronic LBP and age over 40 or 50 years with a decrease of occurrence over 60 years is considered as an established fact because the severity of the radiographic abnormalities makes it logical to infer a cause-and-effect correlation, but the evidence to support these assumptions (with the exception of some degenerative changes) has been inconclusive. ▶▶ Low level of formal education and social class.  For back pain, specifically, some studies have found an inverse relation of formal education, social class, or both to the prevalence of back pain symptoms.53 A tentative conclusion, although not based on an extensive literature review, indicates that lower levels of socioeconomic status and education are better predictors of adverse prognosis for occupational disability from back pain than are risk factors per se.54 ▶▶ Physical workload.  From a number of studies that examined the relation between physical and psychosocial load at work and the occurrence of LBP, it has been concluded that both work-related physical factors of flexion and rotation of the trunk and lifting at work, and low job satisfaction, are risk factors for sickness absence resulting from LBP.53 Physical load on the back has commonly been implicated as a risk factor for LBP and, in particular, for work-related LBP. Repeated lifting of heavy loads is considered a risk factor for LBP, especially if combined with side bending and twisting. ▶▶

TABLE 28-2

EXAMINATION

outer fibers of the annulus fibrosus, zygapophyseal joints, vertebral periosteum, paravertebral musculature and fascia, blood vessels, and spinal nerve roots. A number of associated occupational, psychosocial, and environmental factors can be used to help predict the development of a complicated course of LBP. These include the following:

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EXAMINATION

▶▶

Comorbidity.  Comorbidity may slow or interfere with normal recovery from back pain and may affect an individual’s general sense of health, leading to a decreased self-perception of capability.64

A recent report issued by the Agency for Health Care Policy and Research, now known as the Agency for Healthcare Research and Quality, suggests grouping back pain into five broad categories65: potentially serious spinal conditions such as a spinal tumor, infection, fracture, and cauda equina syndrome. Although the likelihood of a low-back syndrome due to a serious condition is low, the consequences of a missed diagnosis or delayed treatment can be quite costly in terms of prolonged morbidity and, in the extreme, mortality.65 ▶▶ nonspinal causes secondary to abdominal involvement (gallbladder, liver, renal, pelvic inflammatory disease, prostatic carcinoma, ovarian cyst, uterine fibroids, aortic aneurysm, or thoracic disease); ▶▶ sciatica and dural tissue compromise; ▶▶ nonspecific back symptoms, the majority of which are mechanical in nature; ▶▶

THE SPINE AND TMJ

▶▶

psychological causes such as stress and work environment (disability, workers’ compensation, and secondary gain).

CLINICAL PEARL The physical examination of the lumbar spine must include a thorough assessment of the neuromuscular, vascular, and orthopaedic systems of the hip, lower extremities, low back, and pelvic region.66 Figure 28-6 depicts a simple algorithm for decision making during the examination of the lumbar spine.

History The clinician should establish the chief complaint of the patient, in addition to the location, behavior, irritability, and severity of the symptoms. Although dysfunctions of the lumbar spine are very difficult to diagnose, the history can provide some very important clues (Table 28-3). Applying the principles and rationale outlined in Chapters 4 and 5, the clinician uses the history to help with differential diagnosis. A useful organizational acronym for this purpose is LOP4QRST, which represents the following descriptors65: location; onset; ▶▶ prior history/treatment; ▶▶ palliative measures (including medications); ▶▶ provocative factors (including movement/positional factors); ▶▶ progression/course; ▶▶ the quality of symptoms; ▶▶ referral patterns; ▶▶ severity; ▶▶ temporal factors. ▶▶ ▶▶

A lower back medical screening questionnaire is provided in Table 28-4. ▶▶

Location.  Back pain may be localized centrally, unilaterally, or bilaterally. Differential diagnosis should include certain gastrointestinal conditions such as inflammatory bowel disease, appendicitis, or cholelithiasis. Generally speaking, the stronger the pain stimulus, the larger the area of pain reference will be. As the stimulus intensity decreases, the referred pain

LOW BACK ALGORITHM

Do positions, postures, activities, or specific movements increase or decrease the patient's symptoms, and/or produce sciatica?

Are the patient's symptoms unchanged with positions, postures, activities, or specific movements?

Is there evidence of a serious, systemic, (Drop foot, loss of bowel and/or bladder function, areflexia, hyperreflexia, unexplained weight loss, etc.) or psychosomatic component

(This suggests a mechanical, or postural dysfunction)

(This suggests an acute, inflammatory dysfunction)

(This suggests a diagnosis that requires immediate medical intervention)

Referral to Physical Therapy

Rest for 24–48 hours Ice packs Medrol dose packs NSAIDS

Better

Worse

Physical Therapy trial for 4–6 visits

Referral to specialist Referral to Physical Therapy

Physical therapy report with recommendations within 24–48 hours

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FIGURE 28-6  Examination algorithm for the low back.

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Reliability of the Historical Examinationa

Historical Question

Kappa Value or % Agreement

Patient report of (McCombe et al.)   Foot pain   Leg pain   Thigh pain   Buttock pain   Back pain

Group 1:50 patients with low-back pain

Interexaminer reliability   κ = 0.12, 0.73   κ = 0.53, 0.96   κ = 0.39, 0.78   κ = 0.34, 0.44   κ = 0.19, 0.16

Pain ever below the knee Pain ever into the foot Numbness below knee (Waddell et al.)c

475 patients with back pain

Test–retest among patient questionnaire   Agreement 100%   Agreement 92%   Agreement 95%

Increased pain with (Roach et al.)d Sitting  Standing  Walking

53 subjects with a primary complaint of low-back pain 

Test–retest among patient questionnaire   κ = 0.46   κ = 0.70   κ = 0.67

Increased pain with (Vroomen et al.)e  Sitting  Standing  Walking   Lying down

A random selection of 91 patients with low-back pain

Interexaminer reliability   κ = 0.49   κ = 1.0   κ = 0.56   κ = 0.41

Pain with sitting (Van Dillen et al.)f

95 patients with low-back pain

Interexaminer reliability κ = 0.99, 1.0

Pain with bending (Van Dillen et al.)f

 

Interexaminer reliability κ = 0.98, 0.99

Pain with bending (Roach et al.)d

53 subjects with a primary complaint of low-back pain

Test–retest among patient questionnaire   κ = 0.65

Pain with bending (McCombe et al.)b  

Group 1:50 patients with low-back pain Group 2:33 patients with low-back pain

Interexaminer reliability   κ = 0.51, 0.56

Increased pain with coughing/sneezing (Vroomen et al.)e

A random selection of 91 patients with low-back pain

Interexaminer reliability κ = 0.64

Increased pain with coughing (Roach et al.)d

53 subjects with a primary complaint of low-back pain

Test–retest among patient questionnaire   κ = 0.75

Pain with pushing/lifting/carrying (Roach et al.)d

 

Test–retest among patient questionnaire   κ = 0.77, 0.89

Sudden or gradual onset of painc

475 patients with back pain

Test–retest among patient questionnaire Agreement = 79%

  Group 2:33 patients with low-back pain

Lumbar Spine

Population b

EXAMINATION

TABLE 28-3

a

Data from Cleland J. Thoracolumbar Spine, Orthopaedic Clinical Examination: An Evidence-Based Approach for Physical Therapists. Carlstadt, NJ: Icon Learning Systems, LLC; 2005:166–167. b Data from McCombe PF, Fairbank JCT, Cockersole BC, et al. Reproducibility of physical signs in low back pain. Spine. 1989;14:908–918. c Data from Waddell G, Main CJ, Morris EW, et al. Normality and reliability in the clinical assessment of backache. BMJ. 1982;284:1519–1523. d Data from Roach KE, Brown MD, Dunigan KM, et al. Test–retest reliability of patient reports of low back pain. J Orthop Sports Phys Ther. 1997;26:253–259. e Data from Vroomen PC, de Krom MC, Knottnerus JA. Consistency of history taking and physical examination in patients with suspected lumbar nerve root involvement. Spine. 2000;25:91–96; discussion 97. f Data from Van Dillen LR, Sahrmann SA, Norton BJ, et al. Reliability of physical examination items used for classification of patients with low back pain. Phys Ther. 1998;78:979–988.

area becomes smaller, and localization of the pain by the patient becomes easier for the patient. The distribution of the pain should be described by the patient and outlined on a pain diagram. Central back pain is unlikely to be caused by a unilateral structure, such as a zygapophyseal joint or the sacroiliac joint, and bilateral pain hardly ever

Dutton_Ch28_p1335-p1416.indd 1349

has a central origin (one of the exceptions being a central IVD protrusion). ▶▶ An inflammation of the zygapophyseal joints can cause local back pain or buttock pain, but it also has been associated with pain referred to the buttocks and even below the knee.67,68

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EXAMINATION



TABLE 28-4

 edical Screening Questionnaire for the M Low-Back Region

 

THE SPINE AND TMJ

Have you recently had a major trauma, such as a vehicle accident or a fall from a height? Have you ever had a medical practitioner tell you that you have osteoporosis? Do you have a history of cancer? Do you have pain at night that wakes you up? Does your pain ease when you rest in a comfortable position? Have you recently had a fever? Have you recently lost weight even though you have not been attempting to eat less or exercise more? Have you recently taken antibiotics or other medications for an infection? Have you been diagnosed as having an immunosuppressive disorder? Have you noticed a recent onset of difficulty with retaining your urine? Have you noticed a recent need to urinate more frequently? Have you noticed a recent onset of numbness in the area where you would sit on a bicycle seat? Have you recently noticed your legs becoming weak while walking or climbing stairs?

Yes

No  

Data from Bigos S, Bowyer O, Braen G, et al. Acute Low Back Problems in Adults, AHCPR Publication 95–0642. Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, U.S. Department of Health and Human Services, 1994; Wilmarth MA, ed. Medical Screening for the Physical Therapist. Orthopaedic Section Independent Study Course 14.1.1. La Crosse, WI: Orthopaedic Section, APTA, Inc., 2003:1–44.

Groin pain, although also associated with hip pathology and other conditions, is a complaint often present in patients with a high lumbar IVD herniation. On questioning, patients with this form of groin pain often describe the pain as a dull ache lying deep beneath the skin, which they usually find difficult to localize with any degree of accuracy. ▶▶ Leg pain reported by the patient may indicate a radiculopathy or a pseudoradiculopathy. Conditions that may result in radicular symptoms include inflammatory irritation due to tissue injury, disk herniation, and subsequent nerve root irritation. In general, with a disk protrusion, the presence of leg pain indicates a larger protrusion than does back pain alone.69 Other conditions capable of producing radicular-like symptoms include arthrosis involving the facet joints or vertebral body–disk interface, spinal hematoma, and congenital or acquired central or lateral canal stenosis.65 A pseudoradiculopathy, as its name suggests, is pain that is radicular in distribution but is caused by something other than those conditions mentioned. The clinician should also ask the patient about any difficulty with coughing, sneezing, or ▶▶

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abdominal straining (Dejerine’s triad), each of which causes an increase in intrathecal pressure that may provoke radicular symptoms.65 Patients with bilateral root pain should be suspected of having a central disk protrusion, spondylolisthesis, bilateral stenosis of the lateral spinal recesses, a narrowed spinal canal, or malignant disease. ▶▶ Onset.  When did the problem begin, how long has the patient had the problem? Low-back disorders may be acute, chronic, or recurrent. If possible, the clinician should attempt to order the onset of symptoms chronologically and then determine what has occurred to the symptoms since the onset. The mechanism of injury for the lumbar spine usually involves lifting, bending, or twisting, or a combination of all three. However, postural ligamentous pain tends to be more frequent in patients who stand or sit for long periods at work. If an obvious cause is reported, the clinician should confirm the direction, amount, and duration of any forces involved. The forces applied to the lumbar spine and IVD vary according to the task or position of the body (Table 28-5). In general, a sudden onset of pain associated with an activity or movement suggests a ligament, muscle, or IVD as the source, whereas a gradual onset of symptoms suggests a degenerative process or a lesion that is increasing in size, such as a neuroma or neoplasm. While pain is suggestive of mechanical or chemical irritation, paresthesia, anesthesia, and weakness are attributed to decreased nerve or arterial function due to compression, constriction, or other blockage.65 If the onset of symptoms in a female patient is cyclical in nature, the clinician should consider certain gynecologic conditions including endometriosis, pelvic inflammatory disease, and pregnancy. The frequency of the episodes often can give the clinician an indication of severity. Stable episodes of symptoms (e.g., symptoms that only occur every few years and do not change much in severity with each episode) are generally easier to



TABLE 28-5

I ntradiskal Pressures and Forces Generated by Common Tasks

Task

Total Load (kg)a

Lying supine

25

Side lying

75

Standing

150

Bending at waist in standing position

200

Sitting

175

Bending at waist in sitting position

225

a

Represents total load on third lumbar disk in a 70-kg subject.

Data from Nachemson A. Disc pressure measurements. Spine. 1981;6:93–97; Nachemson A, Morris JM. In vivo measurements of intradiscal pressure. J Bone Joint Surg. 1964;46:1077; Nachemson A. Lumbar intradiscal pressure. In: Jayson MIV, ed. The Lumbar Spine and Back Pain. Edinburgh: Churchill Livingstone; 1987:191–203.

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Pathology of nonmechanical origin is usually nonresponsive to provocative movement and may be negatively responsive to positional changes, as in the case of sepsis within the abdominal cavity and neoplastic activity.65,76 ▶▶

Provocative factors (Table 28-6).  Information about the activities or positions that aggravate or relieve the symptoms provides the clinician with an insight as to whether the patient has a mechanically related disorder or one that is nonmechanical. In general, musculoskeletal

Dutton_Ch28_p1335-p1416.indd 1351

Relieving Positions or Movements

Relieving Position or Movement

Probable Cause

Flexion 

Facet joint involvement Low-back strain Lateral stenosis

Extension

Disk involvement Nerve root irritation (disk herniation)

Rest

Neurogenic claudication

pain is reduced with rest although it is worth remembering that in postural syndromes, the symptoms are usually increased by the maintenance of a particular posture and relieved by altering the position. For example, if the patient complains of pain with standing with the feet together, the cause of the pain could be stresses on the structures caused by an increased lordosis, especially if the pain is reduced by placing one foot in front of the other, or if the pain is reduced when the lumbar lordosis is reduced with an active posterior pelvic tilt. Pain that is relieved by sitting and forward bending but aggravated by walking may indicate a zygapophyseal joint problem, spondylolisthesis (in the younger patient), or lateral recess or spinal stenosis (in the elderly patient). Pain that is aggravated by sitting, stooping, or lifting, but is relieved by recumbency and is not increased by brief periods of standing and walking may indicate an IVD lesion such as a protrusion or an annular tear. In addition to those patients with an IVD protrusion, pain with coughing and sneezing also occur in patients with active sacroiliitis, because the sudden increase in intra-abdominal pressure produces a painful distraction of the sacroiliac joints. Once the motion or position that reduces the symptoms is identified, the initial focus of the intervention is teaching the patient strategies that encourage this motion or posture. ▶▶ Progression and course of symptoms.  Questions related to the type and behavior of symptoms can help determine the structure involved and the stage of healing. It is important to determine whether the condition is improving or worsening. Constant pain indicates an inflammatory process. Steadily increasing pain, especially in elderly patients, may indicate malignancy, as does pain that is gradually expanding and increasing as this finding may highlight a lesion that is increasing in size, such as a neuroma or neoplasm. Pain with movement suggests a mechanical cause of pain. If the muscles and ligaments are involved, activity will tend to decrease the pain, but the pain will worsen with repeated movements or sustained positions as the structures become fatigued or overstressed.77 Symptoms of lumbosacral pathology can demonstrate a phenomenon of centralization and peripheralization.69,77 Centralization of symptoms is the progressive retreat of the most distal extent of referred or radicular pain toward the lumbar

Lumbar Spine

Prior history/intervention.  Patients should be asked if they have experienced similar complaints or problems in the past, even if the current complaint feels different. If so, it is helpful to determine what intervention was provided, whether self-administered or by a health-care provider, over what length of time and if that treatment was effective.65 Prognostic factors for the development of recurrent LBP include the history of previous episodes, excessive spinal mobility, and excessive mobility in other joints.70 Prognostic factors for the development of chronic pain include the presence of symptoms below the knee, psychological distress or depression, fear of pain, movement, and reinjury or low expectations of recovery, pain of high intensity, and a passive coping style.70 Painrelated fear (in addition to psychological distress and self-efficacy) mediates the relationship between pain and disability.71,72 In line with the theory that cognitive factors precede emotional reactions, individuals who “catastrophize” about the meaning of their pain may become fearful, subsequently avoiding any physical activity that threatens their well-being, resulting in a vicious cycle, in which the avoidance behavior leads to physical disability and depression that, in turn, can heighten the pain experience.72 With over 50% of primary care patients with LBP presenting with elevated fear,73–75 pain-related fear is an important target for physical therapy intervention.72 ▶▶ Palliative measures.  It is important to determine what attempts have been made to alleviate the symptoms and what effect, if any, was achieved. Depending on the nature of the pathology, certain body positions may bring relief, although it is important to remember that patients often present with symptoms more complex than classic textbook examples allow65: ■■ Lying supine with knees flexed decreases pressure on the spinal column and tension of neural elements. Similar relief may be felt in the side-lying position; however, patients with a neurocompressive disk herniation may find this position unsustainable on one side and tolerable on the other side. ■■ Standing or extension may be less provoking than seated or flexed positions in patients with disk pathology, whereas the opposite is typically true of patients with spinal stenosis. A classic example of positional relief involves the stenotic patient who leans on a shopping cart while walking to alleviate back and lower extremity symptoms. ▶▶

TABLE 28-6

EXAMINATION

treat than episodes that occur daily or weekly and appear to be worsening.

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EXAMINATION

spine midline in response to standardize movement testing during evaluation of the effect of repeated movements on pain location and intensity. Peripheralization of symptoms indicates movement of the symptoms in the opposite direction. Centralization of the symptoms normally indicates improvement in the patient’s diskogenic condition (see “Special Tests” section).

THE SPINE AND TMJ

The quality of symptoms.  Pain is the most common initial complaint involving the low back. Descriptors used by the patient to characterize his or her pain can provide valuable clues to the origin of the problem (Table 28-7). ▶▶ Radiation/referral of symptoms.  LBP that emanates from the bony structures, soft tissues, or neural elements often demonstrates an associated pattern of referral or radiation.65 At a given spinal level, the similar pain patterns of dermatomal, myotomal, and sclerotomal pain represent the distributions of a single nerve root. However, based on the pattern alone, it is difficult to determine the offending structure involved.65 Radicular and dermatomal pain are often used interchangeably although their meanings are distinct: ■■ Radicular pain refers to pain initiated by nerve root irritation and presents itself along the pathway of the root. ▶▶

■■

Dermatomal pain is defined as pain within the distribution of a single sensory nerve root that innervates the skin and presents itself at the surface.

Two additional definitions are pertinent. A myotome consists of groups of muscles supplied by a single spinal segment, whereas a sclerotome is an area of bone or fascia supplied by a single spinal segment.65 ▶▶



1352

■■

Severity.  The most frequently used tool to assess severity is a numerical rating scale, with 0 representing the absence of pain and either 10 or 100 representing the most extreme intensity of pain that the patient has experienced or can imagine. There are several other tools that provide quantification of the patient’s symptoms to a greater or lesser degree65: ■■ The visual analog scale is frequently used, particularly with new patients and during reexaminations. The scale consists of a 10-cm unmarked line, with indicators of “no pain” at the left end of the line and “extreme pain” at the right end of the line. Patients are asked to mark the line at the point corresponding to their pain level. ■■ Color charts are useful for young patients and patients who have difficulty communicating information due TABLE 28-7

 ommon Descriptors of Pain and Their C Origin

Descriptor

Origin

Deep ache and boring

Bony tissues

Dull, achy, sore, burning, and cramping

Muscle/fascia

Sharp, life like, shooting, lancinating, tingling, burning, numbness, and weakness

Nerve

Burning, stabbing, throbbing, tingling, and cold

Vascular

Deep pain, cramping, and stabbing

Visceral

Dutton_Ch28_p1335-p1416.indd 1352

▶▶

to language barriers. The colors extend from red to violet, with red representing extreme pain and violet representing the absence of pain. Verbal descriptors, such as minimal, slight, moderate, and severe, may also be used to categorize pain levels, although they can be subject to misinterpretation. It is important to quantify a patient’s pain intensity at its current level, when it is at its lowest and highest points, and an average estimate over a selected period of time, for example, 1 week.65 This information may then be used as outcome measures for subsequent treatment.

Temporal factors—diurnal or nocturnal variation in symptoms.  Determining the connection between the time of day and onset of symptoms may help differentiate between mechanical and inflammatory disorders. For example, muscle strains may feel slightly sore in the morning on waking but typically result in a greater intensity of pain at the end of the day following activity.65 A patient with an inflammatory condition such as ankylosing spondylitis, an IVD lesion, osteoarthritis, ankylosing spondylitis, or Scheuermann’s disease tend to experience the greatest symptoms in the morning, after the joints and surrounding tissues have had ample time to stiffen. In addition, patients with mechanically based pain often report an increase in symptoms during the evening hours, when their attention is not diverted by work or daily activities.65 This may also be true when looking at pain patterns during the week when much activity occurs at home and work versus during the weekends when rest is more likely.65 Night pain that wakes a patient may be an indicator of neoplastic activity or infection (“Red Flags”) (Table 28-8) and should be addressed immediately. In contrast, a patient who awakens following movement,

TABLE 28-8

Red Flags for the Low-Back Region

Condition

Red Flags

Back-related tumor

Age over 50 years History of cancer Unexplained weight loss Failure of conservative therapy

Back-related infection (spinal osteomyelitis)

Recent infection (e.g., urinary tract or skin infection) Intravenous drug user/abuser Concurrent immunosuppressive disorder

Cauda equina syndrome

Urine retention or incontinence Fecal incontinence Saddle anesthesia Global or progressive weakness in the lower extremities  Sensory deficits in the feet (i.e., L4, L5, and S1 areas)

Reproduced with permission from Wilmarth MA, ed. Medical Screening for the Physical Therapist. Orthopaedic Section Independent Study Course 14.1.1. La Crosse, WI: Orthopaedic Section, APTA, Inc.; 2003.

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Patient’s general health and past medical history.  This component includes checking for a family history of rheumatoid arthritis, IVD lesions, diabetes, osteoporosis, and vascular disease. When collecting information about the patient’s health history, a useful acronym is “FAOMASHL”: family health history, accidents, other associated/unassociated complaints, medications, allergies, surgeries, hospitalizations, and lifestyle factors.65 The clinician should solicit information from the patient regarding the presence or past existence of any major illnesses, including, but not limited to, diabetes, heart disease, cancer, and hypertension. Any allergies should be documented. The dates, provider contact information, and outcomes of hospitalizations and surgical procedures should be noted.65 It is also vital, from a diagnostic as well as treatment viewpoint, to determine the patient’s level of conditioning. ▶▶ Patient age.  Spondylolisthesis is more common among 10–20-year olds.78 Cancer, compression fractures (see Chapter 5), spinal and lateral recess stenosis, and aortic aneurysms are more common among patients older than 65 years of age.79 Inflammatory spondyloarthropathy, which can affect the spine, hips, knees, and feet, is most common in the 15–40-year-old age group, and IVD lesions are more common in this group as well. Osteoarthritis and spondylosis are more common in the 45 years and older age groups.80,81 Effective medication can alter the disease course of spondyloarthropathies, making prompt diagnosis important. All patients under the age of 45 years with symptoms of more than 3 months should be asked four questions82: ▶▶

1. Does the morning back stiffness last over 30 minutes? 2. Does the back pain awaken you during the second half of the night? 3. Does the pain alternate from one buttock to the other? 4. Does rest relieve the pain? If two out of the four questions are positive, there is a 70% sensitivity and 81% specificity for inflammatory back pain.82 If three of four questions are positive, the sensitivity drops to 33%, but the specificity approaches 100%.82 ▶▶

Occupation.  Information regarding the patient’s job description should include the estimated level of

Dutton_Ch28_p1335-p1416.indd 1353

Lumbar Spine

In addition to this list of basic questions, the clinician should also address the following areas:

EXAMINATION

activity, from sedentary to strenuous.65 Also, elements such as lifestyle factors, hobbies, and exercise routines can provide useful information. Flexion and rotation of the trunk, lifting, axial loading, sustained flexed postures, vibration, and low job satisfaction are all considered as risk factors for back pain. The level of impairment or disability that a lesion produces is related to the type of work performed. For example, diskodural back pain produces more disability in a truck driver who has to sit the whole day than in a patient who has light and varying work. The clinician should determine if there are any work stressors that may either physically or emotionally delay recovery or increase the likelihood of chronicity.65 This necessitates a full understanding of the patient’s job description and workplace environment. Depending on the circumstances, lifestyle factors may be a source of either physical or psychosocial irritation for the patient or can be used as a motivational force during treatment.65 Additionally, the patient’s participation in hobbies may be negatively impacted by back pain. Recovery and return to these activities can also be used as a motivational device.65

such as changing positions while sleeping, would be less of a risk for “Red Flags.”65 The same is true of the patient who has difficulty returning to sleep after getting up, for example, to visit the restroom.65 Depending on the size of the patient, prone lying tends to compress the posterior structures and aggravate a zygapophyseal extension dysfunction. Persistent or progressive pain in supine lying may indicate a neurogenic or space-occupying lesion, such as an infection, swelling, or tumor. It may also indicate a zygapophyseal extension dysfunction, especially if the patient has marked adaptive shortening of the hip flexors and rectus femoris. For women, back pain may show a monthly periodicity related to the menstrual cycle.

The impact of symptoms.  The effect the symptoms have on the patient’s work, daily activities, and recreational pursuits can be assessed using the functional assessment tests outlined later. With this information, the clinician can set a baseline with which to measure progress that is meaningful to the patient. In addition, the clinician can determine whether the need for assistive devices is warranted. ▶▶ Medication use.  Pain medications can mask symptoms. If the patient reports taking pain medication prior to the examination, the clinician may not obtain a true symptom-response from the patient. It is important to ask the patient about dosage and frequency of the overthe-counter preparations, prescription medications, particularly corticosteroids and anticoagulants, vitamins, and herbal supplements. ▶▶ Psychosocial factors and nonorganic signs.  During the initial history, it is important to document any psychosocial factors or nonorganic signs and symptoms, as these may directly affect the clinician’s ability to accurately and completely diagnose the patient (see “Examination Conclusions” section). The patient’s response to treatment and prognosis will be impacted as well. ▶▶

Systems Review It must always be kept in mind that pain can be referred to the lumbar spine area from pathologic conditions in other regions. For example, reports of pain in the upper lumbar region could suggest the possibility of aortic thrombosis, neoplasm, chronic appendicitis,83 ankylosing spondylitis, or visceral disease (see Chapter 5) (Table 28-8). The clinician should determine whether there has been any recent and unexplained weight loss, night pain that is unrelated to movement, or changes in bowel and bladder function.

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EXAMINATION

Any one of these findings may indicate the presence of a serious pathology:

THE SPINE AND TMJ

Unexplained weight loss or night pain not associated with movement may indicate a malignancy. In many patients whose LBP is caused by infection or cancer, the pain is not relieved when the patient lies down.84 ▶▶ Bowel or bladder dysfunction may be a symptom of severe compression of the cauda equina (cauda equina syndrome). This rare condition usually is caused by a tumor or a massive midline IVD herniation. Urinary retention with overflow incontinence is usually present, often in association with sensory loss in a saddle distribution, bilateral sciatica, and leg weakness. This condition constitutes a medical emergency. ▶▶

Tests and Measures Observation Observation involves an analysis of the entire patient in terms of how he or she moves and responds, in addition to the positions the patient adopts. Whether the clinician chooses to greet patients personally in the waiting room or in the examination room, the examination should begin with the initial contact.65 The patient’s gait pattern and any antalgia can provide some important clues.

CLINICAL PEARL Muscle weakness and reduced walking capacity are among several functional deficits associated with a lumbar herniated NP.85 Weakness of the gastrocnemius is a clinical sign associated with involvement of the L5–S1 disk (neurologic level S1), whereas weakness of the extensor hallucis longus is a positive sign for involvement of the L4–5 disk (neurologic level L5).

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Once in the examination room, the patient should be gowned appropriately to allow complete inspection of the lumbar spine and lower extremities. Although spinal alignment provides some valuable information, a positive correlation has not been made between abnormal alignment and pain. “Good posture” is a subjective term based on what the clinician believes to be correct, and it is highly variable (see Chapter 6). Posterior Aspect.  The shoulders and pelvis should appear fairly level, and the bony and soft tissue contours should appear symmetric. A horizontal line through the highest points of the iliac crests also passes through the spinous process of the fourth lumbar vertebra. The transtubercular plane to the tubercles on the iliac crest cuts through the body of the fifth lumbar vertebra, and the upper margin of the greater sciatic notch is opposite the spinous process of the first sacral vertebra. There should be no differences in the muscle bulk between both sides and regions of the erector spinae. If atrophy of the paravertebral or extremity muscles is present, the clinician must determine whether it follows a segmental or nonsegmental pattern. A predominance of the thoracolumbar

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TABLE 28-9

 auses of Functional Limb-Length C Difference

Joint

Apparent Lengthening

Apparent Shortening

Sacroiliac

Anterior rotation

Posterior rotation

Hip    

Lowering Extension External rotation

Hiking Flexion Internal rotation

Knee

—

Flexion Valgus Varus

Foot

Supination

Pronation

portion of the erector spinae may indicate poor stabilization of this area, or a rotational asymmetry.86 The inferior angles of the scapulae should be level with the seventh thoracic spinous process; the iliac crests should be level. The PSISs, medial malleoli, and lateral malleoli should all be level with their counterparts on the opposite side. Differences between the two sides may indicate a functional limb-length discrepancy (see Chapter 29). This discrepancy can be caused by altered bone length, altered mechanics, or joint dysfunction (Table 28-9). The thoracic and lumbar vertebrae should be vertically aligned. The curvature of the spine is referred to as scoliosis (see Chapter 6). Deformity, birthmarks, and hairy patches are all evidence of congenital deficits of the integumentary system and can indicate underlying anomalies in the systems derived from the same embryologic segments. A hairy patch or tuft that is located at the base of the lumbar spine may indicate spina bifida occulta or diastematomyelia. Lateral Pelvic Shift. Structural asymmetry in the lumbar region often is associated with pain. For example, patients with disk-related LBP commonly present with a pelvic shift or list when acute sciatica is present. In these cases, the patient may list away from the side of the sciatica, producing a socalled sciatic scoliosis. The lateral pelvic shift is perhaps the most commonly encountered. Under the McKenzie classification system (see Chapter 22), a derangement requires the presence of a relevant lateral shift deformity.69 Determining the presence of a lateral shift deformity may help speed up the recovery from a derangement by first correcting the lateral shift deformity.69 The direction of the list, although still controversial, is believed to result from the relative position of the disk herniation to the spinal nerve (Fig. 28-7). Theoretically, when the disk herniation is lateral to the nerve root, the patient may deviate the back away from the side of the irritated nerve, which has the effect of drawing the nerve root away from the disk fragment (Fig. 28-7). This movement is demonstrated dramatically in patients with extreme lateral disk herniations, whose efforts at side bending to the side of the herniation markedly exaggerate the pain and paresthesia.87 When the herniation is medial to the nerve root, the patient may list toward the side of the lesion, in an effort to decompress the nerve root (Fig. 28-7).

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EXAMINATION

Side bending

Side bending

Nerve compression by medial disk protrusion

FIGURE 28-7  Direction of the lateral list in relation to disk herniation.

The clinician must first determine the presence of the shift and then determine its relevance to the presenting symptoms. To determine its relevance, a side-glide test sequence can be used. The side-glide test sequence is performed by manually correcting the shift by pushing the pelvis into its correct position69 (Fig. 28-8) VIDEO. If the side-glide produces either a centralization or peripheralization of the patient’s symptoms, the test is considered positive for a relevant lateral shift.69 In addition, for a lateral shift to be significant, the patient must exhibit an inability to self-correct past midline when asked to shift in the direction opposite the shift.69 The relevant lateral shift must be corrected, using side-glides, before the patient attempts the McKenzie extension exercises.69 A lateral shift

FIGURE 28-8  Side-glide test.

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Lumbar Spine

Nerve compression by lateral disk protrusion

that is not deemed to be relevant or to be a deformity, per McKenzie’s criteria, may be treated with only sagittal plane movements (e.g., extension principles).69 Lateral Aspect.  From the side, the clinician should observe that the ear lobe is in line with the tip of the shoulder, and the peak of the iliac crest. The amount of lumbar lordosis is noted as to whether it is excessive or reduced. The lumbar lordosis should appear as a smooth and gentle curve, and there should be a gradual transition at the thoracolumbar junction. An excessive lordosis may result in the pelvic crossed syndrome.88 In this syndrome, the erector spinae and the iliopsoas are found to be adaptively shortened, and the abdominal and gluteus maximus muscles are found to be weak. As a result, this syndrome can produce adaptive shortening of the PLL, lower back extensors, and hip flexor muscles and lengthening of the ALL and lower abdominals. An excessive lordosis may also indicate that the patient has a spondylolisthesis. With this condition, the whole spine often lies in a plane anterior to the sacrum. There may also be an associated mid or low lumbar shelf at the spinous processes, which, if not visible, can be palpated. An anterior pelvic tilt posture may also be caused by weakness of the abdominal muscles or an adaptively shortened iliopsoas or TLF, with subsequent lengthening of the hamstring and gluteal muscles.88 ▶▶ A flattened back may indicate that the patient has either a lumbar spinal stenosis, a lateral recess stenosis, or some lateral shifting of the spinal column. A flattened lordosis may be caused by a posterior pelvic tilt, adaptive shortening of the hamstrings, disk protrusion, or weakness of the hip flexor muscles.88 ▶▶ A reversed lordosis, often referred to as a sway back, is caused by a thoracic kyphosis and a posterior pelvic tilt. This posture results in a stretching of the anterior hip ligaments, back extensors, and hip flexors; hip hyperextension; and compression of the vertebrae posteriorly.88 Kyphosis of the lumbar spine may also indicate damage to the SSL complex. ▶▶

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EXAMINATION

The type of footwear that the patient habitually wears can be a factor. For example, high-heeled footwear has a tendency to modify the pelvic angle and increase the lordosis.

Palpation

THE SPINE AND TMJ

There is some disagreement as to when in the examination the palpation assessment should occur, with some authors preferring to perform this portion at the end. The order of examination procedures should reflect an awareness of the patient’s potential discomfort and proceed from least to most invasive.65 For instance, a patient who reports difficulty when lying on his or her stomach should be examined in the prone position only if necessary, saving this position for the end of the examination. For patients who are able to attain all positions without significant distress, it is most convenient for the clinician to perform procedures as gravity suggests, moving from the standing position to seated, supine, side lying, and then prone.65 Whenever it is performed, palpation of the lumbar spine area should be performed in a systematic manner, and in conjunction with palpation of the pelvic area, which is described in Chapter 29, and the hip area, which is described in Chapter 19. Palpation of the lumbar region is best performed with the patient in a prone position but may also be performed on a seated patient. The examiner should begin by assessing the soft tissues for an increase in focal temperature.65 As previously mentioned, in most individuals, the midpoint of an imaginary line drawn between the iliac crests represents the L4–5 interspace and the level of the L4 transverse process. The transverse processes of L3, L2, and L1 each lies two fingerbreadths superior to the vertebra, respectively. Alternatively, they can be found at the level of the lower pole of the spinous process of the vertebra immediately above or below. The lumbar zygapophyseal joints of each motion segment are located approximately 2–3 cm (0.8–1.2 inches) lateral from the spinous processes. The reference point indicating the position of L4 is marked on the patient. The spinous process of L5 is just inferior to this point. The L5 spinous process is short, sharp, and thick compared with those of L4 and L3. The clinician should move superiorly from the L5 spinous process, carefully palpating each segmental level. Evidence of tenderness, altered temperature, muscle spasm, or abnormal alignment during palpation can highlight an underlying impairment. Posterior Aspect.  Palpation of the posterior aspect of the lumbar spine is best achieved by placing the patient in a relaxed prone position, or bent over the treatment table. ▶▶

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The clinician moves the index and middle fingers quickly down the spine, feeling for any abnormal projections or asymmetries of the spinous processes. Any alterations in the alignment of the spinous processes in a posteroanterior (P-A) direction, particularly at the L4–5 or L5–S1 segmental level may indicate the presence of a spondylolisthesis. Specific pain elicited with P-A pressure over the segment serves as further confirmation. Absence of a spinous process may be associated with spina bifida. Side-to-side alterations in the spinous process may

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indicate the presence of a rotational asymmetry of the vertebra.86 ▶▶ The SSLs should be palpated. The ligament is usually supple, springy, and nontender. Because this ligament is the most superficial of the spinal ligaments and the farthest from the axis of flexion, it has a greater potential for sprains. ▶▶ Palpation of the transverse processes of T12 and L5 presents difficulties. That of L3 is easy to feel, being usually the longest of all transverse processes; it is usually possible to feel those of L1, L2, and L4. That of L5 is covered by the posterior ilium. ▶▶ Patients with localized tenderness over the zygapophyseal joints without other root tension signs or neurologic signs may have zygapophyseal joint pain. Anterior Aspect ▶▶ The inguinal area, located between the ASIS and the symphysis pubis, should be palpated carefully for evidence of tenderness, which may be indicative of a hernia, an abscess, sprain of the ligament, or an infection, if the lymph nodes are swollen and tender. ▶▶

In some patients, the anterior aspect of the vertebral bodies may be palpable when the patient is positioned supine with the hips flexed and feet flat on the bed. Tenderness of the anterior aspect of the vertebral bodies may indicate an irritation of the ALL, which may indicate the presence of an anterior instability.89

CLINICAL PEARL Evaluation of the abdominal, inguinal, popliteal arteries, and distal pedal pulses is dependent on the patient’s profile and presentation.65 As a general rule, the abdominal aorta should be assessed for possible enlargement via auscultation and palpation in any patient over the age of 50 with acute onset of LBP.65

Active Range of Motion Normal active motion, which demonstrates considerable variability (Table 28-10) between individuals, involves fully functional contractile and inert tissues and optimal neurologic function.90 It is important to note that ROM may be affected by age and sex. However, it is the quality of motion, and the

TABLE 28-10 Movement

Normal Active ROM of the Lumbar Spine Range (Degrees)

Flexion

70–90

Extension

30–50

Side bending

25–35

Axial rotation

20–40

Data from Ng JK, Kippers V, Richardson CA, et al. Range of motion and lordosis of the lumbar spine: reliability of measurement and normative values. Spine. 2001 Jan 1;26(1):53–60.

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by active ROM may implicate a number of tissues including muscle and tendon, ligament and capsule, and bone and nerve. The active ROM tests should be observed in front of and behind the patient. At the end of each of the active motions, passive overpressure is applied to assess the end-feel, and then resistance tests are performed with the muscles in the lengthened positions. The key to deciphering which offending structure is involved lies in determining the type of pain produced and whether active, passive, and/or resisted motions

EXAMINATION

symptoms provoked, rather than the quantity of motion, that are more important. The reproducibility (precision) of an individual’s effort is one indicator of optimum effort. Measurements should not change significantly ( whites

Observation

Short limb, associated with torticollis

Short limb, obese, Decreased flexion, Short limb, high Irritable child, quadriceps atrophy, abduction, and greater trochanter, motionless hip, and adductor spasm external rotation; quad atrophy, and prominent greater thigh atrophy; and adductor spasm trochanter, and muscle spasm mild illness

Position

Flexed and abducted

Flexed, abducted, and externally rotated

 

Pain

 

Mild pain with palpation and passive motion; often referred to knee

Gradual onset; aching Acute: severe pain in in hip, thigh, and knee; moderate: knee pain in thigh and knee; tenderness over hip

History

May be breech birth

Steroid therapy; fever 20–25% familial, low birth weight, and growth delay

Low-grade fever

May be trauma

Range of motion

Limited abduction

Decreased (capsular pattern)

Limited abduction and extension

Decreased flexion, limited extension, and internal rotation

Limited internal rotation, abduction, and flexion, and increased external adductor spasm

Special tests

Galeazzi sign, Ortolani sign, and Barlow sign

Joint aspiration

 

 

 

Gait

 

Refuses to walk

Antalgic gait after activity

Refuses to walk; antalgic limp

Acute: antalgic; chronic: Trendelenburg external rotation

Radiologic findings

Upward and lateral displacement and delayed development of acetabulum

In stages: increased CT scan: localized density, abscess; increased fragmentation, separation of ossification center and flattening of epiphysis

Normal at first; widened medial joint space

Displacement of upper femoral epiphysis, especially in frog position

 

Flexed, abducted, and externally rotated Vague pain in knee, suprapatellar area, thigh, and hip; pain in extreme motion

Special Populations

Legg–Calvé– Perthes Disease

Septic Arthritis

Data from Richardson JK, Iglarsh ZA. Clinical Orthopaedic Physical Therapy. Philadelphia, PA: WB Saunders; 1994.

show decreased ROM, particularly of IR, abduction, and flexion. On passive flexion of the hip, the patient will frequently externally rotate the leg. SCFE can be classified as a stable or unstable hip from the patient’s history, physical examination, and radiographs.46 In the stable hip, weight bearing is possible with or without crutches. In the unstable hip, the patient presents more with fracture-like symptoms, with pain so severe that weight bearing is impossible.

CLINICAL PEARL Knowledge of SCFE and its manifestations will facilitate prompt referral by the clinician to an orthopaedic surgeon.

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Intervention.  The goals of the intervention are relief of symptoms, containment of the femoral head, and restoration of ROM.46 The current method of choice is in situ surgical fixation. The goal of containment is to maintain the sphericity of the femoral head. Other treatments are epiphysiodesis, osteotomy, salvage procedure, or spica cast. Complications from surgery include chondrolysis and/or necrosis of the femoral head, which increases the likelihood of significant joint degeneration in later years. Conservative intervention includes the use of traction for the relief of symptoms, at home or in the hospital, for periods ranging from 1 or 2 days to several weeks. Gait training postsurgery is initiated as soon as LE strength and ROM are adequate for ambulation skills.

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The weight-bearing status can vary but is usually nonweight bearing or touch down weight bearing. Full weight bearing is permitted when the growth plate has fused (within approximately 3–4 months).

the stretching of the pectoralis major and minor muscles, and muscle strengthening exercises for the thoracic spine extensors (seated rotation and extension in lying exercises), and the scapular adductors.

Low Back Pain CLINICAL PEARL

SPECIAL CONSIDERATIONS 1466

Complications from surgery include chondrolysis and/or necrosis of the femoral head, both of which increase the likelihood of significant joint degeneration in later years.

ROM exercises for the hip should be performed in all planes, but with particular emphasis on hip flexion, IR, and abduction. Strengthening of the affected extremity is introduced when sufficient healing has occurred.

Scheuermann Disease Scheuermann kyphosis, also known as Scheuermann disease, juvenile kyphosis or juvenile discogenic disease, is a condition of hyperkyphosis that involves the vertebral bodies and disks of the spine identified by anterior wedging of greater than or equal to 5 degrees in three or more adjacent vertebral bodies.48 The thoracic spine is most commonly involved (the seventh and tenth thoracic vertebrae are most commonly affected), although involvement can include the thoracolumbar/lumbar region as well.48 The disease, considered to be a form of juvenile osteochondrosis of the spine, involves a defect to the ring apophysis where the vertebrae grow unevenly with respect to the sagittal plane resulting in an anterior angle that is often greater than the posterior angle. These structural changes can cause the vertebral end plate to crack, thus making it possible for disk material to bulge into the vertebral body (Schmorl node). Clinical Findings. Most commonly, diagnosis is made after parents notice a postural deformity or “hunchbacked” appearance combined with complaints of pain in the affected hyperkyphotic region.48 The patient may report pain at the apex of the curve, which can be aggravated by physical activity and by long periods of standing or sitting. As the condition progresses, the patient may complain of an aching sensation in the upper spine. Also, there may be observational evidence of an increased thoracic kyphosis and pain with thoracic extension and rotation, usually detected during a school physical or noted by the parents. Many patients often develop an excessive lordotic curve in the lumbar spine to compensate for the kyphotic curve above. Intervention.  The intervention depends on the severity but typically involves postural education, a modification of the aggravating activity, exercise, or bracing. The Schroth method, which originated in Germany as a treatment for scoliosis, is an exercise system that uses isometric and other exercises to strengthen or lengthen asymmetrical muscles in the spine with the goal to halt or reverse progression of abnormal spinal deviations. The exercise program includes

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Low back pain (LBP) is already common in 14-year-olds, with 30% of adolescent girls and 26% of adolescent boys reporting LBP, and 11% of both sexes reporting chronic LBP (lasting >3 months).49 By the age of 17 years, significant sex differences occur, with 13% of adolescent boys and 26% of adolescent girls reporting the presence of chronic LBP.50,51 Although serious pathology associated with LBP is quite rare, the presence of insidious onset of severe LBP, when associated with a cluster of symptoms such as night pain, fever, unexplained weight loss, neurological deficits, and greater than 30 minutes of morning stiffness, warrants further investigation to rule out pathologies such as malignancy, inflammatory disorders, and infection.52 Although MRI findings such as disc degeneration are prevalent (30%) in adolescents as young as 13 years of age, pathology associated with LBP is relatively rare.53 Other, less serious causes of LBP in this age group include hypermobility syndromes, postural syndromes (such as slump sitting), muscular imbalances, and overuse disorders.52 The prevalence of spondylolysis/spondylolisthesis in adolescents is approximately 6%, making it perhaps the most common cause of LBP in adolescents. Spondylolysis refers to a separation of the pars interarticularis. It is common in patients involved with sports where repetitive extension and rotation of the lumbar spine frequently occur.54 Bilateral spondylolysis at the same vertebral level can result in spondylolisthesis (see Chapter 28).55 ▶▶ Spondylolisthesis refers to anterior slippage of one vertebra over another at the anterior aspect of the spine. Clinical Findings.  The clinical findings for spondylolysis/ spondylolisthesis include the following: ▶▶

The patient typically presents with insidious onset of extension-related LBP. ▶▶ Frequently, there is an associated reduction in hamstring flexibility. ▶▶ Occasionally, radiating pain, numbness, or weakness may be present.55 ▶▶

A physical examination may reveal hyperlordosis, ipsilateral paraspinal muscle spasm, and adaptive shortening of the hamstrings.55 The ROM examination reveals pain with spinal extension. The single-legged hyperextension test may localize the spondylolysis when standing on the ipsilateral leg (Fig. 30-8), although one study found this to be an insensitive test.56 Radiographically, the anteroposterior view may identify anatomic variants or developmental effects, whereas the lateral view may demonstrate spondylolisthesis or a lytic lesion, and oblique views may demonstrate a stress reaction of the pars interarticularis, the pathognomonic neck of the Scottie dog lesion.55

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and validated. Therefore, clinical diagnosis currently relies on plain radiographs and MRI.59 Intervention.  When possible, nonoperative forms of management are attempted first. For OCD of the knee, this can include sports restriction, casting, bracing, and crutch walking (partial or nonweight bearing) and immobilization for the elbow. Approximately 50–67% of OCD of the knee found during childhood will heal within 6–18 months of nonoperative treatments.60

If left untreated, juvenile OCD lesions can progress to adult forms of OCD, resulting in detachment or destruction of a portion of the joint surface and potentially leading to early osteoarthritis.61 Unfortunately, most young patients are diagnosed with OCD a year or more after the onset of symptoms.62 This is because nonspecific knee pain is the most common early symptom, so that OCD can be camouflaged among the many benign juvenile knee pain conditions, such as jumpers knee, OS, and patella femoral pain syndrome.61 Thus, clinicians must be vigilant to identify OCD in young athletes to initiate early treatment.

Special Populations

CLINICAL PEARL

FIGURE 30-8  Single-legged hyperextension test.

Intervention.  The conservative intervention for spondylolysis/spondylolisthesis includes activity modification with avoidance of any activities that cause pain. The exercise program focuses on strengthening of the abdominal muscles and hip flexor and hamstring stretches, while avoiding lumbar extension. Once the athlete becomes pain-free, activity can be gradually increased. Bracing is somewhat controversial. Indeed, one study illustrated that the best results were obtained with a period of rest from sport for 3 months, regardless of whether bracing was used.57

Osteochondritis Dissecans Osteochondritis dissecans (OCD) is a rare cause of anterior knee (it can also affect the elbow) pain in the young athlete. OCD is a joint disorder of unknown etiology in which fissures form in the articular cartilage and the underlying subchondral bone due to vascular deprivation (osteonecrosis). The result is fragmentation (dissection) of both cartilage and bone, and the free movement of these osteochondral fragments within the joint space, causing pain and further damage. If OCD occurs at the knee, it typically involves the weightbearing portions of the medial and lateral femoral condyles, but can also occur in the trochlear groove, patella, and tibial plateau.58 Clinical Findings.  Occasionally, pain may not be the most prominent symptom, but a catching sensation with joint motion may be the primary complaint if there is a loose body in the joint space. If the lesion is small, a painful arc is present during active and passive movement. Unfortunately, an effective clinical examination for OCD has yet to be identified

Dutton_Ch30_p1451-p1500.indd 1467

Surgical treatment varies widely and includes arthroscopic drilling of intact lesions, securing of cartilage flap lesions with pins or screws, drilling and replacement of cartilage plugs, stem cell transplantation, and joint replacement. Although there are few evidence-based recommendations in the literature for postoperative rehabilitation following surgical intervention, the rehabilitation usually involves 4–12 weeks of some form of weight-bearing restriction and physical therapy to gradually increase ROM, maintain quadriceps function, and reduce joint swelling.61 Isometric exercises, straight leg raises and cryotherapy, are commonly used. The exercises are progressed to include stationary bike and deep water running and then, once the patient achieves full ROM and weight bearing, muscle function is restored using closed chain exercises while protecting the joint’s cartilage surface and underlying subchondral bone.

Osgood–Schlatter Disease The apophysis of growing bones differs from the epiphysis of skeletally immature bone in that the apophysis is an independent center of ossification that does not contribute to the longitudinal length of a long bone. The apophysis does, however, contribute to the structure and form of mature long bone by serving as a site of tendinous or ligamentous attachment. Development of the tibial apophysis begins as a cartilaginous outgrowth, with secondary ossification centers appearing with subsequent progression to an epiphyseal phase when the proximal tibial physis closes and the tibial apophysis fuses to the tibia.8 OS disease is a benign traction apophysitis that occurs at the

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SPECIAL CONSIDERATIONS

tibial tubercle. It is a self-limiting knee condition that is one of the most common causes of knee pain in active and nonactive adolescents. The condition occurs in boys and girls aged 11–18 coinciding with periods of growth spurts and occurs more frequently in boys than in girls. 63 During periods of rapid growth, stress from repetitive contractions of the quadriceps is transmitted through the patellar tendon onto a small portion of the partially developed tibial tuberosity. This may result in multiple subacute avulsion fractures and inflammation of the tendon, and subsequent secondary heterotopic bone formation occurring in the tendon near its insertion.63 Clinical Findings.  The diagnosis of OS disease is relatively straightforward. There may or may not be a history of injury. Symptoms are typically unilateral, although 20–30% of cases can be bilateral in nature.8 In the acute phase, the pain is severe and continuous in nature. The pain occurs during activities such as running, jumping, squatting, and especially during kneeling, acute knee impact, and ascending or descending stairs. There is often a visible lump over the site. The pain can be reproduced by extending the knee against resistance or stressing the quadriceps. Intervention.  The intervention for OS disease is usually symptomatic, including antiinflammatory measures, rest from the offending activity, and judicious stretching of the quadriceps and hamstrings (adaptively shortened hamstrings require increased quadriceps force to overcome the tight posterior structures). Bracing or enforced joint immobilization is rarely required, although the most persistent cases may require cast immobilization for 6–8 weeks.63 The progressive quadriceps stretching exercises begin with a bolster placed under the hips of the prone patient to place the muscle on slack at the hip joint. As tolerated, the bolster is removed to place the hip in extension for a complete stretch of the extensor mechanism as indicated. Rarely, individuals will require surgical excision of symptomatic ossicles or degenerated tendons if symptoms persistent into skeletal maturity.

Sever Disease (Calcaneal Apophysitis)

1468

Sever disease (calcaneal apophysitis) is a common cause of heel pain in the skeletally immature athlete due to overuse, with 61% of cases occurring bilaterally.64 The calcaneal apophysis serves as the attachment for the Achilles tendon superiorly and for the plantar fascia and the short muscles of the sole of the foot inferiorly. Sever disease is a traction apophysitis of the growth center of the calcaneus that occurs at the insertion of the Achilles tendon.65 Young gymnasts, soccer players, and dancers are particularly susceptible to this condition because of their repetitive jumping or landing from a height. Clinical Findings.  Sever disease is characterized by pain, point tenderness, and local inflammation at the posterior calcaneus near the insertion of the Achilles tendon. Patients with adaptively shortened calf muscles, internal tibial torsion, forefoot varus, a dorsally mobile first ray, weak

Dutton_Ch30_p1451-p1500.indd 1468

dorsiflexors, and genu varus may be more susceptible to Sever disease.8 There are currently no defined radiographic diagnostic criteria for evaluation of Sever disease, with radiographs generally showing normal appearance of the calcaneal apophysis.65 Intervention.  The intervention for Sever disease initially begins with a shortening of the gastrocnemius-soleus group using heel cups or heel wedges, and avoiding barefoot walking until becoming asymptomatic. Stretching of the gastrocnemius-soleus, with the knee extended and the knee flexed, is only initiated after symptoms have subsided. When stretching in the weight-bearing position, any rear foot to lower leg or forefoot to rear foot abnormality should be corrected before and during the exercise. Dorsiflexion strengthening exercises along with strengthening of the foot intrinsic may also help manage symptoms.8

Little Leaguer Elbow Recent investigations have demonstrated that as many as 30–40% of 7- to 18-year-old baseball players experience elbow and shoulder pain during the baseball season.66,67 Little Leaguer elbow is a common term, credited to Brogden and Cros,68 for an avulsion lesion to the medial apophysis as a result of repetitive valgus stress. The term has since been used to describe a variety of pathoanatomic lesions in the immature athlete, all of which relate to the frequency and mechanics of throwing. For example, overuse, high pitch counts, and the type of pitch (curveball versus fastball) have all been cited as possible factors. Additional factors that influence its development include age, weight, height, skeletal maturity, individual susceptibility, competitive level, and geographic location.69 The increasing popularity of competitive baseball among adolescents has been accompanied by a rise in the incidence of unique throwing-related injuries.70 Each year, nearly 6 out of 10 young pitchers hurt their elbows.71 These injuries can affect pitchers later in their lives making prevention extremely important. It is likely that a confluence of factors, including intrinsic desire for success, participation in multiple leagues, and external pressure from parents and coaches, contributes to longitudinal overuse.67 Repetitive throwing results in muscular and bony hypertrophic changes about the elbow and can also result in ligament damage. This has been reflected by an increase in the number of medial ulnar collateral ligament (UCL) reconstruction (“Tommy John”) procedures being performed on injured throwers.72

CLINICAL PEARL A systematic review study reported that, despite much debate in the baseball community about the safety of the curveball, biomechanical and most epidemiologic studies do not demonstrate an increased risk of pain and/or injury when compared with the fastball.73

The repetitive motions involved in the various phases of throwing place colossal strains on the elbow, particularly

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acute versus progressive injury; the intensity of symptoms; ▶▶ the duration of symptoms; ▶▶ throwing schedule; ■■ frequency of throwing; ■■ intensity; ■■ duration; ▶▶ ▶▶

types and proportion of pitches delivered; delivery style (sidearm versus overhead—the former is more injurious to the elbow); ■■ types and proportions of throws delivered (e.g., curveballs are more deleterious than fastballs); ■■ rest periods employed; ■■ warm-up and cool-down regimens employed; ■■ phase the pain manifests in (e.g., early cocking, acceleration, and follow-through); ▶▶ restriction of motion; ▶▶ numbness. If the ulnar nerve is compromised, numbness in the ulnar distribution and a Tinel sign at the elbow may be present; and ▶▶ locking or checkrein-type symptoms. A locking or “catching” sensation indicates a loose body. ■■ ■■

Intervention.  Management is conservative, involving rest and elimination of the offending activity. Total body conditioning, including hip, back, and LE strengthening, may be able to help optimize a player’s biomechanics to reduce strain on the UE.67 Additionally, playing in a variety of sports to augment athletic dexterity, rather than engaging in early sports specialization, may protect these players while enhancing athleticism.67 Lesions involving less than 0.5–1 cm of apophyseal separation are initially treated with rest. This is followed by a rehabilitation program similar to that described for medial epicondylitis except that resistance exercises are avoided until active range can be performed to full motion without pain (generally 2–3 weeks). Throwing is avoided for 6–12 weeks. If OCD is present, the joint needs protection for several months. Any separation greater than 0.5–1 cm, sudden traumatic avulsions, or a failure to respond to conservative measures are indications for surgery. The patient cannot return

to pitching until full, and normal motion and strength has returned. An interval long-toss throwing program is the staple of a return-to-activity phase.75 The interval throwing program starts skeletally mature players at a throwing distance of 45 ft (14 m) and progressively increases it to 180 ft (55 m).76 The use of proper mechanics is a critical aspect of the interval throwing program. To prevent future elbow disorders, young athletes should adhere to the rules of Little League, which limits the number of pitches per game, per week, and per season and the number of days of rest between pitching. The pitch count is the most important of these statistics.

Proximal Humeral Epiphysitis This condition, often referred to as Little Leaguer shoulder, is also known as osteochondritis, epiphysitis, and epiphysiolysis of the proximal humeral epiphysis.77 The proximal humerus ossifies from four ossification centers: humeral head, greater tuberosity, lesser tuberosity, and humeral shaft. The ossification center for the humeral head is usually radiographically evident within the first year of life, whereas the greater tuberosity appears at age 3 and the lesser tuberosity at age 5.77 The humeral head and tuberosity unite around age 6 to form a large proximal humeral epiphysis, which unites with the shaft around age 20.77 Injury to the proximal humeral epiphysis usually occurs because of the two mechanisms in throwers: distraction and torsion.

Special Populations

during the late cocking and acceleration phases (see section The Throwing Athlete). These strains can result in inflammation, scar formation, loose bodies, ligament sprains or ruptures, and the most serious conditions of osteochondritis or an avulsion fracture. The onset of Little Leaguer elbow can be insidious or sudden, with the latter typically secondary to fracture at the site of the lesion. Clinical Findings.  The child typically presents with pain and local tenderness on the medial side of the elbow. Physical findings depend on the severity but commonly include persistent elbow discomfort or stiffness due to aggravation by the injury. The clinician should seek out details, including74

Clinical Findings.  Patients typically describe pain localized to the proximal humerus during both throwing and resisted shoulder strength testing. Palpation demonstrates local tenderness over the proximal humerus. The differential diagnosis of shoulder pain in adolescents throwers includes glenohumeral instability, rotator cuff tendinopathy, impingement, and proximal humerus physeal fracture.77 Radiographs characteristically show widening of the proximal humeral physis.77 Intervention.  Treatment includes cessation of throwing until the patient has pain-free ROM of the shoulder and radiographs return to normal, which may take up to 1 year.

Supracondylar Fracture of Humerus This type of fracture, which occurs most commonly in children, involves the flat and flared distal metaphysis of the humerus, as a result of hyperextension or a fall on a flexed elbow. The forces are transmitted through the elbow joint to the distal humerus. The distal humeral fragment is usually posteriorly displaced (extension type). Sometimes, a “follow-through” of fragments results in a proximal fragment piercing the anterior periosteum, brachialis muscle, and possibly the brachial artery and median nerve (flexion type). If the brachial artery is pierced, the injury is potentially limb threatening. The child typically presents with marked swelling of the elbow with an obvious deformity and ecchymosis. Because of 1469

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SPECIAL CONSIDERATIONS

the nature of this condition, peripheral circulation and nerve function must be assessed. Intervention.  The intervention is dependent on severity. Nondisplaced fractures are immobilized in a simple sling or shoulder immobilizer, with the elbow flexed for 3 weeks, whereas displaced fractures require closed reduction and immobilization in a cast that does not constrict circulation for 3 weeks. During the period of immobilization, the patient is closely monitored for changes in peripheral circulation. Following the period of immobilization, if the postreduction evaluation is acceptable, active range of motion (AROM) exercises are initiated in an effort to regain full extension. Strengthening of the biceps and triceps is also addressed.

downward pressure on the radial head. A click in the region of the radial head (palpable and sometimes audible) is indicative of a successful reduction. Sometimes, the forearm has to be pronated after forcible supination to reduce the pulled elbow. The click results from the release of the trapped annular ligament. Soon after the manipulation, the child typically begins to use the arm again, but sometimes there can be a delay of a day or two. In such cases, a sling can be used to both give comfort and protect the arm from a recurrence. The parents should be advised to avoid a longitudinal traction strain on the child’s arm by not pulling on the hands or wrists.

Distal Radial Epiphysitis Pulled Elbow The term pulled elbow or “nurse maid’s elbow” refers to a common minor soft-tissue injury of the radiohumeral joint in children of preschool age. The injury is caused by a sudden longitudinal traction force on the pronated wrist and extended elbow resulting in the radial head slipping through the annular ligament, which causes the fibers of the annular ligament to become interposed between the radius and the capitellum of the humerus. The following are the more common causes of pulled elbow: The child is lifted by an adult from the ground by his hands. ▶▶ The child’s forearm, wrist, or hand is being held firmly by a parent as the child attempts to walk away. ▶▶ A mother grabs the hand of a child to prevent a fall as the child wanders toward something potentially harmful. ▶▶ The young child is lifted by the hand from a lying or sitting position. ▶▶ The child is swung around by the hands several times during the course of play. ▶▶

Clinical Findings. There is usually no obvious swelling or deformity, but the child presents with a painful and dangling arm, which hangs limply with the elbow extended and the forearm pronated. The child is reluctant to use the arm and resists attempted supination of the forearm. The common sites of pain are (in order of occurrence) the forearm and wrist, the wrist alone, and the elbow alone. Intervention.  The intervention of choice is manipulation. Before attempting the manipulation, it is important to explain the procedure to the parents and to win the confidence of the child, by gently supporting the injured arm before manipulation. During the procedure, the clinician holds the child’s wrist with one hand while the other hand supports the elbow and palpates the radial head. The child’s attention is diverted, and the forearm is forcibly supinated with one quick motion, together with the application of

Radial physes appear at 12–18 months and fuse by 15–18 years.11 Distal radial apophyseal injuries are most common in male and female gymnasts but occasionally happen in other sports. Clinical Findings.  The patient typically describes a gradual onset of wrist pain made worse by weight-bearing activities while the wrist is in extension. Physical examination often reveals normal ROM but swelling of the distal radius. Tenderness is frequently found over the posterior (dorsal)radial growth plate but may also be elicited on the anterior (volar)-radial physis as well. Radiographic findings depend on the stage of the disease. Although these injuries are usually confined to the distal forearm, the carpus can sometimes be involved. Intervention.  Time to healing is dependent on the stage of the disease in the radiographic findings. When radiographs are negative, 4 weeks of rest usually allow for healing and return to activities. In other cases, immobilization in a cast is the mainstay of treatment.

CLINICAL PEARL Regular participation in organized youth (preadolescence) sports does not ensure adequate exposure to skill- and health-related fitness activities, and sport training without preparatory conditioning does not appear to reduce risk of injury in this population.78 As a global approach to the pediatric athlete, many of whom play multiple sports, sometimes without consideration for cumulative workload, a conceptual training model called integrative neuromuscular training (INT) is recommended.79,80 INT offers a supplemental training program that incorporates both general (e.g. fundamental movements and reduction of abnormal biomechanics), and specific (e.g., exercises targeted to decrease motor control deficits) strength and conditioning activities (eccentric resistance, dynamic stability, core strength, plyometrics, and agility) that are designed to enhance health and skill-related components of physical fitness.78,79,81

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THE AGING ATHLETE

The Aging Process Aging is the declining ability to respond to stress and by virtue of the increasing homeostatic imbalance and incidence of pathology, death remains the ultimate consequence of aging.82 The aging process can be attributed to a combination of development, genetic defects, environment, social and recreational habits, and disease, some or all of which are responsible for sequential alterations that accompany advancing age and the progressive probability of experiencing a chronic debilitating disease. Self-senescence refers to the temporal decrements in the ability of cells to replicate, repair, and maintain tissue, and is induced by both cell-intrinsic and cell-extrinsic mechanisms.82 Oxidative damage from the chronic production of endogenous reactive oxygen species and free radicals has been associated with aging in various human tissues.83 In both young and aged skeletal muscle, it has been shown that oxidative stress increases in response to unloading (lack of activity/immobilization) and may have an important role in mediating muscle atrophy.83,84 The rate of aging, that is, the rate at which aging changes occur, typically varies from individual to individual, resulting in differences in the impact of aging on function. This increase in the incidence of chronic conditions with advancing age occurs largely because this period in life is often accompanied by deterioration in health and a subsequent loss of independence. Complicating matters is the presence of comorbidities at this time of life, such as cardiovascular disorders, osteoporosis, arthritis, and diabetes, which increase the vulnerability of the geriatric patient.

CLINICAL PEARL Geriatrics is the branch of medicine that focuses on health promotion and the prevention and treatment of disease and disability in later life. ▶▶ Gerontology is the study of the aging process and the science related to the care of the elderly. ▶▶ Senescence can be defined as the combination of processes of deterioration, which follow the period of development of an organism. ▶▶

Throughout youth and early adulthood, the body has a number of physiologic reserves from which to draw upon when faced with physical challenges and injury, without a loss of functional abilities. However, older individuals have fewer of these system redundancies due to a gradual decline of health

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Changes Associated with the Aging Athlete A number of changes can negatively impact the performance of the aging athlete, including cardiovascular and neuromusculoskeletal changes. ▶▶

Cardiovascular.  The geriatric patient who has been given a prescription for physical therapy may not have been physically active for some time, and his or her level of fitness may have declined considerably. Age-related changes of the heart and blood vessels, which can either be mitigated or exacerbated by activity level, typically result in reduced capacity for oxygen transport at rest and in response to situations imposing an increase in metabolic demand for oxygen.85 In addition, maximal oxygen consumption decreases after the age of 25 years. As a result, at submaximal exercise, cardiac output and stroke volume are lower in older adults at the same absolute work rates, while BPs tend to be higher. It is very important that elderly patients have a physician’s evaluation of their cardiovascular status before engaging in a rehabilitation program. In addition, the patient should be carefully monitored for their cardiovascular response and tolerance to exercise during their rehabilitation sessions. Heart rate, BP, and rate of perceived exertion (RPE) should be assessed before, during, and after exercise, and the physician should be notified of any abnormal or unusual findings. In addition to the normal aging changes, a number of complications can occur in the elderly86: ■■ Acute inactivity, such as that which occurs with hospitalization, can significantly reduce VO2max and increase blood viscosity and venous status, which increases the risk of thromboembolic disease. Immobility in the elderly can be a common pathway for a host of diseases and further disability. The chronically ill, aged, or disabled are particularly susceptible. ■■ Cardiac diseases, such as coronary artery disease (CAD) and the sequelae of myocardial infarction (MI) and cardiomyopathy: a. CAD is a complex disease of the cardiac arteries resulting in ischemia to the myocardium. The clinical symptoms of CAD include angina (an ache, pressure, pain, or other discomfort in the chest, arms, back, or neck), shortness of breath, a decrease in activity tolerance, or palpitations. b. MI is a development of myocardial necrosis caused by an imbalance between the oxygen supply and demand of the myocardium, typically resulting from plaque rupture with thrombus formation in a coronary vessel, and subsequent acute reduction of blood supply to a portion of the myocardium. This patient population is a much greater risk of an adverse event during exercise, and, therefore, careful consideration, screening, and monitoring must occur to ensure safety with a rehabilitation program.

Special Populations

Due to the rapid growth of an elderly population and its predicted future socioeconomic impact, it is inevitable that future rehabilitation professionals will see an increase in the number of this population seeking services for the management of both acute and chronic conditions that can negatively impact active life expectancy or the number of years that an individual may expect to be independent in ADLs. Therefore, rehabilitation, with its potential to restore function, prolong independence, and improved QoL, can be extremely important in this population.

and increase in the incidence of injury and disease.85 Without these physiologic reserves, an older individual is more susceptible to functional limitations and disability, resulting in frailty— the opposite end of the spectrum from successful aging.85

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■■

■■

▶▶

Left ventricular hypertrophy, left atrial enlargement, aortic root dilatation, arrhythmias, and ischemic heart disease. Hypertension, which may be either essential or secondary, can have a number of negative impacts.

SPECIAL CONSIDERATIONS

Musculoskeletal.  The neuromusculoskeletal changes associated with aging affect all of the soft tissues and bone and many parts of the nervous system. Even healthy and active elderly individuals experience functional loss due to remodeling in the motor system, including muscle cells and upper and lower motor neurons.87 Musculoskeletal impairments are some of the most prevalent and symptomatic health problems of the middle and old age, and can result in a gradual loss of strength, motion, and increasing pain. These changes prevent elderly individuals from participating in regular physical activity, optimum mobility and, in some cases, reduce independence.85

Sarcopenia, often defined as the age-related decrease in lean body mass, has become a topic of significant investigation.88 Although a natural phenomenon, there is a spectrum of changes in aging muscle, some of which are normal (agerelated sarcopenia) and some of which are not (e.g., cancerrelated anorexia and cachexia syndrome*).88 Age-related muscle loss tends to begin at about age 50 in some muscles, and quite relentlessly in others. Decline of muscle mass is primarily due to type II fiber atrophy and loss of muscle fiber numbers.83 This is because type II muscle fibers, which are used primarily in activities requiring more power, are not stimulated by normal ADLs. In contrast, type I muscle fibers are slow contracting, low-tension output fibers that are highly resistant to fatigue and are capable of metabolizing fat for energy expenditure (see Chapter 1). In fact, their overall percentage when compared to type II muscle fibers increases. The rate of muscle loss has been estimated to range from 1% to 2% per year past the age of 50, as a result of which 25% in persons under the age of 70 and 40% of those older than 80 years are sarcopenic.89

CLINICAL PEARL According to the 2010 European Working Group on Sarcopenia in Older People, there are three stages of the muscle aging process90: ▶▶ Presarcopenia is simply a loss of muscle mass. ▶▶ Sarcopenia is muscle loss that occurs in conjunction with loss of strength or physical performance. ▶▶ Severe sarcopenia occurs when muscle loss is present with both strength and physical performance loss. Muscle is at the end of the chain of events in movement, so virtually every step involved from oxygenating the blood to the delivery of oxygen to working muscles may contribute in some manner to sarcopenia.88 With advancing age, *

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Cachexia is a pathological process that involves increases in muscle protein synthesis and degradation, basal metabolic rate and energy expenditure, inflammation, and insulin resistance, which results in a loss of muscle and fat mass.

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muscles display hybrid muscle fiber characteristics, which demonstrate selective loss of fast motor neurons that partially convert to slow-twitch fibers, ending with a hybrid phenotype showing the characteristics of both fast and slow fibers.83,91 These changes create irregularities in the size distribution of motor units which, in turn, affect both motor accuracy, especially with low flow movements, as the recruitment order does not adjust well to the previously small motor units having grown bigger and stronger.83 Finally, the ability of cells involved in the musculoskeletal system to sense, process, and respond to mechanical stimuli deteriorates with age and these changes may be involved in the etiology of aging-associated disease.83,92 Fortunately, skeletal muscle demonstrates a high degree of plasticity and is able to adapt to its demands throughout life. Thus, strength can be enhanced in adults, and quite substantially in the sedentary using customized exercise programs. Given the predominant loss of type II muscle fibers, the focus on this age group should be the prescription of exercises that develop coordinated movements, the speed of movement, strength, and power.

CLINICAL PEARL One pharmacological direction under investigation to prevent sarcopenia is the development of selective androgen receptor modulators (SARMs), which are a synthetic group of compounds that bind to specific areas of androgen receptors and are designed to encourage muscle growth while at the same time preventing some of the unwanted aspects of hormone therapy.88,93 In addition to the age-related changes in muscle, aging changes also occur in the biology, healing capacity, and biomechanical function of tendons and ligaments. Tendons.  There are structural changes in tendon such as collagen disorganization and decreased collagen content with aging, which can alter the biomechanical response of tendon tissue.94 The most common clinical tendon problems for the aging population are in the rotator cuff, Achilles, lateral elbow epicondyle, quadriceps, and patella tendon.95 Ligaments.  With aging, collagen fiber disorientation occurs that results in decreased linear stiffness and ultimate load.

CLINICAL PEARL Two musculoskeletal conditions that can severely impact function in the aging athlete are osteoporosis (see Chapter 5) and osteoarthritis. Spine.  Spinal degenerative and age-related changes have an extremely high prevalence in adult populations. Normal physiological strains are well accommodated by each functional mobile segment, but the natural aging process coupled with attrition and associated with a degenerative cascade can impact the segment, either individually or regionally.83 The general pattern is for spinal motion to decline in all directions with age, but the mobile cervical and lumbar segments and

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Rotator cuff pathology. Rotator cuff pathology in this age range runs the gamut from tendinopathy to massive tear. Partial thickness tears are quite common. A 2010 in vivo study,96 evaluating the vascularity of rotator cuff tears using ultrasound, showed that there was a significant decrease in blood flow in the intratendinous region in elderly subjects compared with younger subjects but no differences in the bursal blood flow suggesting an agerelated decrease in intratendinous vascularity.95 ▶▶ Adhesive capsulitis. This condition is described in detail in Chapter 16. For the aging athlete, conservative management is a reasonable, evidence-based approach with one study97 finding that physical therapy with steroid injections significantly better than that without at 3-month follow-up, although both groups were similar at 1 year. ▶▶ Osteoarthritis. While osteoarthritis of the shoulder is not as common as it is in the knee and hip, it is not uncommon, and can be debilitating if added to the myriad of pain generators in the biceps, acromioclavicular joint, and subacromial space.98 However, for the older recreational patient who is able to limit activity, total shoulder arthroplasty provides excellent long-term survival rates and return to sport is high.99 ▶▶

CLINICAL PEARL Fractures, which can have a significant impact on morbidity, mortality, and functional dependence, commonly occur among the elderly. Such fractures include pathologic fractures, proximal femur fractures, proximal humerus fractures, distal radius fractures, compression fractures of the spine, and stress fractures. ▶▶

Neurological.  In the central nervous system (CNS), there are age-related reductions in the total number of brain cells and fibers and the organization of fibers within the brain’s white matter in addition to the reduction to the large diameter (A-beta proprioceptive) fibers in peripheral nerves.83,91 In addition to reductions in the number of fast myelinated fibers, the speed of signal conduction within the axon of the nerve also reduces with age, thereby reducing the efficiency of the efferent transmission to the muscles.83,89

The history and physical examination of the aging athlete must differentiate between the effects of aging, inactivity, and disease on the underlying impairments and functional limitations that result in movement dysfunction. For example, mild

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impairments in ROM may be due to increased stiffness associated with aging that occurs in the tendinous or ligamentous structures around a joint, or it could be due to acute immobilization, or chronic inactivity and reduced demands on a particular joint for full ROM.86

THE FEMALE ATHLETE Both male and female children are basically equal in physical condition and have the same strength before puberty. After puberty (Table 30-2), females aged 11–12 years are 90% as strong as their male counterparts versus 85% as strong at ages 13–14, and 75% at ages 15–16 years.100

ACL Injury Although skeletal muscle physiology in men and women does not differ significantly—the actual number of muscle fibers is similar between genders—men do appear to demonstrate larger absolute strength gains due to a larger cross-sectional muscle fiber size. When comparing strength to lean body mass or cross-sectional area, women are about equal to men and are equally capable of developing strength relative to total muscle mass. However, differences in anatomy make the female more prone to certain injuries. A variety of studies have reported that female athletes are more likely to sustain an ACL injury than their male counterparts, and most of these injuries occur without contact. Theories about the higher rates of ACL injury in women have centered on the following101: Anatomic alignment and structural differences.  These include the differences in pelvic width and the tibiofemoral angle between males and females, which can affect the entire LE. For example, women demonstrate greater amounts of static external knee rotation, greater active internal hip rotation, and increased hip width when normalized to femoral length than men, resulting in a number of structural combinations.102 In addition, the magnitude of the quadriceps femoris angle (Q-angle) and the width of the femoral notch are thought to be anatomic factors that have contributed to the disparity of ACL injury rates between males and females.101 Hypothetically, a larger Q-angle increases the lateral pull of the quadriceps femoris muscle on the patella placing medial stress on the knee, decreasing the effectiveness of the quadriceps as a knee extensor, and diminishing the ability of the hamstrings to exert their protective influence on the ACL. ■■ Femoral notch.  A narrow intercondylar notch appears to increase the potential for ACL ruptures.101 The shape of the femoral notch varies with gender and may contribute to the incidence of ACL injury.101 ■■ Joint laxity.  Joint laxity tends to be greater in women than in men, although the correlation between ligamentous laxity and injury is not clear. ▶▶ Hormonal influence.  Hormones, especially estrogen, estradiol, and relaxin, may be involved indirectly in increased ACL injury in females.

Special Populations

their respective stiffer transitional junctions (cervicothoracic and thoracolumbar) display different trends. For example, in the segments adjacent to the transitional junctions, which have less relative motion, the actual compressive load is greater so there is a higher rate of arthrosis in the synovial joints, whereas in those areas in the middle of the lordosis or kyphosis the trend is for greater disc degeneration.83 Shoulder.  The normal high degree of mobility associated with the shoulder declines not only with age but with long-term sports participation. A number of musculoskeletal conditions are common in the aging shoulder including the following:

▶▶

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ACL size.  Females typically have a smaller ACL than males, which would tend to enhance the risk of tissue failure.103 ▶▶ Muscular strength and muscular activation patterns.  Several studies have demonstrated that women have significantly less muscle strength in the quadriceps and hamstrings compared with men, even when muscle strength is normalized for body weight. Approximately 30% of all ACL injuries are classified as contact injuries, and the remaining 70% are not related to direct contact and are therefore classified as noncontact.104,105 The most common noncontact ACL injuries in females are as follows104,105: ▶▶

SPECIAL CONSIDERATIONS

■■ ■■ ■■ ■■

Planting and cutting Straight knee landings One-step stop with the knee hyperextended Sudden deceleration

While landing injuries to the ACL are common in both males and females, male athletes appear to employ different mechanisms to compensate for high landing forces than females, resulting in a decrease in both varus and valgus laxity of the knee during the landing.106–109 Females have some unique characteristics that may predispose them to ACL injury, including increased genu valgum, a poor hamstringquadriceps strength ratio, running and landing on a more extended knee, quadriceps-dominant knee posture, hormonal changes, and hip/core weakness.110 Because a common mechanism of noncontact ACL injury is valgus stress with rotation at the knee, it is important that the female athlete learns to control this valgus moment111,112 using exercises designed to control this moment including front step downs, lateral step downs with resistance, and squats with resistance around the distal femur.110 In addition, the following should be emphasized110: Patient education on optimal knee alignment (keeping the knee over the second toe). ▶▶ Exercises to train the patient to stabilize the knee through coactivation of the quadriceps and hamstrings, including tilt board balance exercises while performing a throw and catch. ▶▶ Dynamic stabilization drills to teach the patient to land with the knee flexed to approximately 30 degrees to promote better alignment and activation of the quadriceps and hamstrings. ▶▶ Exercises to train the hip extensors, external rotators, abductors, and core stabilizers while emphasizing a flexed-knee posture while running, cutting, and jumping. ▶▶

Pregnancy

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Pregnancy is a state of wellness that spans approximately 40 weeks from conception to delivery. A number of physiologic changes occur during pregnancy and the postpartum period within the various body systems that can present the clinician with some unique challenges. Given the number of physiologic changes during pregnancy and the postpartum

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period within the various body systems, the extent of the physical therapy intervention will depend on the findings of the examination.

Endocrine System Changes that occur in the endocrine system include but are not limited to the following: Enlargement of the adrenal, thyroid, parathyroid, and pituitary glands. ▶▶ An increase in hormonal levels to support the pregnancy and the placenta and in preparation for labor. For example, a female hormone (relaxin) is released that assists in the softening of the pubic symphysis so that during delivery, the female pelvis can expand sufficiently to allow birth. Unfortunately, the hormone is not specific to this region and produces greater laxity in all joints.113,114 This can result in an increased susceptibility to musculoskeletal injury. ▶▶

Musculoskeletal System Pregnancy can produce a number of changes within the musculoskeletal system: The abdominal muscles are stretched to the point of their elastic limit and become weakened. ▶▶ The development of relative ligamentous laxity, both capsular and extracapsular. Ehlers–Danlos syndromes (genetic connective tissue disorders; see Chapter 5) place the individual at greater risk for pain and other complications and often result in the patient having looser shoulders, neck, and abdominal muscles increasing the need for extra patient education in body mechanics. ▶▶ The rib cage circumference increases resulting in a natural state of hyperventilation to meet the oxygen demands. ▶▶ Pelvic floor muscle (PFM) weakness. Due to the increased weight and pressure directly over these muscles, the muscles of the pelvic floor become stretched and compromised during labor—the pelvic floor drops as much as 2.5 cm (1 in) as a result of pregnancy.115 On occasions, the pelvic floor musculature may also be torn or incised during the birth process. This can lead to a number of dysfunctions including pain, prolapse, urinary or fecal incontinence, and hypertonus. Interventions include neuromuscular reeducation, patient education, biofeedback with instrumentation, and specific exercises (see “Pelvic Floor Dysfunction” section). ▶▶ Postural compensations to maintain stability and balance. These changes are related to the weight of growing breasts, uterus, and fetus, resulting in a shift in the woman’s center of gravity in an anterior and superior direction. Specific postural changes include an increased lumbar lordosis, an increased thoracic kyphosis with scapular retraction and rounded shoulders, and an increased cervical lordosis and forward head. These changes in posture can become habitual postpartum. ▶▶ Changes in gait. Since the weight increases, and the body mass is redistributed, compensations are necessary to maintain balance and perform even simple functions such ▶▶

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as walking. In advanced pregnancy, the patient develops a wider base of support and increased ER at the hips and demonstrates increased difficulty with walking, stair climbing, and rapid changes in position.

CLINICAL PEARL During pregnancy, the most common areas where women experience pain are the pelvic girdle, lumbar region, and hips due mainly to the ligamentous laxity that results from hormonal changes and the changing of the woman’s center of gravity and body mass. Common diagnoses associated with some of the above includes the following: ▶▶

Symphysis pubis dysfunction (SPD).  This disorder can occur as a result of trauma during vaginal delivery. SPD should always be considered when treating patients in the postpartum period who are experiencing suprapubic, sacroiliac, or thigh pain (see Chapter 29).

CLINICAL PEARL SPD should always be considered when treating patients in the postpartum period who are experiencing suprapubic, sacroiliac, or thigh pain.

Special Populations

pelvic region (with or without radiation) that started during pregnancy or within 3 weeks after delivery. About 49% of pregnant women experiences some type of pelvic pain,171 with 33% of these women experiencing severe pain.127 Women who have had multiple babies are at higher risk for PGP, as are those with hypermobility, an increased body mass index, and/or history of trauma to the pelvis. The pain is typically experienced in the lumbar region and over the sacroiliac joints (with no findings suggesting nerve root involvement). Although the etiology of PPPP is unknown, it has been linked to the many physiological adaptations that occur in preparation for childbirth. The previously mentioned change in the center of gravity leads to a change in the degree of lordosis of the spine, which in turn affects the paraspinal musculature. In addition, the hormonal changes that occur during pregnancy may cause an imbalance between the ligaments, muscles, and joints in the posterior aspect of the pelvis.159 Although a systematic review160 of the literature investigating the effectiveness of physical therapy interventions in the treatment of PPPP and LBP found scant evidence to support the use of exercise or mobilization in this patient population, exercise is thought to be beneficial in the postpartum period. In addition, the patient should be given posture/body mechanics advice using the suggestions listed for SPD. Coccydynia.128-130 Pain in and around the region of the coccyx, especially with sitting, is relatively common postpartum. Seating adaptations such as a donut cushion can be prescribed to lessen the weight on the coccyx and to support the lumbar lordosis. Also, the patient should be advised to lie on the side instead of in supine. If symptoms persist for more than a few weeks, the displaced coccyx can often be corrected manually (see Chapter 29). ▶▶ Diastasis recti abdominis (DRA).  A DRA, a split between the two rectus abdominis (RA) muscles to the extent that the linea alba may split under the strain, is common in pre- and postpartum women. The size of the DRA can vary from 2–3 to 12–20 cm in width and from 12 to 15 cm to the entire length of the recti muscles. It has not been determined whether the separation is a true tear or a relaxation of the tissue. Predisposing factors for a DRA in women include obesity, a narrow pelvis, multipara, multiple births, excess uterine fluid, large babies, and weak abdominals prior to pregnancy.131 The separation may develop during the second and third trimesters of pregnancy, during second stage labor and during the postpartum period.131 It is believed that a DRA may hinder the abdominal wall function related to posture, trunk stability and strength, respiration, visceral support, diminished pelvic floor facilitation, and delivery of the fetus. An umbilical hernia may result as well. The DRA is believed to contribute to chronic pelvic and LBP.132 ▶▶

▶▶

Lumbopelvic pain.116-120 Pregnancy-related lumbar pelvic pain during pregnancy, defined as pregnancy-related LBP and/or pregnancy-related pelvic girdle pain (PGP), is a complex problem, with both a physical and psychological burden.121 The prevalence is reported to range from 24% to 90%, largely in part because of the lack of a clear definition and classification of the condition.122-125 The most common location of back pain in pregnant women126 is the sacroiliac region. The cause of back pain during the childbearing year is thought to be related to the mechanical and hormonal changes. It is not clear whether the LBP is the result of the shift in the center of gravity, the associated postural changes, or changes to an intervertebral disk due to the release of relaxin. However, disk herniations are no more common during pregnancy than at other times. It is also important to consider systemic causes for LBP in this population. Kidney or urinary tract infections can both cause LBP. A 2014 systematic review of the literature by Van Benten et al.121 found that all of the included studies on exercise therapy, and most of the studies on interventions combined with patient education, reported a positive effect on pain, disability, and/or sick leave.

CLINICAL PEARL It is worth remembering that complaints of LBP in this population may also be because of a kidney or urinary tract infection. ▶▶

Peripartum posterior pelvic pain (PPPP).  PPPP can be defined as unexplained and undiagnosed pain in the

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Diagnosis includes clinical examination and assessment of symptoms. Criteria have been established for determining a DRA.131,133,134 Physical characteristics include a midline abdominal bulge without a fascial defect.131 The patient is positioned in the hook-lying position. The clinician palpates with fingers horizontally, at the umbilicus and 2 in above and

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SPECIAL CONSIDERATIONS

below the umbilicus, and the patient is asked to raise their head and shoulders while reaching toward their feet. Any separation will be palpable, and a wide ridge of bulging tissue may actually be visible. If a DRA of 1–2 fingers width (1–2 cm) is present, this is considered within normal limits. Any separation greater than two-finger wide constitutes a DRA, and, therefore, restrictions on abdominal exercise prescription should apply. However, it is worth remembering that the interrater reliability for measuring a DRA by manually inserting the fingers into the gap has been considered poor. With regard to conservative treatment, particularly exercises to prevent or reduce DRA, the verdict is inconclusive. A 2018 randomized controlled trial133 that examined the effect of a postpartum training program on the prevalence of DRA in postpartum primiparous women concluded that a weekly, postpartum, supervised exercise program, including strength training of the pelvic floor and abdominal muscles, in addition to daily home training of the PFMs, did not reduce the prevalence of diastasis. In contrast, another 2018 study135 that compared trunk muscle function between women with and without DRA at 1 year postpartum found that women with DRA demonstrated significantly lower trunk muscle rotation torque, and scored lower on the sit-up test than those without DRA.

Neurologic Swelling and increased fluid volume can cause symptoms of thoracic outlet syndrome due to compression of the brachial plexus, carpal tunnel syndrome due to median nerve compression, or meralgia paresthetica, which is compression of the lateral (femoral) cutaneous nerve of the thigh (see Chapter 3). Pregnancy-related depression and postpartum depression have been documented to occur in 5–20% of all postpartum mothers,136–138 but can also occur in fathers.139 These disorders can range from a mild “postpartum blues,” which occurs from 1 to 5 days after birth and lasts for only a few days, to the more severe forms that include postpartum depression and postpartum psychosis, which require medical or social intervention.140–142 Comorbidities such as multiple sclerosis have an impact on this population. In addition to emphasizing correct body mechanics and focusing on strengthening, equipment for new parent such as a very light stroller to prevent excessive lifting and an appropriate changing table height to prevent excessive bending should be recommended.

Gastrointestinal Nausea and vomiting may occur in early pregnancy and are generally confined to the first 16 weeks of pregnancy but occasionally remain throughout the entire 10 lunar months (hyperemesis gravidarum).140,143–146 The causes of hyperemesis gravidarum are largely unknown.

Cardiopulmonary System To meet the increased metabolic demands of the mother and fetus, various pregnancy-induced changes occur in the cardiovascular system. These changes include the following: ▶▶

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A predominance of costal versus abdominal breathing as the diaphragm elevates with a widening of the thoracic cage.

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Mild increases in oxygen consumption due to increased respiratory center sensitivity and drive.147 Even with mild exercise there is a greater than normal increase in respiratory frequency and oxygen consumption to meet the greater oxygen demand.147 However, pregnant women demonstrate decreased respiratory frequency and maximal oxygen consumption as exercise increases to moderate and maximal levels.147 ▶▶ A compensated respiratory alkalosis. ▶▶ A low expiratory reserve volume.147 ▶▶ Increased blood volume. ■■ To facilitates maternal and fetal exchanges of respiratory gases, nutrients, and metabolites. ■■ To reduce the impact of maternal blood loss at delivery. ▶▶ Increased plasma volume is relatively greater than that of red cell mass resulting in hemodilution and a decrease in hemoglobin. ▶▶ Increased cardiac output.

▶▶

CLINICAL PEARL Hypertensive disorders complicating pregnancy are the most common medical risk factor responsible for maternal morbidity and death related to pregnancy.140 Although BP decreases early in the first trimester, it gradually rises from mid pregnancy. Hypertensive disorders complicating pregnancy have been divided into five types.   Changes in BP during pregnancy include the following: ▶▶ Systemic arterial pressure should not increase during normal gestation. ▶▶ Pulmonary arterial pressure also maintains a constant level. ▶▶ Hypotension develops more readily and more markedly. ▶▶ Central venous and brachial venous pressures remain unchanged during pregnancy. During pregnancy, a condition called supine hypotension (also known as inferior vena cava syndrome), manifested by a decrease in BP, may develop in the supine position, especially after the first trimester. The decrease in BP is thought to be caused by the occlusion of the aorta and inferior vena cava by the increased weight and size of the uterus as spontaneous recovery usually occurs upon a change of maternal position. However, although a change in position is necessary, patients should not be allowed to stand up quickly to avoid another condition related to a decrease in BP; orthostatic hypotension. Signs and symptoms of this condition run the gamut from a headache, bradycardia, dizziness, and shortness of breath to numbness in extremities, nausea and vomiting, and syncope (fainting). Ideally, the time spent in supine should be limited to approximately 5 minutes. Alternative positions include side lying (best position for minimizing compression), supine reclined, or supine with a small wedge under the right hip.

Metabolic System The metabolic rate increases during both exercise and pregnancy. Thus, an additional intake of 300 cal per day is needed

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▶▶

genetic predisposition; ■■ high-risk populations include people of Aboriginal, Hispanic, Asian, or African descent; ■■ a family history of diabetes, gestational diabetes, or glucose intolerance; and ■■ increased tissue resistance to insulin during pregnancy, due to increased levels of estrogen and progesterone. Current risk factors include

maternal obesity (>20% above ideal weight). The recommended weight gain during pregnancy is 25–27 lb. Maternal obesity during the first pregnancy increases the risk for gestational diabetes in any subsequent pregnancy, but also increases the risk for conversion to type II diabetes later in life; ▶▶ low level of high-density lipoprotein cholesterol (2.8 mmol/L); ▶▶ hypertension or preeclampsia (risk for gestational diabetes is increased to 10–15% when hypertension is diagnosed); and ▶▶ maternal age >25 years. ▶▶

Most individuals with gestational diabetes are asymptomatic. However, subjectively the patient may complain of polydipsia; polyuria; ▶▶ polyphagia; and ▶▶ weight loss. ▶▶ ▶▶

Renal and Urologic Systems Anatomic and hormonal changes during pregnancy place the pregnant woman at risk for both lower and upper urinary tract infections and for urinary incontinence (UI).140 The size of the uterus increases fivefold, and 20 times in weight by the end of pregnancy. In addition, the ureter enter the bladder at a perpendicular angle because of the uterine enlargement and this can result in a reflux of urine out of the bladder and back into the ureter, which can result in urinary tract infections. As the fetus grows, stress on the mother’s bladder can increase. This can result in UI (refer to “Pelvic Floor Dysfunction”). Although urine leaking is normal for 3–4 weeks postpartum as the pelvic floor become stretched, leaking that persists beyond this time frame could be problematic. For example, a 2016, 12-year longitudinal cohort study, that investigated the extent of persistent UI 12 years after birth found that among

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those who had reported UI at 3 months, 76.4% reported it at 12 years.148

Exercise Prescription The goals of therapeutic exercise during pregnancy are to improve muscle balance and posture, help provide support of the growing uterus, stabilization of the trunk and pelvis, and maintenance of function for more rapid recovery after delivery.140 Unless there is a serious condition present, exercise during pregnancy is healthy. In fact, the American College of Obstetricians and Gynecologists recommend 30 minutes of moderate-intensity exercise most days of the week throughout pregnancy. Contraindications to exercise include the following149: An incompetent cervix (early dilation of the cervix before pregnancy is full-term). ▶▶ Vaginal bleeding (especially second or third trimester). ▶▶ Placenta previa (the placenta is located on the uterus in a position where it may detach before the baby is delivered). ▶▶ Multiple gestations with risk of premature labor. ▶▶ Pregnancy-induced hypertension. ▶▶

Special Populations

to meet the basic metabolic needs of pregnancy. Fetoplacental metabolism generates additional heat, which maintains fetal temperature at 0.5–1°C (0.9–1.8°F) above maternal levels.11 Because of the increased demand for tissue growth, insulin is elevated from plasma expansion, and blood glucose is reduced for a given insulin load. Fats and minerals are stored for maternal use. Gestational diabetes is defined as carbohydrate intolerance of variable severity, with onset or first recognition during pregnancy. After the birth, blood sugars usually return to normal levels; however, frank diabetes often develops later in life. Typical causes include:

Premature labor (labor beginning before the 37th week of pregnancy). ▶▶ Maternal heart disease. ▶▶ Maternal type I diabetes. ▶▶ Intrauterine growth retardation.149 ▶▶

Even without these conditions, the patient requires permission from her physician before beginning an exercise program. Some precautions should be observed during exercise.150–157 Exercise programs for high-risk pregnancies should be individually established based on diagnosis, limitations, physical therapy examination and evaluation, and in consultation with the physician. Exercises for the pelvic floor are described in the section “Pelvic Floor Dysfunction.” Objective data on the impact of exercise on the mother, the fetus, and the course of pregnancy are limited, and results of the few studies in humans are often equivocal or contradictory.155 No human research has conclusively proven a detrimental feature response to mild-, moderate-, or highintensity exercise during pregnancy. However, as both exercise and pregnancy are associated with a high demand for energy, the competing energy demands of the exercising mother and the growing fetus raise the theoretic concern that excessive exercise might adversely affect fetal development.140 Therefore, theoretically, because of the physiologic changes associated with pregnancy, as well as the hemodynamic response to exercise, some precautions should be observed during exercise (Table 30-4).150–157 Warning signs associated with exercise during pregnancy include pain, vaginal bleeding, tachycardia, dyspnea, uterine contractions, and chest pain. Adjunctive Interventions.  Modalities that increase body heat (hot packs, ultrasound, shortwave, or microwave diathermy) should be used with caution, especially over the abdomen or uterus. Except for the use of transcutaneous electrical stimulation during labor and delivery, electrical stimulation is contraindicated during pregnancy.

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TABLE 30-4

Exercise Precautions During Pregnancy

SPECIAL CONSIDERATIONS

Exercise intensity    

Exercise programs for high-risk pregnancies should be individually established based on diagnosis, limitations, physical therapy examination and evaluation, and in consultation with the physician. Exercise acts in concert with pregnancy to increase heart rate, stroke volume, and cardiac output. However, during exercise, blood is diverted from abdominal viscera, including the uterus, to supply exercising muscle. The decrease in splanchnic blood flow can reach 50% and raises theoretic concerns about fetal hypoxemia. Women should avoid becoming overtired. Hypoglycemia occurs more readily during pregnancy necessitating adequate carbohydrate intake. Exercise activity should be performed at a moderate rate during a low-risk pregnancy. Aerobic exercise causes a redistribution of blood flow away from the internal organs and toward the working muscles. The maternal respiration rate appears to adapt to mild exercise but does not increase proportionately with moderate and severe exercise when compared with a nonpregnant state. Guidelines for a low-risk pregnancy permit women to remain at 50–60% (12–14 on the Borg scale of perceived exertion) of their maximal heart rate (monitored intermittently) for approximately 15–30 minutes per session.

Exercise type  

Recommended activities include stationary cycling, swimming, or water aerobics. Weight-bearing exercises and high-impact exercises should be prescribed judiciously as increases in joint laxity may lead to a higher risk of strains or sprains.

Exercise position      

Patients should not exercise in the supine position for more than 5 minutes after the first trimester (see “Supine Hypotension”). To prevent inferior vena cava compression when the patient is lying supine, a folded towel can be placed under the right side of the pelvis so that the patient is tipped slightly to the left. If the supine position is contraindicated, exercises can be performed in side lying, the quadruped position or sitting. Positions that involve abdominal compression (flat prone lying) should be avoided in mid to late pregnancy. Modifications to exercise for the abdominal muscles must be made for a woman with diastasis recti, as the presence of this condition potentially reduces the ability of the abdominal wall muscles to contribute to their role in trunk and pelvic girdle alignment, motion, and stability. Traditional abdominal exercises, such as full sit-ups or bilateral straight leg raises, are not recommended as they may encourage further separation. However, these exercises can be resumed when the separation is