Foundations for Osteopathic Medicine

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FOUNDATIONS FOR OSTEOPATHIC MEDICINE SECOND EDITION

FOUNDATIONS FOR OSTEOPATHIC MEDICINE Published under the auspices of the American Osteopathic Association

SECOND EDITION Executive Editor ROBERT C. WARD, D.O., F.A.A.O. Professor Department 0/ Osteopathic Manipulative Medicine and Family Medicine College o/ Osteopathic Medicine Michigan State University East Lansing, Michigan

Section Editors RAYMOND J. HRUBY, D.O., M.S., F.A.A.O.

WILLIAM A. KUCHERA, D.O., F.A.A.O.

Professor and Chairman

Professor Emeritus oJOsteopathic Manipulative Medicine

Department oJOsteopathic Manipulative Medicine

Kirksville College oJOsteopathic Medicine

College ojOsteopathic Medicine ojthe Pacific

Kirksville, Missouri

Western University ojHealth Sciences

MICHAEL M. PATTERSON, Ph.D.

Pomona, California

Professor and Assistant Chair

JOHN A. JEROME, Ph.D., B.C.F.E.

Department ojOsteopathic Principles and Practice

Associate Professor oJClinical Medicine

College oJOsteopathic Medicine

Department oJOsteopathic Medicine

Nova Southeastern University

Michigan State University

Ft. Lauderdale, Florida

East Laming, Michigan

BERNARD R. RUBIN, D.O., M.P.H.

Clinical Director

Professor ojMedicine

Pain Clinic

Chief Division ojRheumatology

Pain Management Specialists, PLLC

Department ojMedicine

Lansing, Michigan

University ojNorth Texas Health Science Center

JOHN M. JONES, III, D.O., AOBFP

Fort Worth. Texas

Professor

MICHAEL A. SEFFINCER, D.O., C.S.P.O.M.M., F.A.A.F.P.

Department oJOsteopathic Manipulative Medicine College oJOsteopathic Medicine oJthe Pacific

Assistant Professor



Pomona, California

College oJOsteopathic Medicine oJthe Pacific

ROBERT E. KAPPLER, D.O., F.A.A.O.


Professor and Chair

Pomona. California


SARAH A. SPRAFKA, Ph.D.

Chicago College oJOsteopathic Medicine Midwestern Univenity

Director, Predoctoral Education

Downer's Grove, Illinois

College ojOsteopathic Medicine

MICHAEL L. KUCHERA, D.O., F.A.A.O.

University ojNew England Biddeford, Maine

Professor oJOsteopathic Manipulative Medicine

RICHARD VAN BUSKIRK, D.O., Ph.D.

Director oJOsteopathic Manipulative Medicine Research Philadelphia College oJOsteopathic Medicine

Private Practice

Philadelphia. Penmylvania

Sarasota. Florida

4� LIpPINCOTT WILLIAMS •

& WILKINS

A Wolters Kluwer Company Philadelphia Buenos Aires

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Acquisitions Editor: Timothy Y Hiscock DevelopmentaL Editor: MicheLLe LaPLante Production Editor: Robin E. Cook Manufocturing Manager: Tim Reynolds Cover Designer: Mark Lerner Compositor: TechBooks Printer: Courier Westford

© 2003 by LIP PINCOTT WILLIAMS & WILKINS 530 Walnut St. Philadelphia, PA 19106 USA www.Lww.com

All righrs reserved. This book is prorecred by copyright. No part of rhis book may be reproduced in any form or by any means, including phorocopying, or urilized by any informarion srorage and retrieval sysrem wirhour wrirren permission from rhe copyrighr owner, excepr for brief quotations embodied in crirical articles and reviews. Marerials appearing in this book prepared by individuals as parr of rheir official duries as U.S. governmenr employees are not covered by rhe above-menrioned copyright. Prinred in the USA

Library of Congress Cataloging-in-Publicauon Data

Foundarions for osteoparhic medicine / edited by Roben C. Ward .. . [er al.].- 2nd ed. p.; cm. Includes bibliographical references and index. ISBN 0-7817-3497-5

I. Osreoparhic medicine.

2. Osteoparhic medicine-Philosophy.

I. Ward, Roben c., DO. [DNLM: I. Osreoparhic Medicine-merhods. WE 940 F771 2002] RZ342 .F68

2002

615.5'33-dc21

2002016285

Care has been raken ro confirm the accuracy of rhe information presenred and ro describe generally accepred pracrices. However, rhe aurhors, edirors, and publisher are nor responsible for errors or omissions or for any consequences from applicarion of rhe informarion in rhis book and make no warranty, expressed or implied, with respecr ro rhe currency, complereness, or accuracy of rhe conrenrs of rhe publicarion. Applicarion of rhis informarion in a particular siruarion remains rhe professional responsibility of rhe pracririoner. The aurhors, edirors, and publisher have exerted every effort ro ensure rhar drug selection and dosage ser forth in rhis rexr are in accordance wirh currenr recommendations and pracrice ar rhe rime of publicarion. However, in view of ongoing research, changes in governmenr regularions, and the constanr Aow of inform arion relaring ro drug rherapy and drug reacrions, rhe reader is urged ro check rhe package inserr for each drug for any change in indicarions and dosage and for added warnings and precaurions. This is particularly imporranr when rhe recommended agenr is a new or infrequenrly employed drug. Some drugs and medical devices presenred in rhis publicarion have Food and Drug Adminisrrarion (FDA) clearance for limired use in resrricred research serrings. Ir is rhe responsibility of rhe healrh care provider ro ascertain rhe FDA starus of each drug or device planned for use in [heir clinical pracrice. 10 9 8 7 6 5 4 3 2

This second edition of Foundations for Osteopathic Medicine is dedicated to three icons of osteopathic medicine. Each, in his own very special way, made remarkable contributions to the growth and evolutions of the osteopathic profession, and all it stands for.

George Northup George Northup, D.O., F.A.A.O. ( 1 9 1 5- 1 996), was the son of Thomas Northup, D.O., the first secretary treasurer of the American Academy of Osteopathy. Among his many accomplishments, Dr. Northup was the 1 958- 1 959 president of the American Osteopathic Association (AOA) . Born in Syracuse, New York, he lived for a short time in Kirksville, Missouri, while his father was a student. In 1 939, he graduated from the Philadelphia College of Osteopathic Medicine and established practices in Morristown and Livingston, New Jersey. From the beginning, he dedicated his career to " . . . [gaining] . . . acceptance of the profession by the rest of organized medicine and the public" ( 1 ). Particularly skilled at politics, Dr. Northup worked diligently for greater osteopathic recognition as a full-service health profession. Always dedicated to excellence, he was appointed editor-in-chief for AOA publications in 1 96 1 , serving 26 years until his retirement in 1 987. Among his greatest successes were his many insightful editorials dealing with a wide array of osteopathically oriented and general health policy issues. Among his many publications is his classic book, Osteopathic Medicine: An American Reformation (2).

I

Irving M. Korr

,.

Irvin M . Korr, Ph.D., ( 1 9 1 0-), led a distinguished career as both a re spected researcher and educator at the Kirksville College of Osteopathic Medicine (KCOM) . Beginning his career as a cellular physiologist, he re ceived his PhD from Princeton University in 1 935. From 1 936 to 1 942, he was an instructor in physiology at the New York University School of Medicine in New York City. During World War II he worked for the U.S. War Department researching aspects of aviation medicine, wound ballis tics, and climate physiology. After the war, Korr was recruited to Ki rksville College of Osteopathic Medicine by]. Stedman Denslow, D.O., himself a distinguished faculty member actively pursuing osteopathically related research. Shortly after arriving at Kirksville, Dr. Korr realized that his real interests lay in exploring the relationship of the autonomic nervous system to somatic dysfunction. Some refer to Korr's tenure at Kirksville as a golden age for osteopathic research. After a 3D-year career, he retired from KCOM having written or cowritten many papers that conrinue to be widely quoted and used in most osteopathic curricula. After leaving Kirksville, he spenr a number of years teaching osteopathic philosophy and principles of healthy lifestyles at both Michigan State University College of Osteopathic Medicine, and the University of North Texas College of Osteopathic Medicine.

Paul E. Kimberly Paul E Kimber!y, D.O., EAA 0., Professor and Chairman Emeri tus, Kirksville College of Osteopathic Medicine ( 1 9 1 5-) a quiet and unassuming osteopathic giant, was born into an osteopathic family. He graduated from the Des Moines Still College of Osteopathic Medicine in 1 940. Through a mixture of preclinical and postdoctoral teaching, writing, and pragmatically useful approaches to osteo pathic patient care, Dr. Kimberly's contributions are legendary for over three generations of osteopathic physicians. He is renowned for his detailed and clinically useful grasp offunctional anatomy and credits much ofhis career to his first mentor, H. Virgil Halliday, D.O., Professor of Anatomy at the Des Moines School. Halladay, himself a consummate functional anatomist, was a student of AT. Still. Recognizing Kimberly's special combination of anatomical knowledge and communication skills, Halladay hired the rising young star as a teaching assistant. Eventually, the opportunity led Kimberly to directly involve himself in the development of many aspects of contemporary osteopathic skills teaching programs. Among his contributions are the following: A collaboration with O. Edwin Owen, D.O., that collated and published the first edition of Chapman's Reflexes. Publication rights now lie with the American Academy of Osteopathy. Collaboration with Fred L Mitchell, Sr, of Chattanooga, Tennessee, in the development of the original muscle energy concepts. Organization and development of the first detailed anatomy courses highlighting WG. Sutherland's cranial osteopathy concepts. Several decades later, he published a manual on cranial osteopathic methods that is widely in use today. Development and participation in the first clinical teaching teams sponsored by the American Academy of Osteopathy. His central role in helping the Educational Council on Osteopathic Principles (ECOP) develop and clarify its long-range agenda, much of which is represented in this text. His major role in introducing and developing international cooperation among allopathic and American osteopathic physician groups in collaboration with the International Federation of Musculoskeletal and Manual Medicine (FIMM). His major participation in developing and standardizing postdoctoral continuing education programs at the Michigan State University College of Osteopathic Medicine, which were begun at the request of the North American Academy of Musculoskeletal and Manual Medicine (NAMM) and F IMM.

(I) Fitzgerald M. Hail to our ex-chief, The DO, 1 997:32 (2) Northup C. Osteopathic Medicine: An American Reformation, Chicago: American Osteopathic Association, 1 966.

THIS PAGE INTENTIONALLY LEFT BLANK

CONTENTS

Contributing Authors xi Mission Statement xv Preface xvii Preface to the First Edition Foreword xxi Acknowledgments xxiii

1 0.

Microbiologic Considerations and Infectious Diseases 165 Lauritz A. Jensen and James B. Jensen

X1X

11.

Endocrine System and Body Unity: Osteopathic Principles at a Chemical Level 179 Ronald Portanova

SECTION I: OSTEOPATHIC PHILOSOPHY AND HISTORY 1 1.

1 2.

Pharmacologic and Osteopathic Basic Principles 189 Robert] Theobald, Jr.

Osteopathic Philosophy 3 Michael A. Seffinger, Hollis H. King, Robert C. Ward,

John M. Jones, II!, Felix] Rogers, and Michael M. Patterson

2.

Major Events in Osteopathic History 19

SECTION III: OSTEOPATHIC CONSIDERATIONS IN THE BEHAVIORAL SCIENCES 1 95

Barbara E. Peterson

Introduction 196 John A. Jerome

SECTION II: OSTEOPATHIC CONSIDERATIONS IN THE BASIC SCIENCES 31

1 3.

Gerald G. Osborn

1 4. Introduction 32 Michael M. Patterson

3.

Rules of Anatomy 37 Lex C. Towns

4.

Anatomy 44

Biomechanics: An Osteopathic Perspective 63

1 5.

Autonomic Nervous System 90 Frank H. Willard

7.

Pain Management 212 John A. Jerome

1 6.

Life Phases and Health 227 Jed Magen

1 7.

Stress Management in Primary Care 233

Michael R. Wells

6.

Introduction to Psychoneuroimmunology 208 David A. Baron

Allen W Jacobs and William M. Falls

5.

Health Promotion and Maintenance 197

John A. Jerome

1 8.

Osteopathic Psychiatry 245 Ronald H. Bradley, Gerald G. Osborn,

Neurophysiologic Mechanisms of Integration

John A. Jerome, and Mary C. Williams

and Disintegration 120 Michael M. Patterson and Robert D. Wurster

8.

Nociception, the Neuroendocrine Immune System, and Osteopathic Medicine 137 Frank H. Willard

9.

Tissue Respiration and Circulation 157 Harvey V Sparks, Jr.

SECTION IV: OSTEOPATHIC CONSIDERATIONS IN CLINICAL PROBLEM SOLVING 255 1 9.

Clinical Problem Solving 257 Sarah A. Sprafka

viii

Contents

SECTION V: OSTEOPATHIC CONSIDERATIONS IN FAMILY PRACTICE AND PRIMARY CARE 281

34.

Pulmonology 500 Gilbert E. D'Alonzo, Jr. and Samuel L. Krachman

35.

Osteopathic Physical Medicine and Rehabilitation 516

J

Introduction 282 Richard L. Vtm Buskirk and Robert E. Kappler

20.

of the Primary Care Model 289 Richard L. Vtm Buskirk and Kenneth E. Nelson

21 .

36.

Osteopathic Family Practice: An Application

37.

General Pediatrics 305 Shawn Centers, Mary Anne Morelli, Colleen Vallad-Hix, and Michael A. Seffinger

23.

Geriatrics 327

Rheumatology 526

J

Michael Finley

An Osteopathic Approach to Sports Medicine 534

P Gunnar Brolinson, Kurt Heinking, and Albert J Kozar

General Internal Medicine 298 Donald R. Noll, John M. Willis, and Terri Turner

22.

Michael Wieting and James A. Lipton

SECTION VII: OSTEOPATHIC CONSIDERATIONS IN PALPATORY DIAGNOSIS AND MANIPULATIVE TREATMENT 551

Thomas A. Cavalieri

Introduction 552 John M Jones, III and Robert E. Kappler

SECTION VI: OSTEOPATHIC CONSIDERATIONS IN THE CLINICAL SPECIALTIES 339

Part A: Overview: Evaluation and Management 557

38. Introduction 340 Michael A. Seffinger

24.

An Osteopathic Perspective on Cardiology 345

25.

Osteopathic Management of Ear, Nose,

Felix J Rogers

and T hroat Disease 370

Robert E. Kappler

39.

Osteopathic Medicine in the Practice of Emergency Medicine 383

40.

27.

Robert E. Kappler and William A. Kuchera

41 .

28.

42. 43.

Michael L. Kuchera

44.

Manipulative Medicine 420

31 .

Obstetrics 450 Melicien Tettambel

32.

William A. Kuchera and Robert E. Kappler

Neurology 435 Mitchell L. Elkiss and Louis E. Rentz

Oncology 462

Part B: Regional Examination and Treatment 660

45.

33.

46.

and Jeff] Patterson

Cervical Spine 684 Robert E. Kappler

47.

Upper Extremities 690 Robert E. Kappler and Kenneth A. Ramey

Orthopedics 477 Richard A. Scott, Michael L. Kuchera,

Head: Diagnosis and Treatment 660 Robert E. Kappler and Kenneth A. Ramey

Michael J Opipari, Augustine L. Perrotta, and David R. Essig-Beatty

Musculoskeletal Examination for Somatic Dysfunction 633

Raymond J Hruby

30.

Postural Considerations in Coronal, Horizontal, and Sagittal Planes 603

Gynecology 409 Neuromusculoskeletal Medicine and Osteopathic

Radiographic Aspects of the Postural Study 591 Michael L. Kuchera and William A. Kuchera

Melicien Tettambel

29.

Considerations of Posture and Group Curves 580 Michael L. Kuchera and Robert E. Kappler

General Surgery 399 Constance Cashen and Sydney PRoss

Diagnosis and Plan for Manual Treatment: A Prescription 574

Peter Adler-Michaelson, Bernadette Brandon, and Raul Garcia

Examination and Diagnosis: An Introduction 566 Michael L. Kuchera

Harriet H. Shaw and Michael B. Shaw

26.

Palpatory Skills and Exercises for Developing the Sense of Touch 557

48.

T horacic Region 705

Raymond J Hruby

Contents

49.

50.

T he Rib Cage 718

67.

Lumbar Region 727

68.

Raymond j. Hruby

52. 53.

Elaine Wallace, john M. McPartland, john M jones,

III, William A. Kuchera, and Boyd R. Buser 69.

Pelvis and Sacrum 762 Kurt P Heinking and Robert E. Kappler

70.

54.

Alexander S. Nicholas

55.

71 .

Treatment of the Acutely III Hospitalized Patient 1115 Hugh Ettlinger

72.

Efficacy and Complications 1143 Michael L. Kuchera, Eileen L. Di Giovanna, and Philip E. Greenman

Articulatory Techniques 834 David A. Patriquin and john M. jones, III

56.

Dr. Andrew Taylor Still 1094 Richard L. Vtm Buskirk

Soft Tissue Techniques 819 Walter C. Ehrenfeuchter, David Heilig, and

Treatment of Somatic Dysfunction with an Osteopathic Manipulative Method of

Michael L. Kuchera

Treatment 819

V isceral Manipulation 1078 Kenneth Lossing

Lower Extremities 784

Part C: Palpatory Diagnosis and Manipulative

Lymphatic System: Lymphatic Manipulative Techniques 1056

T he Abdominal Region 751

Raymond j. Hruby

Chapman Reflexes 1051 David A. Patriquin

William A. Kuchera

51 .

73.

Somatic Dysfunction 1153

H james jones

T hrust (High-Velocity/Low-Amplitude) Techniques 852 Robert E. Kappler and john M. jones, III

57.

Muscle Energy Techniques 881 Walter C. Ehrenfeuchter and Mark Sandhouse

58.

SECTION VIII: BASIC AND CLINICAL RESEARCH FOR OSTEOPATHIC THEORY AND PRACTICE 1 1 63 Introduction 1164

Fascial-Ligamentous Release: Indirect

Albert E Kelso and Bernard R. Rubin

Approach 908 Anthony G. Chila

59.

74.

Integrated Neuromusculoskeletal Release and

Michael M. Patterson

75.

61 .

Functional Technique: An Indirect Method 969

Deborah M. Heath and Norman Gevitz

76.

William L. johnston

62.

Osteopathy in the Cranial Field 985 Hollis H King and Edna M. Lay

63.

77.

Brian H Foresman, Gilbert E. D'Alonzo, jr.,

Strain and Counterstrain Techniques 1002

and john A. jerome

Facilitated Positional Release 1017

78.

Dennis j. Dowling

79.

Progressive Inhibition of Neuromuscular Structures Technique 1026

Dennis j. Dowling

66.

Biobehavioral Interactions with Disease and Health 1203

Clinical Research and Clinical Trials 1215 Bernard R. Rubin

Stanley Schiowitz, Eileen L. Di Giovanna, and

65.

Outcomes Research and Design 1194

Richard j. Snow, john C. Licciardone and Russell G. Gamber

john C. Glover and Paul R. Rennie

64.

T he Research Status of Somatic Dysfunction 1188

Myofascial Release 931 Robert C. Ward

Foundations for Osteopathic Medical Research 1167

Balanced Ligamentous Tension Techniques 916 jane E. Carreiro

60.

ix

Osteopathic Research: Challenges of the Future 1219 Michael M. Patterson

Glossary o/Osteopathic Terminology 1229

Myofascial Trigger Points as Somatic

Appendix I 1255

Dysfunction 1034

Appendix II 1258

Michael L. Kuchera and john M. McPartland

Subject Index 1263


CONTRIBUTORS

Peter Adler-Michaelson, D.O., Ph.D.

Assistant Professor

Eileen L. DiGiovanna, D.O.

of Osteopathic Medicine, Philadelphia College of Osteo

pathic Medicine, Old Westbury, New York, and Attend

pathic Medicine, Philadelphia, Pennsy lvania David A. Baron, M.S.Ed., D.O.

ing Physician, Department of Family Practice, Good

Professor and Chair,

Samaritan Hospital, West Islip, New York

Department of Psychiatry, Temple University School of Medicine, Philadelphia, Pennsylvania Ronald H. Bradley, D.O., Ph.D.

Dennis J. Dowling, D.O.

Clinical Professor ofIn

York College of Osteopathic Medicine, Old Westbury, New York, and Director of Manipulation, Attending

Michigan, and Vice Chairman, Department of Psychia

Physician, Department of Physical Medicine and Re

try,Ingham Regional Medical Center, Lansing, Michigan

Residency

Brandon, Director,

D.O. St.

Emergency

Barnabas

Bronx,

New York P. Gunnar Brolinson, D.O. Boyd R. Buser, D.O.

habilitation, Nassau University Medical Center, East

Medicine

Hospital,

Meadow, New York Walter C. Ehrenfeuchter, D.O., EA.A.O.

phia College of Osteopathic Manipulative Medicine, Bala Cynwyd, Pennsylvania

Associate Dean, Clinical Mfairs,

Jane E. Carreiro, D.O.

Mitchell L. Elkiss, D.O.

Associate Professor and Chair,

Department of Osteopathic

Manipulative Medicine,

ing, Michigan, and Associates in Neurology, P.c., Farm ington Hills, Michigan David R. Essig-Beatty, D.O.

Constance Cashen, D.O., EA.C.O.S.

Clinical Associate

A.

Cavalieri,

D.O.

Professor

of

Clinical

of Osteopathic Medicine, Lewisburg, West Virginia Hugh Ettlinger, D.O.

Osteopathic Medicine, Old Westbury, New York, and

Osteopathic Medicine, University of Medicine and Den Shawn Centers, D.O.

Clinical Attending and Assis

St. Barnabas Hospital, Bronx, New York W illiam M. Falls, Ph.D.

partment of Radiology, Division of Anatomy and Struc

Manipulative Medicine, Osteopathic Center for Children California Anthony G. Chila, D.O. Ohio

University

Professor of Family Medicine,

College of Osteopathic Medicine,

Athens, Ohio Gilbert E. D'A1onzo, Jr., D.O., EA.C.O.I.

Professor of

Medicine, Division of Pulmonary and Critical Care, Tem

Associate Dean of Student Ser

vices, College of Osteopathic Medicine, Professor, De

tant Professor of Pediatrics, Department of Osteopathic of Western University of Health Sciences, San Diego,

Associate Professor of Osteo

pathic Manipulative Medicine, New York College of

Medicine, Chairman, Department of Medicine, School of tistry, Stratford, New Jersey

Associate Professor of Os

teopathic Principles and Practice, West Virginia School

Professor of General Surgery, St. Vincent Mercy Medical Center, Toledo Surgical Associates, Toledo, Ohio Thomas

Assistant Clinical Professor of

Internal Medicine, Michigan State University, East Lans

University of New England College of Osteopathic Medicine, Biddeford, Maine

Clinical Pro

fessor of Osteopathic Manipulative Medicine, Philadel

Private Practice, Toledo, Ohio

University of New England, Biddeford, Maine

Professor and Chairman De

partment of Osteopathic Manipulative Medicine, New

ternal Medicine, Michigan State University, East Lansing,

Bernadette

Professor of Osteopathic

Manipulative Medicine, New York College of Osteo

tural Biology, East Lansing, Michigan J.

Michael

Finley,

D.O.

Department

of

Internal

Medicine, Western University College of Osteopathic Medicine, Pomona, California Brian H. Foresman, D.O., M.S.

Associate Professor

of Clinical Medicine, Indiana University

School of

Medicine, Indianapolis, Indiana

ple University School of Medicine, Deputy Chief Divi

Russell G. Gamber, D.O.

sion of Pulmonary and Critical Care, Temple University

Manipulative Medicine,

Hospital, Philadelphia, Pennsylvania

Health Science Center, Fort Worth, Texas

Department of Osteopathic University

of North Texas

Contributors

xii

Raul Garcia, D.O.

Senior Emergency Medicine Resident,

New York College of Osteopathic Medicine, St. Barnabas

Professor and Chair, Department

of Social Medicine, Ohio University College of Osteo

Oklahoma

State

Physicians Health Care Center,

University

College

of Osteopathic

Professor Emeritus of Osteo

pathic Manipulative Medicine, College of Osteopathic Medicine,

Michigan State University, East Lansing,

Michigan Deborah M. Heath, D.O., M.D.(H)

Private Practice,

Arizona Center for Health and Medicine, Scottsdale, Arizona David

Heilig,

D.O. (Deceased)

Emeritus

Professor,

Department of Osteopathic Manipulative Medicine, Philadelphia College of Osteopathic Medicine, Philadel phia, Pennsylvania Kurt Heinking, D.O.

H. James Jones, D.O.

Assistant Professor of Neurology/

of Health Sciences, College of Osteopathic Medicine of the Pacific, Pomona, California Robert E. Kappler, D.O., EA.A.O.

Medicine, Tulsa, Oklahoma Philip E. Greenman, D.O.

ences, Pomona, California

Osteopathic Manipulative Medicine, Western University

pathic Medicine, Athens, Ohio John C. Glover, D.O.

Professor, Department of Os

teopathic Manipulative Medicine, College of Osteopathic Medicine of the Pacific, Western University of Health Sci

Hospital, Bronx, New York Norman Gevitz, Ph.D.

John M. Jones, III, D.O.

Assistant Chair, Department of

Osteopathic Manipulative Medicine, Chicago College of Osteopathic Medicine, Midwestern University, Downer's Grove, Illinois, and Staff Member, Department of Family Medicine, Hinsdale Hospital, Hinsdale, Illinois Raymond J. Hruby, D.O., M.S., EA.A.O.

Professor

and Chair, Department of Osteopathic Manipulative Medicine, Western University of Health Sciences, Col lege of Osteopathic Medicine of the Pacific, Pomona, California

Professor and Chair,

Department of Osteopathic Manipulative Medicine, Chicago College of Osteopathic Medicine, Midwestern University, Downer's Grove, Illinois Albert E Kelso, Ph.D., D.Sci. (Hon.)

Professor Emeri

tus, Center for Osteopathic Education and Research, Uni versity Health Sciences, Chicago College of Osteopathy, Chicago, Illinois Hollis H. King, D.O., Ph.D.

Associate Professor of Os

teopathic Manipulative Medicine, College of Osteopathic Medicine, Pacific Western University of the Health Sci ences, San Diego, California AlbertJ. Kozar, D.O.

SportS Care, Toledo, Ohio

Samuel L. Krachman, D.O.

Director, Sleep Disorders

Center, Tuberculosis Program, Department of Pulmonary Medicine, Temple University, Philadelphia, Pennsy lvania Michael L. Kuchera, D.O.

Professor of Osteopathic

Manipulative Medicine, Director of Osteopathic Manip ulative Medicine Research, Philadelphia College of Os teopathic Medicine, Philadelphia, Pennsy lvania Wuliam A. Kuchera, D.O., EA.A.O.

Professor Emeritus,

Department of Osteopathic Manipulative Medicine,

Allen W. Jacobs, D.O., Ph.D. (Deceased)

Dean, College

of Osteopathic Medicine, Professor and Team Physician, Department of Osteopathic Manipulative Medicine, Michigan State University, East Lansing, Michigan Lauritz A. Jensen, D.A.

Kirksville College of Osteopathic Medicine, Kirksville, Missouri Edna M. Lay, D.O.

Private Practice, Bozeman, Montana

John C. Licciardone, D.O., M.S., M.B.A.

Professor of

Director of Pre-Clinical Educa

Family Medicine, Director of Grants and Funding, De

tion, Nova Southeastern University College of Osteo

partment of Family Medicine, Texas College of Osteo

pathic Medicine, Ft. Lauderdale, Florida James

B. Jensen,

D.O.

Microbiology

pathic Medicine, University of North Texas Health Sci Department,

Brigham Young University, Provo, Utah John A. Jerome, Ph.D.

James A. Lipton, D.O., EA.A.O., EA.A.P.M.R.

Associate Professor of Clinical

Medicine, Michigan State University College of Osteo pathic Medicine, East Lansing, Michigan, and Clini cal Director, Pain Clinic, Pain Management Specialists, PLLC, Lansing, Michigan Ptofessor Emeri

tus, Department of Family and Community Medicine, State

University,

College

Medicine, East Lansing, Michigan

of

Osteopathic

Adjunct

Clinical Professor, Osteopathic Manipulative Medicine, New York College of Osteopathic Medicine, Adjunct Clinical Associate Professor, Family Medicine, Midwest ern University, Downer's Grove, Illinois Kenneth Lossing, D.O.

William L. Johnston, D.O., EA.A.O. Michigan

ence Center, Fort Worth, Texas

Private Practice, San Rafael,

California Jed Magen, D.O.

Director, Residency Education, Depart

ment of Psychiatry, Michigan State University College of Osteopathic Medicine, East Lansing, Michigan

Contributors John M. McPartland, M.S. (Hons), D.O.

Faculty of

Health and Environmental Sciences, U NITEC, Auck land, New Zealand

FelixJ. Rogers, D.O.

Downriver Cardiology Consultants,

Trenton, Michigan Sydney P. Ross, D.O.

Mary Anne Morelli, D.O.

Private Practice, Osteopathic

Kenneth E. Nelson, D.O., EA.A.O., EA.C.O.EP.

As

sociate Professor, Osteopathic Manipulative Medicine, Department of Osteopathic Manipulative Medicine, Chicago College of Osteopathic Medicine, Midwestern University, Downer's Grove, Illinois Alexander S. Nicholas, D.O.

Pennsylvania College of Os

Associate Professor, Kirksville Col

BiCounty Community Hospi

Kirksville College of Osteo

pathic Medicine, Kirksville, Missouri David A. Patriquin, D.O.

Mark Sandhouse, D.O.

Assistant Professor, Department

of Osteopathic Principle and Practice, Nova Southeastern University College of Osteopathic Medicine, Fort Laud

Stanley Schiowitz, D.O.

New York College of Osteo

Richard A. Scott, D.O.

Associate Clinical Professor,

Department of Osteopathic Medicine and Orthopedic

tal, Warren, Michigan Gerald G. Osborn, D.O.

Health Science Center, Fon Worth, Texas

pathic Medicine, Old Westbury, New York

lege of Osteopathic Medicine, Kirksville, Missouri Michael I. Opipari, D.O.

Professor of Medicine, Chief,

Division of Rheumatology, University of North Texas

erdale, Florida

teopathic Medicine, Philadelphia, Pennsylvania Donald R. Noll, D.O.

Kirksville College of Osteopathic

Medicine, Kirksville, Missouri Bernard R. Rubin, D.O.

Center for Children, San Diego, California

xiii

Surgery, Michigan State University College of Osteo pathic Medicine, East Lansing, Michigan, and Depart mem of Orthopedic Surgery, BiCounty Community Hospital, Warren, Michigan Michael A. Seffinger, D.O.

Assistant Professor, Depart

Professor Emeritus, Depart

mem of Osteopathic Manipulative Medicine, College of

ment of Family Medicine, Ohio University College of

Osteopathic Medicine of the Pacific, Western University

Osteopathic Medicine, Athens, Ohio

of Health Sciences, Pomona, California

Michael M. Patterson, Ph.D.

Professor and Assistam

Chair, Depanment of Osteopathic Principles and Prac tice, College of Osteopathic Medicine, Nova Sourheast ern University, Ft. Lauderdale, Florida Jeff J. Patterson, D.O. Deparrment

of

Professor of Family Medicine,

Family

Medicine,

University

of

Wisconsin, Northeast Family Medical Cemer, Madison, Wisconsin Augustine L. Perrotta, D.O.

Clinical Professor of Med

icine, Michigan State University College of Osteopathic Medicine, East Lansing, Michigan, and Chairman, De partment of Medicine, Chief, Section of Hemarologyl Oncology, BiCounty Community

Hospital, Warren,

Michigan Evanston, Illinois

Ronald P. Portanova, Ph.D.

Chair,

Department of

Biomedical Sciences, Ohio University College of Osteo pathic Medicine, Athens, Ohio Kenneth A. Ramey, D.O. Paul R. Rennie, D.O.

Michael B. Shaw, D.O.

Clinical Professor of Family

Medicine, College of Osteopathic Medicine, Oklahoma State University Cemer for Health Sciences, Tulsa, Oklahoma RichardJ. Snow, D.O., M.P.H.

Doctor's Hospital Family

Practice, Grove City, Ohio Harvey V. Sparks, Jr., M.D., Ph.D.

Department of

Physiology, Michigan State University, East Lansing, Michigan Sarah A. Sprafka, Ph.D.

Director of Predoctoral Edu

Clinical Assistant Professor, De

RennieMatrix,

Inc.,

New England, Biddeford, Maine Melicien Tettambel, D.O.

Chair, Division of Female and

Child Health and Professor of Osteopathic Manipulative Medicine, Department of Obstetrics and Gy necology, Missouri

gan State University College of Osteopathic Medicine, Williamston,

Michigan Louis E. Rentz, D.O.

Oklahoma State University Center for Health Sciences, Tulsa, Oklahoma

Kirksville College of Osteopathic Medicine, Kirksville,

Oviedo, Florida

partment of Osteopathic Manipulative Medicine, Michi President,

Clinical Professor Department

of Family Medicine, College of Osteopathic Medicine,

cation, College of Osteopathic Medicine, University of

Barbara E. Peterson, D.Litt.

and

Harriet H. Shaw, D.O.

RobertJ. T heobald, Jr., Ph.D.

Professor and Chairman,

Depanment of Pharmacology, Kirksville College of Os teopathic Medicine, Kirksville, Missouri Lex C. Towns, Ph.D.

Professor and Chair, Department

of Anatomy, Kirksville College of Osteopathic Medicine, Michigan lnstiture for Neurological

Disorders, Farmington Hills, Michigan

Kirksville, Missouri Terri Turner, D.O.

Sebastopol, California

xiv

Contributors

Colleen Vallad-Hix, D.O.

Apnea Clinic, Michigan State

Richard L. Van Buskirk, D.O., Ph.D. Elaine M. Wallace, D.O.

Sarasota, Florida

Professor and Chair, Depart

ment of Osteopathic Practices and Principles, Nova Southeastern University Health Conference Division, College of Osteopathic Medicine, Ft. Lauderdale, Florida Robert C. Ward, D.O.

J. Michael Wieting, M.A., D.O. Department

University, Lansing, Michigan

Professor, Department of Osteo

of

Phy sical

Associate Professor,

Medicine

and

Rehabilita

tion, Michigan State University College of Osteopathic Medicine, East Lansing, Michigan Frank

H.

W illard,

Ph.D.

College

of

Osteopathic

Medicine, University of New England, Biddeford, Maine Mary C. Williams, D.O. John M. Willis, D.O.

Roanoke, Virginia

Assistant Professor, Internal Medi

pathic Manipulative Medicine, Michigan State Univer

cine, Chief, Division of General Internal Medicine, Uni

sity, East Lansing, Michigan

versity of North Texas Health Science Center, Texas Col

Michael R. Wells, Ph.D.

Associate Professor and Chair

man, Department of Biomechanics and Bioengineering, New York College of Osteopathic Medicine, New York Institute of Technology, Old Westbury, New York

lege of Osteopathic Medicine, Ft. Worth, Texas Robert D. Wurster, D.O.

Professor, Department of Phys

iology, Loyola University Medical Center, Maywood, Illinois

MISSION STATEMENT

Osteopathic medicine (hisrorically, osteopathy) is a philosophy, a science, and an an. Irs philosophy embraces the concept of the unity of the living organism's structure and function in health and disease. Its science includes the biological, behav ioral, chemical, physical, and spiritual knowledge related ro the maintenance and resroration of health, as well as identification, prevention, cure, and alleviation of disease. Its an is the applica-

Edirors at first meeting: John Harakal, D.O., FA.A.O. (deceased) Jill Hendra, D.O. John J. Jones, D.O. Robert E. Kappler, D.O., FA.A.O. Albert F. Kelso, Ph.D., DSci. (Hon.) William A. Kuchera, D.O. , F.A.A.O.

tion of the philosophy in the practice of medicine and surgery in all its branches and specialties.

Editorial Board First Meeting, July 1990 Chicago, Illinois

Howard M. Levine, D.O. Ward Perrin, D.O . , FA.CO.I. Barbara A. Peterson, D. Litt. Felix J . Rogers, D.O. , F.A.CO. I. , F.A.CC Sarah A. Sprafka, Ph.D. Roben C Ward, D.O., FA.A.O.


PREFACE

Welcome to the second edition of Foundations for Osteopathic Medicine. Based on feedback ftom the first edition, this edi tion is considerably changed and, we believe, improved. T he preface from the first edition is included for the reader's perspective. Several chapters were replaced, covering the same topic areas, but in greater depth. T he number of sections has been shortened from ten to eight with better location for areas with overlapping interests. For example, the primary care fields of family medicine, pediatrics, internal medicine, and geriatrics are now in one place. Importantly, three of the four are extensively restructured to reflect both osteopathic philosophical concepts and their relationships with 21st-century practice requirements. Only two chapters are untouched, Chapter 23, "Geriatrics" and Chapter 30, "Neurology. " On the other hand, we decided to add a new chapter, "Somatic Dysfunction," which deals with current neurological and biomechanical concepts affecting this Important area. Along with extensive revisions to other chapters, the fol lowing are completely new: Chapter 5: Biomechanics: An Osteopathic Perspective Chapter 1 0: Microbiological Considerations and Infectious Diseases Chapter 1 3: Health Promotion and Maintenance Chapter 1 8: Osteopathic Psychiatry Chapter 26: Osteopathic Medicine in the Practice ofEmer gency Medicine Chapter 29: Neuromusculoskeletal Medicine and Osteo pathic Manipulative Medicine Chapter 35: Osteopathic Physical Medicine and Rehabil itation Chapter 37: An Osteopathic Approach to Sports Medicine Chapter 65: Progressive Inhibition of Neuromuscular Structures (PINS) Chapter 69: Visceral Manipulation Chapter 70: Treatment of Somatic Dysfunction with an Osteopathic Manipulative Method of Dr. Andrew Taylor Still Chapter 7 1 : Treatment of the Acutely III Hospital Patient Chapter 7 3: Somatic Dysfunction Chapter 76: Outcomes Research and Design Chapter 77: Biobehavioral Interactions with Disease and Health Chapter 78: Clinical Research and Clinical Trials Here is a brief overview of the eight major sections:

Part I. Osteopathic Philosophy and History

Osteopathic philosophy and the profession's history are inextri cably mixed together. Each offering is significantly revised with considerable cross-references between the two in an effort to give a better sense of context and continuity. In addition, the dedications and a number of chapters offer further perspective and cross-referencing.

Part /I. Osteopathic Considerations in the Basic Sciences

Each chapter is expanded and refined, with better integration with other parts of the text. Osteopathic philosophical concepts are highlighted in a context of evolving scientific breakthroughs.

Part /II. Osteopathic Considerations in the Behavioral Sciences

Further refinements occur throughout, along with the addition of a new, well-designed descriptive chapter highlighting osteo p athically oriented psychiatry as a discipline.

Part IV. Osteopathic Considerations in Clinical Problem Solving

Revisions further refine Dr. Sprafka's original work.

Part V. Osteopathic Considerations in Family Practice and Primary Care

T his invaluable section presents three major revisions and one repeat from the first edition, "Geriatrics." Three rather large chapters: "Family Practice, " "General Internal Medicine, " and "General Pediatrics," add considerable osteopathic perspective for all three disciplines.

Part VI. Osteopathic Considerations in the Clinical Specialties

Among all segments of this text, this section adds more new os teopathically oriented perspectives than any other. Many offer ings are expanded, with surgery, orthopedics, and rheumatology as prime examples.

xviii

Preface

Part VII. Osteopathic Considerations in Palpatory

Part VIII. Basic and Clinical Research for

Diagnosis and Manipulative Treatment

Osteopathic Theory and Practice

As with the first edition, this comprises almost half the book. T he associate editors and previous authors have done masterful work.expanding, clarifying, and illustrating their material. We hope you agree. Five new chapters strengthen the material even more: Chapter 65: Progressive Inhibition of Neuromuscular Structures (PINS) Chapter 69: Visceral Manipulation Chapter 70: Treatment of Somatic Dysfunction with an Osteopathic Manipulative Method of Dr. Andrew Taylor Still Chapter 7 1 : Treatment of the Acutely III Hospital Patient Chapter 73: Somatic Dysfunction

Under new leadership, this important section has been changed considerably to reflect the important and evolving roles of both basic and clinical research methodologies as they relate to the osteopathic philosophy and its principles.

Glossary of Osteopathic Terminology

T he Glossary, first published in 1 98 1 , is an ongoing project under continuing revision by the Educational Coun cil on Osteopathic Principles. T his edition is the most current.

PREFACE TO THE FIRST EDITION

Osteopathic medical students and physicians alike have ex pressed the need for a major text dealing with the broad aspects of osteopathic medicine. For this and many other reasons, the American Osteopathic Association concluded that a wide vari ety of venues would benefit from a straightforward and prac tical explanation of osteopathic philosophy and its principles as practiced in a modern context. Foundations for Osteopathic Medicine reflects the current understanding and knowledge of osteopathic philosophy and principles as reflected by more than 70 osteopathically oriented authors and even greater number of peer reviewers from a variery of basic science, behavioral, and clinical disciplines. This text provides an up-to-date multidisciplinary overview of osteopathic philosophy and principles with exam ples of clinical perspectives gleaned from a variery of disciplines. The book has been organized in ten sections, many of which are introduced with an editorial overview from the section editor. A brief overview of the ten sections follows. I. Osteopathic Philosophy This consensus statement comes from the Editors of Founda tions for Osteopathic Medicine after an extensive peer-review process. The reader will note that many other philosophy refer ences are scattered throughout the text, including the Mission Statement. II. History No text of this sort gives proper perspective to its essential ideas and practices without discussing its ancestry and evolution. In the United States, accelerating reorganization of health care ser vices of all rypes emphasizes the importance of this profession's historical memory. Sometimes forgotten are the many individ ual and collective Struggles for full medical licensure in all 50 states; general ostracism, then acceptance into military and pub lic sector positions; moves from within sectors of the profession to restrict osteopathic physician licensure for their own short term gain; and, most recently, the substantial growth of osteo pathic education and training programs in universities, colleges, and schools, while at the same time there is a merging/closure and downsizing of hospitals in response to economic pressures. III. Basic Sciences From its earliest beginnings, osteopathic medicine emphasized the scientific basis for applications of its fundamental ideas. In

the 1 9th century, there was little to go on other than clinical in stincts and intuition. On the other hand, formal scientific inves tigation was exploding in many areas. Now, a century later, re search and evidence-based clinical practices are becoming rules rather than exceptions. With this in mind, the section editors recognized the need for presentation of current osteopathic per spectives among the basic science disciplines. To this end, au thors from a variety of basic science disciplines have skillfully crafted creative, pertinent, and current perspectives representing their fields of inquiry. A number of clinically applicable discus sions relating the particular disciplines to neuromusculoskeletal srrucrure and function perspectives are of particular interest. IV. Behavioral Sciences This offering is a first effort from within osteopathic medicine to highlight some of the important and complex behavioral, psy chosocial, and cultural issues in a context that uses osteopathic philosophy and its principles as a frame of reference. Patients and physicians alike behave and are affected by their genetic endowments, cultural values, belief systems, gender, age, fam ily background, education, and working environments. Health, impairment, and disease/illness outcomes are often determined by individual, family, and social group responses and choices deriving from these background elements. Authors highlight some of these important issues, such as life stages, stress, and depression. V. Clinical Problem Solving Like the Behavioral Science Section, this too is an osteopathic textbook first. Written by one of the pioneers in the field, the offering lays out both general and specific problem-solving strategies that enhance comprehensive clinical evaluations in a context that highlights osteopathic philosophy and principles. Emphasis is placed on integrative thinking processes in the clin ical setting. VI. Family Practice and Primary Care Family practice and primary care form the backbone of os teopathic medicine. When these chapters were written, ap proximately 60% of graduates nationwide were entering the fields of family practice, general pediatrics, and general inter nal medicine. If general obstetrics and gynecology is added, the

XX

Preface to the First Edition

figures are higher. T he authors have given general overviews of their disciplines, with an emphasis on osteopathic philosophy and principles.

osteopathic medical treatment program. T hese survey chapters address some of the pertinent issues. X. Applications of Basic and Clinical Research

VII. Clinical Specialties In our complex, high technology, medically oriented society, applications of osteopathic medicine principles may, at times, be difficult to articulate. One outcome has been the inaccurate notion that osteopathic philosophy and its principles reflect alternative or complementary medicine rather than mainstream practices. Among many complex reasons for this view is the reality that some specialties and subspecialties seem less holistic than others, often inappropriately so.

VIII. Palpatory Diagnosis and Manipulative Treatment

Approximately half of this text presents a perspective on aspects of osteopathic palpatory diagnosis and manipulative treatment processes. Survey chapters cover the major curriculum content areas taught in American colleges of osteopathic medicine. Con tributions have been peer reviewed by members of the Educa tional Council on Osteopathic Principles, an osteopathic ma nipulative skills teaching arm of the American Association of Colleges of Osteopathic Medicine.

IX. Health Restoration Osteopathic palpatory diagnosis, manipulative treatment, and rehabilitative procedures are essential components of an

for Osteopathic Theory and Practice

This section discusses appropriate research methods and op portunities confronting osteopathic medical practice. Particu lar emphasis is placed on appropriate research planning, data acquisition and documentation, basic science perspectives, clin ical trials, epidemiologic considerations, and outcomes research in relation to somatic dysfunction. In addition, the Glossary of Osteopathic Terminology, pre pared by the Educational Council on Osteopathic Principles of the American Association of Colleges of Osteopathic Medicine, endorsed by the American Osteopathic Association, is included. T he text concludes with a comprehensive Index. T he time for this text has been long in coming. One idea for such a textbook was informally discussed during the 1 970s as part ofa longitudinal osteopathic principles curriculum effort by the Educational Council on Osteopathic Principles. Other such forums had discussed additional alternatives over the years. However, the concept and plan for this text was developed within the Bureau of Research of the AOA. T he Bureau officially termed the development activity the "Osteopathic Principles Textbook Project." Our goal has been to introduce both future and present osteopathic physicians to the rationale behind ap plications of osteopathic principles and the appropriate use of palpatory diagnosis and manipulative treatment in a wide range of disciplines. After years of soul-searching and peer review, our efforts are in your hands. We have given our best. We hope you agree.

FOREWORD

"The theory of a free press is that truth will emerge from discussion, not that It. wd! be presented pe1fietly and instantly in any one account. "

-Walter Lippmann]

As Editor-in-Chief of the American Osteopathic Association, it is my pleasure to present the second edition of Foundations for Osteopathic Medicine. In the spirit of Walter Lippmann, this text reflects many illustrations of ongoing and evolving dlscussI � n� wahln the osteopathic profession. For those seeking greater l l1slght and perspective, this authoritative text explores the osteopathic philosophy and its evolving relationships with the behavioral, basic and clinical sciences. It is our hope that readers will find it a useful addition for classrooms, offices, hospitals, and osteopathic principles' l earning laboratories. As in the first edition, 79 chapters and the Glossary of Os t�opathic Terminology blend osteopathic principles and prac . tIces with contemporary multidisciplinary health care. Over half of the book is dedicated to palpatory diagnosis and osteopathic manipulative treatment. In addition, many as pects of osteopathically oriented problem solving as it applies . to pnmary care and specialty practices are also highlighted. T hrough extensive cross-referencing, osteopathic con�idera tions are repeatedly emphasized in order to give the reader bener insights. Robert C. Ward, D.O., his 1 1 associate editors, almost 1 00 authors, and numerous peer reviewers have worked extremely hard producing a more valuable, meaningful, and relevant text book for our profession. Seventy-seven have been extensively revised, and several others added. In the foreword to the first edition, Howard Levine, D.O. asked readers to use the textbook to "think osteopathically." Through the vision and commitments of both Dr. Levine and Dr. Ward, this textbook has come to life. With further editions, it is expected that additional changes will occur.

T his text is significant not for only students, but also for osteopathic physicians already in practice. More than five years ago, having already been in practice for many years, I read p� rtions of �he fi rst edition that focused on the etiology and . clinical applications relating to somatic dysfunction. In these materials, I found plausible scientific information that helped me bener understand this particular concept in greater depth. T he result was that it allowed me to apply osteopathic princi ples and practices to pulmonary and critical care medicine in ways I had never envisioned before. Visceral disease and its ef fect ? n th� musculoskeletal system took on new meaning. T he relationship between somatic dysfunction and visceral physiol ogy and its pathophysiology had always been appreciated, but after reviewing these materials carefully, these special osteopath . Ically onented relationships became more understandable. As an osteopathic physician, I became much stronger. More impor tantly, my inquisitive and scientifically oriented mind under took numerous new j ourneys, the first steps in pursuing newly directed research. As a pulmonologist, the second edition of Foundations has taken my personal understanding to a higher level than ever expecte . example of how one pair of authors' evolving os teopathiC inSights are changing is found by comparing the first and second edition respiratory systems chapters, coauthored by Samuel Krachman and myself. Not only are there numerous content changes, but our method of presentation and osteo pathic perspectives have changed dramatically. It is my hope that my personal experience with this project provides some insight for future readers of this text. As Dr. Levine recommends, use this text as a template for learning "to think osteopathically," while using all available scientific and clinical information that make the science and art of practicing of osteopathic medicine so special and distinctive.

� �.

GILBERT E. D'ALONZO, D.O., EA.C.O.1. ]

Walter Lippmann, Pulitzer Prize winner, syndicated columnist, and editor

of the New York World.

Editor-in-Chiej AOA Publications American Osteopathic A ssociation


ACKNOWLEDGMENTS

Development of this second edition of Foundations for Osteo pathic Medicine has been a remarkable, often stress-inducing, but worthwhile experience for all concerned. Initial planning began at the October 2000 AOA meeting in New Orleans. Only rwo face-to-face meetings were needed to implement and eval uate project goals and objectives. The first occurred over rwo days in Philadelphia in March 200 1 at the corporate offices of Lippincott Williams & W ilkins. T he second took place over a rwo-hour breakfast meeting at the AOA convention in San Diego, California in October 200 1 . As expected, there were a number of conceptual and detail type problems putting the project together. Most noteworthy, however, is the fact that vir rually aU the work occurred in cyberspace. Among the benefits were fast rurnaround times and reasonably quick fixes for major problems. One comes away with a sense that a diverse group of associate editQl's, authors and staff have worked unbelievably hard meeting project expectations deadlines. Dedication to our profession, once again, has been the byword. In literal terms, the project moved from concept to production in less than 1 2 months! What more can be said, except an enormous thank you to everyone involved. On a sad note, one of our anatomy coauthors, Allen Jacobs, D.O., Ph. D., Dean of the Michigan State University College of Osteopathic Medicine, died suddenly and unexpectedly in December 200 1 . His dedication to osteopathic medicine, and its students in particular, was legendary. Special thanks goes to the following: Section Editors: Raymond J. Hruby John A. Jerome John M. Jones, III Robert E. Kappler Michael L. Kuchera William A. Kuchera Michael M. Patterson Bernard R. Rubin Michael A. Seffinger Sarah A. Sprafka Richard L. Van Buskirk Project Managers: For the Osteopathic Principles Textbook Project Jane A. Walsh

For Lippincott W illiams & Wilkins Timothy Y. Hiscock, Acquisitions Editor Michelle M. LaPlante, Senior Developmental Editor Robin E. Cook, Senior Production Editor For the American Osteopathic Association John Crosby, J . D., Executive Director, American Osteo pathic Association Gilbert A. D'Alonzo, D.O., FA.e.O.I., Editor-in-Chief, Publications, American Osteopathic Association Philip A. Saigh, J r., Director of the Department of Com munications, American Osteopathic Association Michael Fitzgerald, Director of the Division of Publica tions, American Osteopathic Association Peer Reviewers

Constance Cashen, D.O., FA.e.O.S. Anthony G. Chila, D.O., FA.A.O. Eileen L. DiGiovanna, D.O., FA.A.O. Lori Dillard, D.O. Chester DeGroat, Ph.D . Dennis Dowling, D . O . , FA.A.O. John Duhn, MS I I I : MSU-COM Walter Ehrenfeuchter, D.O., FA.A.O. Mitchell Elkiss, D.O., FA.e.N. Thomas Gilson, D.O. Philip Greenman, D.O., FA.A.O. Andra Grosser, MS I I:COMp, OMM Teaching Fellow Raymond J . Hruby, D.O., F.A.A.O. Sheru Hurlong, MS II:COMp, OMM Teaching Fellow John A. Jerome, Ph.D. William L. Johnston, D.O., FA.A.O. Robert E. Kappler, D.O., FA.A.O. Albert F Kelso, Ph. D. Hollis King, D.O., Ph.D., FA.A.O. Steven Kopka, M.A. Michael L. Kuchera, D.O., FA.A.O. W illiam A. Kuchera, D.O., FA.A.O. Edna M. Lay, D.O., FA.A.O. Wesley Lockhart, D.O. Jayne H.-W. Martin, D.O. Chindeum Olsekeka, MS II:COMP, OMM Teaching Fellow Gerald G. Osborn, D.O., FA.e.N. David A. Patriquin, D.O., FA.A.O. Michael M. Patterson, Ph. D.

xxiv

Acknowledgments

Chrisropher Pohlod, MS I I I : MSU-COM, OMM Teaching Fellow Felix J. Rogers, D.O . , FA.CO.I. Bernard R. Rubin, D.O., FA.CO.I. Jesus Sanchez, MS II:COMp, OMM Teaching Fellow Michael A. Seffinger, D.O. Serh Torregiani, MS II:COMP, OMM Teaching Fellow Richard L. VanBuskirk, D.O., FA.A.O. Angela Wagner, D.O. Elaine Wallace, D.O. Roben C Ward, I I I , D.O. Robert Wursrer, Ph.D.

Major Project Contributors

Michael Firzgerald, AOA Philip Saigh, AOA Ms. Jane Walsh, Projecr Coordinaror, Department of Osreoparhic Manipularive Medicine, MSU-COM Ms. Parricia Grauer, Informarion officer, MSU-COM Ms. Sharon Husch, Execurive secrerary, Department of Osreoparhic Manipularive Medicine, MSU-COM

ROBERT C. WARD, D.O., EA.A.O.

Executive Editor

S

E

C

T

I

O

N

OSTEOPATHIC PHILOSOPHY AND HISTORY


OSTEOPATHIC PHILOSOPHY MICHAEL A. SEFFINGER HOLLIS H. KING ROBERT C. WARD JOHN M. JONES, III FELIX J. ROGERS MICHAEL M. PATTERSON

INTRODUCTION

The osteopathic philosophy, deceptively simple in its presenta tion, forms the basis for osteopathic medici ne's distinctive ap proach to health care. The philosophy acts as a unifying set of ideas for the organization of scientific knowledge in rela tion to all phases of physical, mental, emotional, and spiritual health, along with distinctive patient management principles. As such, its concepts form the foundation for practicing osteopathic medicine. Viewpoints and attitudes arising from osteopathic principles give osteopathic practitioners an important template for clinical problem solving and patient education. In the 21st century, this viewpoint is particularly useful as practitioners from a wide va riety of disciplines confront increasingly complex physical, psy chosocial, and spiritual problems affecting individuals, families, and populations from a wide variety of cultures and back grounds.

HOW IT ALL BEGAN

Andrew Taylor Still, M.D., D.O.

(1828-1917)

KEY CONCEPTS

Origin of osteopathic philosophy Classic osteopathic philosophy • Historical development of osteopathic concepts • Evolution of the osteopathic philosophy from A.T. Still to present • Applications of osteopathic principles as guidelines to patient care

•

•

Andrew Taylor Still (1828-19 1 7) was an American frontier doc tor who was convinced that 19th century patient care was severely inadequate. This resulted in an intense desire on his part to im prove surgery, obstetrics, and the general treatmen t of diseases, placing them on a more rational and scientific basis. As his perspectives and clinical understanding evolved, Still created an i nnovative system of diagnosis and treatment with two major emphases. The first highlights treatment of physi cal and mental ailments (i.e. , diseases) while emphasizing the normalization of body structures and functions. Its hallmark was a detailed knowledge of anatomy that became the basis for much of his diagnostic and clinical work, most notably palpa tory diagnosis and manipulative treatment. The second empha sizes the importance of health and well being in its broadest sense, including mental, emotional, and spiritual health, and the avoidance of alcohol and drugs, and other negative health habits.

4

f Osteopathic Philosophy and History

ORIGINS OF OSTEOPATHIC PH ILOSOPHY

Hiswrically, Still was not the first w call attention w i nade quacies of the health care of his time. Hippocrates (c. 460c. 377 BeE. ) , Galen (c. 130-c. 200), and Sydenham (1624- 1 689) are others. Each, in his own way, criticized the inadequacies of existing medical practices, while focusing contemporary thinking on the patient's natural abil iry w heal. In addition, Still was deeply influenced by a number of philosophers, scientists, and medical practitioners of his time. There is also evidence he was well versed i n the religious philoso phies and concepts of the Methodist, Spiritualist, and Universalist movements of the period (1) . Following the loss of three children w spinal meningitis i n 1864, Still immersed himselfin the study of the nature of health, ill ness, and disease (2). His goal was w discover definitive methods for curing and preventing all that ailed his patients. He implicitly believed there was "a God of truth ," and thar: "All His works, spiritual and material, are harmonious. His law of animal life is absolute. So wise a God had certainly placed the remedy within the material house i n which the spirit of life dwells." Further more, he believed he could access these natural inherent remedies " . . . by adjusting the body in such a manner that the remedies may naturally associate themselves wgether, hear the cries, and relieve the afflicted" (2) . In this quest, he combined contempo rary philosophical concepts and principles with existing scientific theories. Always a pragmatist, Still accepted aspects of different philosophies, concepts, and practices that worked for him and his patients. He then int egrated them with personal discoveries of his own from in-depth studies of anawmy, physics, chemistry, and biology (I). The result was the formulation of his new philosophy and its applications. He called it: "Osteopathy." Still's moment of clariry came on June 22, 1874. He writes, "1 was shot, not in the heart, but in the dome of reason" (2). " Like a burst of sunshine the whole truth dawned on my mind, that I was gradually approaching a science by study, research, and observation that would be a great benefit w the world" (2) . He realized that all living things, especially humans, were created by a perfect God. If humans were the embodiment of perfection, then they were fundamentally made w be healthy. There should be no defect in their structures and functions. Since he believed that "the greatest study of man is man," he dissected numerous cadavers w test his hypothesis (2). He believed that if he could understand the construction (anawmy) of the human body, he would comprehend Nature's laws and unlock the keys w health. Still found no flaws in the concepts of the body's well-designed structure, proving w him that his hypothesis was correct. A corollary to Still's revelation was that the physician does not

In his view, it was the job of the physician w correct structural disturbances so the body works normally, just as a mechanic adjusts his machine. In Research and Practice he wrote, "The God of Nature is the fountain of skill and wisdom and the mechanical work done i n all natural bodies is the result of absolute knowledge. Man cannot add anything w this perfect work nor improve the functioning of the normal body. . . . Man's power w cure is good as far as he has a knowledge of the right or normal position, and so far as he has the skill to adjust the cure diseases.

bones, muscles and l igaments and give freedom w nerves, blood, secretions and excretions, and no farther. We credit God with wisdom and skill to perform perfect work on the house of life i n which m a n l ives. I t is only justice that God should receive this credit and we are ready w adjust the parts and trust the results" (3) . While Stil l practiced the orthodox medicine of his day from 1853 to 1879, including the use of oral medications such as p urgatives, diuretics, stimulants, sedatives, and analgesics, and externally applied salves and plasters, once he began using his new philosophical system he virtually ceased using drugs. This occurred after several years where he experimented with com binations of drugs and manipulative treatment. In addition, he compared his results with those of patients who received no treat ment at all (2). After several years' experience, he became con vinced that his mechanical corrections consistently achieved the same or better results without using medications. It was at that point that Still philosophically divorced him self from the orthodox practices of 19th century medicine (2). He writes, " H aving been familiar myself for years with all their methods and having experimented with them I became disheart ened and dropped them" (3) . His unerring fai th in the natural healing capabilities of the mechanically adjusted body formed the foundation for his new philosophy. Unsure of what to call his new hands-on approach in the early years, Still at times referred w himself as a "magnetic healer" and "lightning bone-setter" (1,4). In the 1880s Still began pub licly using the term "osteopathy" as the chosen name for his new p rofession (1, 5) . He writes: "Osteopathy is compounded of two words, osteon , meaning bone, (and) pathos, (or) pathine, w suf fer. I reasoned that the bone, 'Osteon,' was the starting point from which I was to ascertain the cause of pathological condi tions, and so I combined the 'Osteo' with the 'pathy' and had as a result, Osteopathy" (2) . As the name osteopathy implies, Still used the bony skelewn as his reference point for understanding clinical problems and their pathological processes. On the surface, he was most i nter ested in anawmy. On the other hand, he taught that there is more to the skeleton than 206 bones attached wgether by ligaments and connective tissue. In his discourses, Still would describe the anatomy of the arterial supply to the femur, for example, trace it back to the heart and l ungs, and relate it w all of the sur rounding and interrelated nerves, soft tissues, and organs along the way. He would then demonstrate how the obstruction of ar terial flow anywhere along the pathway toward the femur would result in pathophysiologic changes in the bone, producing pain or dysfunction. He writes of his treatment concepts: "Bones can be used as levers w relieve pressure on nerves, veins and arteries" (2). This can be understood in the context that vascular and neural struc tures pass between bones or through orifices (foramina) within a bone. These are places where they are most vulnerable to bony compression and disruption of their functions. In addition, fas cia is a rype of connective tissue that attaches w bones. Fascia also envelops all muscles, nerves, and vascular structures. When strained or twisted by overuse or trauma myofascial structures not only restrict bony mobiliry, but also compress neurovascu lar structures and disturb their functions. By using the bones as

1. Osteopathic Philosophy

manual levers, bony or myofascial entrapments of nerves or vas cular structures can be removed, thus restoring normal nervous and vascular functions.

5

not the effect is disease. When the parts are readjusted disease gives place

[0

health. The work of the osteopath is to adjust the body from

the abnormal [ 0 the normal, then the abnormal conditions give place to the normal and health is the result of the normal condition

(3).

The Philosophy Involves More Than Neuromusculoskeletal Diagnosis and Treatment

Osteopathy is not only a neuromusculoskeletal-oriented diagnos tic and treatment system, it is also a comprehensive and scien tifically based school of medicine that embraces a philosophy. In answer to the question, "What is osteopathy?" Still stated, "It is a scientific knowledge of anatomy and physiology in the hands of a person of intelligence and skill, who can apply that knowl edge to the use of man when sick or wounded by strains, shocks, falls, or mechanical derangement or injury of any kind to the body" (6) . Furthermore, osteopathy had a greater calling. I n what could be considered a mission statement, Still wrote, "The object of Osteopathy is to improve upon the present systems of surgery, midwifery, and treatment of general diseases" (2) . And, "To find health should be the object of the doctor. Anyone can find disease" (6) .

CLASSIC OSTEOPAT HIC P H ILOSOP HY OF HEALT H Health Is a Natural State of Harmony

Still believed health to be the natural state of the human being (Table 1.1). In his own words: Osteopathy is based on the perfection of Nature's work. When all parts of the human body are in line we have health. When they are

TABLE 1.1. CLASSIC OSTEOPATHIC PHILOSOPHY A. T. Still's fundamental concepts of Osteopathy can be organized in terms of health, d isease, and patient care.

Health 1. Health is a natural state of harmony. 2. The human body is a perfect machine created for health and activity.

3. A healthy state exists as long as there is normal flow of body fluids and nerve activity.

Disease 4. Disease is an effect of underlying, often multifactorial causes. 5. Illness is often caused by mechanical impediments to normal flow of body fluids and nerve activity.

6. Environmental, social, mental, and behavioral factors contribute to the etiology of d isease and illness.

Patient Care 7. The human body provides all the chemicals necessary for the needs of its t issues and organs.

8. Removal of mechanical impediments allows optimal body fluid flow, nerve function, and restoration of health.

9. Environmental, cultural, social, mental, and behavioral factors need to be addressed as part of any management plan.

10. Any management plan should realistically meet the needs of the individual patient.

Mechanics and Health

Still's concept of a healthy person is insightful. It places his belief of the importance of structural and mechanical integrity within the perspective of a comprehensive view of a human being within society: When complete, he is a self-acting, individual ized, separate person age, endowed with the power

[0

move, and mind to di rect i n lo

comotion, with a care for comfort and a thought for his contin ued existence in the preparation and consumption of food in size and form to suit the duties he may have

[0

[0

perform

keep him

(6).

Still believed that life exists as a unification of vi tal forces and matter. Since the body is controlled by the mind ro exhibit pur poseful motion in attai ning the needs and goals of the organism, he stated that, "Osteopathy . . . is the law of mind, matter and mo tion" (2). Once Still accepted that motion is an inherent quality of life itself, it was a small step to inquiring into what is mov ing and how it moves. Through his in-depth study of anatomy, he could see the interdependent relationships among different tissues and their component parts. He observed that each part developed as the body was moving, growing, and developing from embryo to fetus to newborn and throughout life. Thus, each tis sue, organ, and structure is designed for motion. "As motion is the fi rst and only evidence of life, by this thought we are conducted to the machinery through which life works to accomplish these results" (7). I f "life is matter in motion"(6), then what is the effect on a body part that is not moving? Still reasoned that a lack of motion is not conducive to life or health. "[The osteopath's] duties as a philosopher admonish him that life and matter can be united, and that that union cannot continue with any hindrance to free and absolute motion" (6) . Further, he boldly states that the practice of osteopathy "covers all phases of disease and it is the law that keeps life in motion" (2) . Normal Nerve Activity and Flow of Body Fluids

A machine cannot run without proper lubrication, fuel, and mechanisms to remove the by-products of combustion. In teach ing his students, Still identified each component of the body's intricate mechanisms as he knew them. In the process, he dis cussed various forces that he reasoned create motion and main tain life. He explained how lubricating and nourishing Auids Aow through the arteries, veins, lymphatics, and nerves. He also noted that they turn over by-products of metabolism through the ve nous and lymphatic systems. "The human body is a machine run by the unseen force called life, and that it may be run harmo niously it is necessary that there be liberty of blood, nerves and arteries from their generating point to their destination" (2) . Another component of Still's machine concept was the power source. He identified the brain as the dynamo, the electric battery

6

1. Osteopathic Philosophy and History

that keeps the body moving and working: The brain furnishes nerve-action and forces to suit each class of work to be done by that set of nerves which is to construct forms and to keep blood constantly i n motion in the arreries and fro m all parts back to the hean through the veins that it may be purified, renewed, and re-enter ci rculation

(6).

CLASSIC OSTEOPAT H IC P H ILOSOP HY OF D ISEASE Disease Is an Effect of an Underlying Cause or Causes

From the time of Hippocrates through the first half of the 20th century, diseases were identified primarily through simple and complex descriptions of symptoms and signs. Many afflictions were without clear etiology. In spite of our current greater lev els of knowledge and understanding, this is still true in many cases. Still taught that disease is the effect of an abnormal anatomic state with subsequent physiologic breakdown and decreased host adaptability. Germs were first discovered in the 17th century with the inven tion of the microscope, but the germ theory of disease was not accepted until Pasteur provided convincing scientific ev idence in the mid-19th century. However, experienced clinicians like Still, as well as an emerging group oflaboratory scientists, saw germs as opportunists to decreased host function, not as primary in themselves. They speculated that infections resulted from an interaction berween the degree of virulence and quantity of the infecting agen t and the level of host immunity. Still also realized that there were multifactorial components to disease processes (8,9). He believed that disease was a combi nation of influences arising from decreased host adaptability and adverse environmental conditions. He recognized that symptoms often were a manifestation of nerves irritated by pathophysio logic processes commonly created by an accumulation of fluids (congestion and inflammation). This diminished the patient's ability to adapt to the environment (2). Additionally, Still was keenly aware of the deleterious effects ofenvironmentally induced trauma, or abrupt changes in the atmosphere, causing physical or emotional "shock" or inertia, and therefore obstructing normal metabolic processes, body fl uids, and nerve activity (3).

Mechanical Impediments to Flow of Body

and congestion by mechanical obstruction, interruption, or im pediment to normal flow of vital fluids. Still understood that the flow of body fluids was under the con trol of the nerves that innervated the blood vessel walls, adjusting the diameter of the vessels and thus controlling the amount and rate of blood flow to the tissues and organs. " While the vascular and nervous systems are dependent upon each other, it must be remembered that the bloodstream is under the control of the ner vous system, not only indirectly through the heart, but directly through the vasoconstrictor and vasodilator nerve fibers, which regulate the caliber and rhythm of the blood vessels" (9). Still writes: "All diseases are mere effects, the cause being a partial or complete failure of the nerves to properly conduct the fluids of life" (2). Although he emphasized that "the rule of the artery is absolute, universal, and it must be unobstructed, or disease will result"(2), he also pointed out the importance of unimpeded flow of lymphatics: "[W]e must keep the lymphatics normal all the time or see confused Nature in the form of disease. We strike at the source of life and death when we go to the lymphatics" (6). However, even if the blood and lymph are flowing normally, Still pointed out that, "the cerebro spinal fluid is the highest known element that is contained in the human body, and unless the brain furnishes this fluid in abundance a disabled condition of the body will remain. He who is able to reason will see that this great river oflife must be tapped and the withering field irrigated at once, or the harvest of health be forever lost" (7). Holistic Aspects-Environmental, Social, Mental, and Behavioral Etiologies

For the most part, Still described the origins of disease and illness as a result of "anatomic disturbances followed by physiologic dis cord." However, at the same time, he acknowledged the potential detrimental influences of heredity, lifestyle, environmental condi tions, contagious diseases, inactivity and other personal behavior choices, and psychological and social stress on health (6,8,9). Still also recognized that substance abuse (e.g., alcohol and opium) as well as poor sanitation, personal hygiene and dietary indiscretion, lack of exercise or fitness all contributed to illness and disease. He lectured passionately against the social forces that promulgated these deleterious behaviors and social situations, including slavery and economic inequities. Indeed, he talked from personal experience as he and his family members suffered from these challenging social circumstances during the pioneer days of the 19th century Midwest.

Fluids and Nerve Activity

Still's study of pathology found that in all forms of disease there is mechanical interruption of normal circulation of body fluids and nerve force to and from cells, tissues, and organs (3). "Sick ness is an effect caused by the stoppage of some supply of fluid or quality of life" (2). He understood that it is the combination of free circulation of wholesome blood and motor, n utrient, and sensory nerve activity that creates tissues and organs, and facil itates their growth, maintenance, and repair. Through cadaver dissection studies he reasoned that strains, rwists, or distortions in fascia, ligaments, or muscle fibers surrounding the small capil laries and nerve bundles could very well be the cause of ischemia

CLASS IC OSTEOPAT H IC P H ILOSOPHY AND PAT IENT CARE The Body Provides Its Own Drug Store

Like many others, Still observed that some people are more sus ceptible to epidemic diseases than others. It was also recognized that host resistance to disease is more apparent in certain indi viduals ( 1 0); so-called natural immunity, that is either i nherited or acquired ( 1 1,12). Still believed that promoting free flow of arterial blood to an infected area would enable "Nature's own germicide" to eradicate the infectious agent (3). Still's philosophy


places complete trust in the innate self-healing ability of the body. Removing all hindrances to health wasn't enough however, as it was incumbent upon the physician to ensure that the body's nat ural chemicals were able to work effectively in alleviating any pathophysiologic processes (2).

7

First and foremost, Still clearly believed that the osteopathic physician should strive to help the patient's body release its own medicine for a particular problem. He writes: The brain of man was God's drug srore, and had in it all liquids, drugs, lubricating oils, opiates, acids, and antacids, and every qual ity of drugs that the wisdom of God thought necessary for human happiness and health

Use of Medications I was born and raised ro respect and confide in the remedial power of drugs, but after many years of practice in close conformity ro the dictations of the very best medical authors and in consultation with rep' resentatives of the various schools, I failed ro get fro m drugs the results hoped for and I was face ro face with the evidence that medication was not only untrustworthy but was dangerous

(3).

I nitially, Still conceived of osteopathy as "a system of heali ng that reaches both i nternal and external diseases by manual opera tion and without drugs" (2) . Although he stated, " Osteopathy is a drugless science," he clarified this statement by explaining that he believed that drugs "should not be used as remedial agents," since the medications of his era only addressed symptoms or abnormal bodily responses to an unknown cause. In osteopathy, there is no place for injurious medications, whose risks outweigh their benefits, especially if safer and equally effective alternatives exist. Specifically, Still was against the irrational use of drugs that (a) showed no benefit, (b) had proven to be harmful, and (c) had no proven relationship to the cause of disease processes. He accepted anesthetics, poison antidotes, and a few others that had proven beneficial. "Osteopathy has no use for drugs as remedies, but a great use for chemistry when dealing with poisons and antidotes" (13). Still supports his reasons by listing the life-threatening risks of using drugs commonly employed in the late 19th century, namely, calomel, digitalis, aloe, morphine, chloral hydrate, ver atrine, pulsatilla, and sedatives (2). Still persuasively argued that a detailed physical examination, with focus on the neuromus culoskeletal system, followed by a well-designed, manipulative treatment, often removes impediments to motion and function. Where he differed from others was his view that manipulative treatment should always be used before deciding that the body has failed in its own efforrs. Vaccinations jenner introduced the smallpox vaccine in the 17th century, with considerable success. Still acknowledged this by stating, " I believe the philosophy of fighting one infection with another infectious substance that could hold the body immune by long and contin uous possession is good and was good" (6). Without disrespect to jenner, he describes shortcomings of jenner's methods, pointing out that there were many patients on whom the vaccine did not work or who became disabled or fatally ill. He states his belief that there is a less harmful method of vaccination and requests that Jenner's methods be improved. His rejection of drugs and vacci nations showed up in the initial mission statement for the American School of Osteopathy (ASO) (3). However, in 1910, even while Still was president, the school changed its stance and accepted vacci nations and serums as part of osteopathic practices.

(13).

The Mechanical Approach to Treating the Cause of Disease

Still reasoned that the cause of most diseases was mechanical, therefore, treatment must follow the laws of mechanics. As a con sequence, he used manipulative approaches designed to release bony and soft tissue barriers to nervous and circulatory functions in order to improve chances for healing (Fig. 1.1). He claimed that mobilization of these structures improved the outcomes of his patients (3) . However, manipulation procedures were not only applied to relieve musculoskeletal strains and inj uries, but to treat internal organ diseases as well. For example, he found characteris tic paraspinal muscle rigidity and other abnormal myofascial ten sions in patients with infectious diseases. He noted improvement in the health of these patients as well when the musculoskele tal and myofascial i mpediments to normal physiologic processes were alleviated. I n a majority of cases the patient's condition was seemingly cured, leading him to believe that the mechani cal aspects of dysfunction or disease were vitally important (3). Still thus proposed, that in all diseases, mobil ization of all the spinal joints not in their proper positional and functional rela tionships was necessary to ensure proper nerve activity and blood and lymph flow throughout the body. This included everyth i ng from the occipur to the coccyx, and indicated adjustment of the pelvis, clavicles, scapulae, costal cage, and diaphragm. Comprehensive Treatment

While heavily com m itted to the use of palpatory diagnosis and manipulative treatment, Dr. Still continued many other aspects of patient care. He practiced surgery and midwifery (obstetrics), although little is documented about specific activities. His patient education strategies highlighted moderation . He included advice for removing noxious or toxic substances from the diet and environment and behavioral adjustments such as adding exercises and stopping smoking. He also admonished his parients for abusing alcohol, opium, and heroin. Mental illness and stress-related problems were also important to Still (2,3) . He wrote about the role the p hysician can take in providing emotional support and encouragement to patients with end-stage medical problems. He described the importance of giving hope to patients and, at the same time, providing them with a realistic approach to managing their clinical condition (3) . Individualized Treatment

Each person is treated as a unique individual, not as a disease entity. Still taught that the history and physical evaluation of each person would turn up unhealthy self-care behaviors or cir cumstances and parts of the body not moving normally; the

-

8


FIGURE 1.1. Like many physicians before and after him, Dr. Still applied his new philosophy first to himself and then to his patients. In a famous early anecdote, he stopped a headache by suspending his neck across a low-lying rope swing. He later applied self-adjustments of spinal joint dysfunction to abate an attack of "flux" (bloody dysentery). After he was successful at curing 17 children of the same affliction by adjusting their spinal joint dysfunctions, he realized he was onto something worthwhile. (From Still AT. Autobiography of Andrew T. Still. Rev ed. Kirksville, MO: Published by the author; 1908. Distributed, Indianapolis: American Academy of Osteopathy.)

combination interfering with the body's natural ability to heal itself. The treatment would need to be tailored specifically for each patient's particular needs.

H ISTORICAL DEVELOP MENT OF OSTEOPATHIC CONCEP TS

Exactly how much influence previous or contemporary philoso phies and practices had on Still is purely speculative, since he never discussed specific attachments for any particular philosopher or scientist. The writings of contemporary philosophers of science and biology, like Herbert Spencer (1820-1903) and Alfred Rus sel Wallace (J 823-1913), resonated with those of Still (1) . They ptomoted the theories of evolution and the interdependence of the environment and the organism in all biologic processes, in cluding the origins of disease. They also promoted the concepts of the interdependence ofstructure and function, the importance of differentiating cause and effect, and emphasized the unity of the organism and interrelatedness of its pans. Throughout his life, however, Still maintained that his discoveries and thoughts were based on personal observation, experimentation, applica tions of factual knowledge, and the power of reasoning. After nearly 50 years of developing his concepts, he stated: I have explored by reading and inquiry much that has been wrirren on kindred subjects, hoping to get something on this great law wrirren by the ancient philosophers, but I come back as empry as I started (2).

A n umber of scholars and educators have attempted to trace both the historical development and evolution of thoughts and practices that may have influenced Still's thinking (10-12, 14-18) . In general, the authors compare Still's ideas with well known discourses passed on principally through Western cultural ideas. In 1901, Littlejohn wrote, "Osteopathy did not invent a new anatomy or physiology or construct a new pathology. It has built upon the foundation ofsciences already deeply seated in the

philosophy of truth, chemistry, anatomy and physiology, a new etiology ofdiseases, gathering together, adding to and reinforcing natural methods of treating disease that have been accumulating since the art of healing began" (l0). However, CM.T. Hulett emphatically stated that "Osteopathy is a new system of thought, a new philosophy of life" (19). Whereas Littlejohn (14) finds the foundation of osteopathy in Greek and Roman medicine, G.D. Hulett (12) and Downing (15) trace the origins of various osteo pathic concepts to the philosophy and practice of medicine found in other ancient writings, such as those of the Ptolemies, Brah mins, Chinese, and Hebrews. All agree on the further develop ment of medicine throughout Europe as a precursor to American osteopathic medical practice. Northup compares osteopathy to the concepts of Hippocrates and the Cnidian schools (18). Korr contrasts the contributions of Asclepian and Hygeian roots (17) . Whereas G.D. Hulett (12) and Korr (17) describe osteopathy as part of an evolution of the philosophy of medicine, Lane (II) and Northup (18) consider it a reformation of medical theory and practice. Still's use of spinal manipulation had many precedents. Schiotz and Cyriax (20) and Lomax (21) , among many, document the use of manual treatments for millennia. Hippocrates discussed "sub l uxations" or minor displacements of vertebra in his treatise "On the Articulations" and the manual adjustments used to correct them (22) . I n the 18th and 19th centuries many American and European practitioners acknowledged that there are relationships among displaced or "subluxed" vertebrae, and "irritated" spinal nerves in relation to both musculoskeletal and visceral disorders (23) .

EVOLUTION OF OSTEOPAT HIC P H ILOSOP HY

I n his unique way, Still integrated many of these concepts into his new system and molded it into a distinctive medical school curriculum that continues to evolve to this day. Still was adamant


that he did nor expect his studenrs and colleagues ro take what he advocated as dogma. He taught, "You must reason. I say reason, or you will finally fail in all enrerprises. Form your own opin ions, select all facts you can obtain. Compare, decide, then ace. Use no man's opinion; accept his works only" (6) . He urged his scudenrs ro study, test, and improve upon his ideas. An example of this evolution is a shifc from Still's early, and vircually exclusive, emphasis on anaromy ro a more i nclusive scress on primary physiologic functions that screngthen his concepts. Initially, J. Marcin Linlejohn (J 4), and later, Burns (24), Cole (25), Denslow (26), and Korr (27,28) promoted inregrative neu rophysiologic and neuroendocrine concepts. Whereas Linlejohn inr erpreted Still's concepts in light of 19th cenrury physiologic theories, Burns, Cole, Denslow, and Korr pi oneered distinctive osteopathic approaches ro physiologic inves tigations, making significant scientific contributions. Korr was particularly inAuenrial in i nrerpreting osteopathic concepts in light of the rapidly developing science of physiology in the 20th crnrury. He has been referred ro as "the second great osteopathic philosopher" (29). Irvin Korr, Ph.D., received his physiology degree from Prince ron University. Most of his teachi ng and research career was spent at the Kirksville College of Osteopathic Medicine i n Missouri, with later appoinrmenrs a t both M ichigan State Uni versity College of Osteopathic Medicine and The Texas College of Osteopathic Medicine (University of North Texas) . A multital ented individual, Korr was an accomplished violinist, sometimes playing chamber music with AJbert Einstein, who was in res idence at the time of his postgraduate train ing. He published extensively with several colleagues, i ncluding ].S. Denslow, A . D. Krems, Marcin J. Goldstein, Price E. Thomas, Harry M . Wright, and Gustavo S.L. Appeltauer. In 1947, Korr's i n itial publication, with Denslow and Krems, focused on facilitation of neural im pulses in moroneuron pools. Original research papers followed this on dermal auronomic activity, electrical skin resistance, and trophic function of nerves (28 ) . As Korr gained insight i nto Still's concepts, he lectured widely and published a number of impor tanr treatises tying osteopathic concepts rogether with proven physiologic models that emphasized the importanr roles p layed by the neuromusculoskeletal system. Whereas Still emphasized a focus on bones as the starring place from which he was ro discern the cause of pathology, Korr expanded this concept ro include the i nregrative activity of the spinal cord and its relationships with the musculoskeletal and the sympathetic nervous systems (28). Sim ilar ro Still, however, Korr often referred ro the neuro musculoskeletal system as the "Primary Machinery of Life." (See Korr's "An Explication of Osteopathic Principles" later in this chapter).

The Definition of Osteopathy

Osteopathic philosophy has been defined various ways over the years. To get a better sense of the evolution of the osteopathic philosophy since its inception, it is i nstructive ro follow how it has been defined over time. In his aurobiography, Still gave a "technical" definition as follows:

9

under the scientific treatment peculiar to osteopathic practice ... in harmonious accord with its own mechanical principles . .. may re cover from displacements, d isorganizations, derangements, and con sequent disease and regain its normal equilibrium of form and func tion i n health and strength.

(2)

Besides Still, several other American osteopath ic scholars wrote treatises on osteopathic ph ilosophy and principles ( I 1 , 1 2, 1 5, 1 6,25,30-36) . Each author had his or her own definition and explanation of osteopathic philosophy. There have been several attempts over the past century ro obtain consensus, or agreemenr, on a unifying definition and clearly stated tenets or principles that govern the practice of osteopathic medicine. According ro Littlejohn, the first consensus definition of os teopathy, among m ul tiple faculty members, represenring several osteopathic medical schools, was published in 1 900 (10). In 1 922, another consensus statemenr was developed and published by the A.T Still Research I nstitute as a revised edition of a popular classic textbook by G.D. Hulen (12) . By this time in medical thought, it was widely accepted that cellular level activity was a strong determinant of health or disease states. In an anempt ro update osteopathic philosophy in light of emerging concepts in cellular biology, the authors applied Still's mechanistic viewpoinr ro cel lular physiology. The following passage not only illustrates this approach, but demonstrates the desire of rhe profession ro state osteopathic philosophy and principles in terms of concise tenets based on contemporary scientific knowledge: The osteopathic view of the cell .. . is largely covered by the following statements: •

Normal strucrure is essential to normal function.

•

Normal function is essential if normal strucrure is to be main

•

Normal environment is essential to normal function and strucrure,

tained. though some degree of adaptation is possible for a time, even under abnormal conditions.

I n the human body, with its diversified functions, we may add also, •

The blood preserves and defends the cells of the body.

•

The nervous system unifies the body in its activities.

•

Disease symptoms are due either to failure of the organism

to

meet

adverse circumstances efficiently, or to strucrural abnormali ties. •

Rational methods of treatment are based upon an attempt

to

pro

vide normal nutrition, i n nervation and drainage to all tissues of the body, and these depend chiefly upon the maintenance of normal structural relations

(12).

The addition of medications in the practices of osteopathic physicians and surgeons over the years affected how the philoso phy was stated. For example, in 1 948, the faculty at the College of Osteopathic Physicians and Surgeons in Los Angeles added the following phrase ro their basic osteopathic principles statement: "Like a machine, the body can function efficiently only when in proper adjustment and when its chemical needs are satisfied either by food or medical substances" (37). Furcher evolution occurred in 1953, when the faculty of the Kirksville College of Osteopathy and Surgery (KCOS) agreed on the following: Osteopathy, or Osteopathic Medicine is a phi losophy, a science and an art. I ts philosophy embraces the concept of the unity of body

Osteopathy is that science which consists of .. . knowledge of the

structure and function in healrh and disease. Irs science includes rhe

structure and functions of the human mechanism . . .by which narure

chemical, physical and biological sciences related

to

rhe maintenance


10

of health and the prevenrion, cure, and alleviation of d isease. Irs arr is the application of the p h i losophy and the science i n the prac

The editors modified the four key principles of osteopathic philosophy as follows:

tice of osteopathic medicine and surgery in all i ts branches and specialties. Health is based on the natural capaciry of the human organism ro

resist and combat noxious i n A uences i n the environmenr and

ro

compensate for their effects; ro meet, with adequate reserve, the

usual stresses of daily l ife and the occasional severe stresses i mposed by extremes of environmenr and activi ry. Disease begins when this natural capaciry is reduced, or when i t is exceeded or overcome by noxious i n A uences. Osteopathic medicine recognizes that many facrors i mpair this capaciry and the natural tendency rowards recovery, and that among the most i m porram of these facrors are the local disturbances or le sions of the musculoskeletal system. Osteopathic medicine is there fore concerned with l iberating and developing all the resources that constitute the capaciry for resistance and recovery, thus recogn izing the validiry of rhe anciem observarion that the physician deals with a patient as well as a disease

(38).

They then combined several concepts and restated them as four principles: The osteopath ic concept em phasizes four general pri nci pies from which are derived an etiological concept, a philosophy and a thera

I . The body is a unit; the person is a unit of body, m i nd, and spirit. 2 . The body is capable of self-regulation, self-heali ng, and health maimenance.

3. Structure and function are reciprocally i nterrelated.

4.

Rational treatment is based upon an understanding of the basic principles of body u n i ry, self-regulation, and the imerrelationship of structure and function

(43).

Although Korr applies 20th century physiologic concepts in his explication of osteopathic principles, he maintains Still's basic premise: "It is the patient who gets well, and not the practitioner or the treatment that makes them well" (44). In order to represent an increasingly diverse group of osteo pathic physicians, the American Osteopathic Association (AOA) adopted a general statement regarding osteoparhic medicine. Since 1991, the official AOA definition of osteopathic medicine has been reviewed periodically. The latest rendition is available by consulting the AOA website at www. aoa-net. org and clicking on the "yearbook" icon. I t was last reviewed and accepted as policy by the AOA House of Delegates in 1 998:

peutic tech nic that are distinctive, but not the only features of osteo pathic diagnosis and treatment.

I . The body is a un it. 2 . The body possesses self-regularory mechanisms. 3 . Structure and function are reciprocally i mer-related.

4.

Osteopathy (Osteopathic Medicine): A complete system of medical care with a philosophy that combines the needs of the patient with

Rational therapy is based upon an understand i ng of body u n i ry,

current practice of medicine, surgery and obstetrics; that emphasizes the in terrelationship between structure and function; and that has an appreciation of the body's abil i ty

ro

heal i tself.

self-regularory mechanisms, and the i n ter-relationship of struc ture and function

The Educational Council on

(38).

Osteopathic Principles

Over the ensuing 40 years, advances in the biologic sciences elucidated many mechanisms in suPPOrt of the concept that op timal health calls for integration of countless functions ranging from the molecular to the behavioral level. When this integra tion breaks down, dysfunction and disease commonly follow. Infectious and metabolic diseases, as well as diseases of aging and genetics are frequent examples. Interdisciplinary fields of study have been developed to investigate and delineate the complex in teractions of numerous coordinated body functions in health and disease. Psychoneuroimmunology, for example, provides substan tial evidence linking mind, body, and spiritual activities with a wide variety of biologic observations (39-42). Clinical applications of the advances in molecular, cellular, neurologic, and behavioral sciences, combined with the decreased emphasis on mechanical factors within osteopathic medical prac tice, demanded a new consensus statement. Using the 1953 Ki rksville faculty statement as a beginning, the associate editors of the first edition of this text ( 1 997) stated:

In the contemporary era, the evolution, growth, and teaching of osteopathic philosophy have been coordinated through the Edu cational Council on Osteopathic Principles (ECOP) of the Amer ican Association of Colleges of Osteopathic Medicine. This orga nization consists of the chairs of the departments of osteopathic manipulative medicine and osteopathic principles and practice from each osteopathic medical school. It is the "expert panel" in the osteopathic profession in regard to osteopathic manipula tive medicine and osteopathic philosophy and principles. These osteopathic physicians are considered leading-edge thinkers in terms of osteopathic philosophy and principles. One of ECOP's charges is to obtain consensus on the usage of terms within the profession. The Glossary o/Osteopathic Termi nology was first published in 1981 (45), and is updated annually. The 2002 edition is included at the back of this text. The Glos sary elaborates upon the AOA definition of osteopathic medi cme:

Health is the adaptive and optimal attainment of physical, mental,

Osteopathic medicine is a phi losophy of health care and a distinc

emotional, and spiritual well-being. It is based on our natural capaciry

tive arr, supporred by expanding scienr ific knowledge; its philosophy

to meet, with adequate reserves, the usual stresses of daily l ife and

embraces the concept of uniry of the l iving organism's structure

the occasional severe stresses im posed by extremes of environment

(anaromy) and function (physiology). Its art is the application of the

and activi ty. I t i ncludes our abil iry ro resist and combat noxious

philosophy in the practice of medicine and surgery in all its branches

i n A uences in our environment and ro compensate for their effects.

and specialties. lrs science includes the behavioral, chemical, physi

One's health at any given time depends on many facrors including

cal, spiritual and biological knowledge related ro the establish ment

h is or her polygenetic i n heritance, environmemal i n A uences, and

and mai nrenance of health as well as the prevenrion and alleviation

adaptive response ro stressors

(43).

of disease.


TABLE 1 .2 . OSTEOPATHIC PATIENT G U I DANCE FOR SE LF-CARE

EDUCATION

11

AND

While osteopathically oriented medical care emphasizes competent comprehensive patient management, it also places importance on restoration of well being appropriate for the patient's age and health potential. This includes addressing: •

Physical, mental, and spiritual components

•

Personal safety, such as wearing seat belts

•

Sufficient rest and relaxation

•

Proper nutrition

•

Regular aerobic, stretching, and strengthening exercises

•

Maintaining rewarding social relationships

•

Avoidance of tobacco, and other abused substances

•

Eliminating or modifying abusive personal, interpersonal, family, and work-related behavior patterns

•

FIGURE 1.2. Osteopathic philosophy of health d isplayed as the coor dinated activity of five basic body functions, integrated by the muscu loskeletal system, adapting to environmental stressors. Evaluation and treatment of the musculoskeletal system is performed in light of its ability to affect not only the five functions, but also how it ultimately affects the person's ability to adapt to internal and external stressors.

One of the products of ECOP's work is the development of a method of organizing osteopathic concepts using systems theory and modern concepts in physiology. The primary approach taken was ro adopt a health-oriented perspective while also focusing on competent diagnosis and clinical management. Five basic integrative and coordinated body functions and cop ing srrategies are considered in a conrext of healthful adaptation ro life and its circumstances: I.

Posture and motion, including fundamental stfllcrural and biomechanical reliabiliry

2. Neurologic inregration, including cennal, peripheral, au ronomic, neuroendocrine, neurocircularory, and somanc elemenrs 3. Macro- and microrespirarory and circularory facrors 4. Metabolic processes of all rypes 5. Psychosocial, cultural, behavioral, and spiritual elements Figure 1.2 depicts the musculoskeletal system as the core or hub of a five-spoked wheel. Careful observation and educated palpation help make the musculoskeletal system a natural entry poinr for both diagnosis and rreatmenr. Imporranrly, the muscu loskeletal system often reflects numerous signs relating ro internal diseases.

Avoidance of environmental radiation and toxins

for long-term self-health care. Emphasis is on health resroration and disease prevention. An ad hoc interdisciplinary commirree of osteopathic educa tors, philosophers, and researchers recenrly proposed osteopathic principles for patient care: The Patient Is the Focus for Health Care All osreoparhic physicians, irrespecrive of rhe specialty of the prac titioner, are trained ro focus on the individual patienr. The relation ship between clinician and patient is a partnership in which both parties are actively engaged. The osteopathic physician is an advo cate for the patient, supporting his or her efforts ro optim ize rhe circumstances to maintain, improve, or resrore healt h .

The Patient Has the Primary Responsibility for His or Her Health While rhe physician is the professional charged with the respon sibility to assisr a patient in being well, the physician can no more impart health to another person than he or she can impart charm, wis dom, wit or any orher desirable trair. Although the patient-physician relarionsh ip is a partnership, and rhe physician has significant obliga tions to the parient, ultimately the patient has primary responsibility for h is or her health. The parient has inherent healing powers and must nurture these through diet and exercise, as well as adherence to appropriate advice in regard to stress, sleep, body weight, and avoidance of abuse.

An Effective Treatment Program for Patient Care An effective treatment program for patient care is founded on the above reners and incorporates evidenced-based guideli nes, op timizes the parient's narural healing capacity, addresses the primary cause of disease, and emphasizes health mai ntenance and disease prevention. The emphasis on the musculoskeleral system as an in tegral part of patient care is one of the defining characteristics of osteopathic medicine. When applied as part of a coherent ph iloso

OSTEOPAT HIC PR INCIPLES AS

phy of the pracrice of medicine, these teners represent a distinct and

PRACTICE GUIDELINES

necessary approach to health care . . . .

The conrributions of A.T. Still and the osteopathic medical pro fession affecr many aspects of general patient care. First, irre spective of diagnoses or practitioner, the patient is of central im ponance. Second, a competenr differential diagnosis is essenrial. This includes all aspects of the person (body, mind, and spirit) (Table 1.2). Third, clinical activities integrate realistic expecta tions with measurable outcomes. Finally, and ideally, patient oriented educational efforts pragmatically address both personal and family-related concerns. The patient is ultimately responsible

treatments with p roven efficacy and to discourage those that a re

Evidence-based guidelines should be used ro encou rage those not beneficial, or even harmful. Osteopathic medicine embraces the concept of evidence-based medicine as part of a valuable reformation of clin ical pracrice. Andrew Taylor Still told his students to "look for heal th; any one can find disease." This precept provides a useful orientation in parient care. An emphasis on health rather rhan disease helps to pro mote optimism. It may facilitare efforts to engage the patient as an active participant i n recovery from illness. Ir may also encourage the realization that no single treatment approach is successful for every

12


patient. Rather, optimal approaches will use diet, exercise, medica

SU M MARY

tions, manipulative rreatmenr, surgery, or other modalities according to the needs and wishes of the patienr and the skill and aptitude of the practitioner

(46).

In end-stage conditions, treatment may be only palliative, yet, as Korr points out, [ I ] t is the physician's responsibility, while giving palliative and reme dial arrenrion to the patien t's immediate problem, to support each patienr's internal health care system, to remove impedimenrs to its competence, and above all, to do i t no harm. It is also the respon sibility of physicians ro instruct patienrs on how to do the same for themselves and own example

ro

strive to motivate them to do so, especially by their

(44).

Osteopathically oriented problem-solving and treatment plans help guide the application of osteopathic principles in med ical, behavioral, and surgical care. In 1 987, ECOP developed guidelines for use by osteopathic physicians in developing an osteopathic management plan (47). The extent to which palpa tory diagnosis and manipulative treatment are specifically useful interventions for a wide variety of neuromusculoskeletal prob lems remains to be seen th rough research. However, since many clinical presentations commonly interfere with a patient's ability to meet the requirements of normal daily activities, including appropriate exercise, it stands to reason that improving the ef ficiency of the neurom usculoskeletal system would benefit each patient. "There is a somatic component in all clinical situations. The somatic component is addressed to the extent that it inAu ences patient well-being. Conceprually, osteopathic manipulative treatment is designed to address both structural abnormalities and self-regulatory capabilities."

Based on a health-oriented medical philosophy, osteopathic medicine uses a n umber of concepts to implement its principles. The neuromusculoskeletal system is used as a common point of reference, because it directly relates the individual to the physical environment on a day-to-day basis. The practitioner's primary roles are to: Address primary cause(s) of disease using available evidence based practices • Enhance the parien t's healing capacity • Individualize patient management plans with an emphasis on health restoration and disease prevention • Use palpatory diagnosis and manipulative treatment to focus on and affect somatic signs of altered structural, mechanical, and physiologic states •

Osteopathic philosophy is meant to guide osteopathic physi cians in the best use of scientific knowledge to optim ize health and diminish disease processes. Upon founding his profession and school, Still expressed the hope that "the osteopath will take up the subject and travel a few miles farther toward the fountain of this great source of knowledge and apply the re sults to the relief and comfort of the afAicted who come for counsel and advice" (6) . It is the intention of the authors to organize current medical knowledge and place it on a foun dation of osteopathic philosophy. We do this in order to pro vide the osteopathic medical student with a road map that will lead to the further study of the science of osteopathy and the practice of the highest quality patient-centered health care possible.

Editor's note: For 50 years, Irwin M. Korr, scientist, philosopher, and humanist, has led and inspired several generations of osteopathic physicians and educators. His fi nal treatise on osteopathic philosophy was written for the first edition of this text.

A N E X P L I C AT I O N O F O S T E O PAT H I C P R I N C I P L E S I RV I N M . K O R R

At this stage o f your medical training, you have become famil iar with osteopathic principles and can recite them in their usual brief, maxim form. The purpose of this section is to explore more fully the meani ng, biological foundations, and clinical implica tions of the founding principles of osteopathic medicine.

Remember that these principles began to evolve centuries ago, even before the time of Hippocrates. However, their basis in an imal and, more specifically, human biology did not begin to be come evident through research until late in the 1 9th century. The origin of these principles, therefore, was largely empirical; that is,


they were the product of thoughtful and widely shared observa tions of ill and inj ured people. For example, it could hardly escape notice, even in primitive societies, that people (and animals) re covered from ill ness and wounds healed without i ntervention and, therefore, some natural indwelling heali ng power must be at work. Even at the time of the founding of the osteopathic profes sion in 1 892, the available knowledge in the sciences of phys iology, biochemistry, microbiology, immunology, and pathol ogy was meager. Indeed, immunology, biochemistry, and various other neurosciences and biomedical sciences had yet to appear as distinct disciplines. Therefore, these principles could only be expressed as aphorisms, embellished perhaps with conjectures about their biological basis. It is to the credit and honor of the osteopathic profession that it contributed cogent elaboration of the principles, developed effective methods for their implemen tation, built a system of practice upon those principles, and dis closed much about their basis in biological mechanisms through research. In view of the enormous amount of biomedical knowledge recorded throughout the 20th century, it is timely to exami ne the principles that guide osteopathic practice in the light of that knowledge and to explore their relevance to clinical practice and to current and future health problems. What follows is an effort in that direction, without detailed reference to individual research .

T HE PERSON AS A WHOLE The Body

The principle of the unity of the body, so central to osteopathic practice, states that every part of the body depends on other parts for maintenance of its optimal function and even of its in tegrity. This interdependence of body components is mediated by the communication systems of the body: exchange of sub stances via circulating blood and other body Auids and exchange of nerve impulses and neurotransmitters through the nervous system. The circulatory and nervous systems also mediate the regula tion and coordi nation of cellular, tissue, and organ functions and thus the maintenance of the integrity of the body as a whole. The organized and integrated collaboration of the body components is reAected in the concept of homeostasis, the maintenance of the relative constancy of the internal environment in which all the cells live and function. In view of this interdependence and exchange of inAuences, it is i nevitable that dysfunction or failure of a major body com ponent will adversely affect the competence of other organs and tissues and, therefore, one's health. The Person

Important and valid as is the concept of body unity, it is in complete in that it is, by impl ication, limited to the physical realm. Physicians minister not to bodies but to individuals, each of whom is unique by virtue of his or her genetic endowment, personal history, and the variety of environments in which that history has been lived.

13

The person, obviously, is more than a body, for the person has a mind, also the product of heredity and biography. Separation of body and mind, whether conceptually or in practice, is an anachronistic remnant of such dualistic thinking as that of the 1 7th century philosopher-scientist, Rene Descartes. It was his belief that body and mind are separate domains, one publicly visible and palpable, the other invisible, impalpable, and private. This dualistic concept is anachronistic because, while it is almost universally rejected as a concept, it is still acted out in much of clinical practice and in biomedical research. Clin ical and biomedical research (as well as everyday experi ence) has irrefutably shown that body and mind are so i nsepara ble, so pervasive to each other, that they can be regarded-and treated-as a single entity. It is now widely recognized (whether or not it is demonstrated in practice) that what goes on (or goes wrong) in either body or mind has repercussions in the other. It is for reasons such as these that I prefer unity of the person to unity of the body, conveying totally integrated humanity and i ndivid ual i ty. The Person as Conte xt

Phenomena assigned to mind (cons.ciousness, thought, feeli ngs, beliefs, attitudes, etc.) have their physiological and behavioral counterpartS; conversely, bodily and behavioral changes have psy chological concomitants, such as altered feelings and perceptions. It m ust be noted, however, that it is the person who is feeli ng, per ceiving, and responding not the body or the mind. It is you who feels well, ill, happy, or sad, and not your body or mind. What goes on in body and mind is conditioned by who the person is and their entire history. I n short, the person is far more than the union of body and mind, in the same sense that water is more than the union of hy drogen and oxygen. Nothing that we know about either oxygen or hydrogen accounts for the three states of water (liquid, solid, and gas) , their respective properties, the boiling and freezing points, viscosity, and so forth. Water incorporates yet transcends oxy gen and hydrogen. To understand water we must study water and not only its components. In the same way, at an enormously more complex level, the person com prises yet transcends body and mind. Moreover, once hydrogen and oxygen are joined to form water, they become subject to the laws that govern water. [n the same but infinitely more complex sense, it is you who makes up your mind, changes your mind, trains and entiches your mind, and puts it to work. I t is you who determines from moment to moment whether and in what way you will express, through your body, what is in or on your mind. Thus the person is the context, the environment, in which all the body parts live and function and in which the mind finds expression. Everything about the person-genetics, history from conception to the present moment, nutrition, use and abuse of body and mind, parental and school conditioning, physical and sociocultural environments, and so on-enters into determin i ng the qual i ty of physical and mental fu nction . The better the qual i ty of the environment provided by the person for the men tal and bodily components, the better they will function. For example, someone who has a peptic ulcer is not ill because of

14

I. Osteopathic Philosophy and History

the ulcer. The ulcer exists because of an unfavorable internal environment. In conclusion, just as the proper study of mankind is man (Alexander Pope), so is the study of human health and illness also man. As will become evident, the principle of the unity of the person leads us naturally to the next principle.

THE PLACE O F THE MUSCULOSKELETAL

Indeed, most of the fibers in the spinal nerves are those converg ing impulses to and from the muscles and other components of the musculoskeletal system. In addition, the nervous system, i ts autonomic components, and the circulatory system mediate communication and exchange of signals and substances between the soma and the viscera. In this way, visceral, metabolic, and endocrine activity is continually tuned to moment-to-moment requirements of the musculoskeletal system, that is, to what the person is doing from moment to moment.

SYSTE M IN HUMAN L I FE The Means of E xpression of Our Humanity and Individuality

Structure determines function, structure and function are recip rocally interrelated, and similar aphorisms have traditionally rep resented another osteopathic principle. That principle recognizes the special place of the musculoskeletal system among the body systems and its relation to the health of the person. We examine now the basis for the osteopathic emphasis on the musculoskeletal system in total health care. Human life is expressed in human behavior, in humans do ing the things that humans do. And whatever humans do, they do with the musculoskeletal system. That system is the ultimate instrument for carrying out human action and behavior. It is the means through which we manifest our human qualities and our personal uniqueness-personality, intellect, imagination, creativ ity, perceptions, love, compassion, values, and philosophies. The most noble ethical, moral, or religious principle has· value only i nsofar as it can be overtly expressed through behavior. That expression is made possible by the coordinated contrac tions and relaxations of striated muscles, most of them acting upon bones and joints. The musculoskeletal system is the means through which we communicate with each other, whether it be by written, spoken, or signed language, or by gesture or facial ex pression. Agriculture, i ndustry, technology, l iterature, the arts and sciences-our very civilization-are the products of human ac tion, interaction, communication, and behavior, that is, by the or chestrated contractions and relaxations of the body's musculature. Relation to the Body Economy

The musculoskeletal system is the most massive system in the community of body systems. Its muscular components are col lectively the largest consumer in the body economy. This is true not only because of their mass, but because of their high energy requirements. Furthermore, those requirements may vary widely from moment to moment according to what the person is doing, with what feelings and in what environments. The high and varying metabolic requirements of the muscu loskeletal system are met by the cardiovascular, respiratory, diges tive, renal, and other visceral systems. Together, they supply the required fuels and nutrients, remove the products of metabolism, and control the composition and physical properties of the inter nal environment. In servicing the musculoskeletal system in this manner, these organ systems are at the same time servicing each other (and, of course, the nervous system). The nervous system is also, to a great degree, occupied with the musculoskeletal system, that is, with behavior and motor control.

Consequences of Visceral Dysfunction

Impairment or failure of some visceral function or of commu nication between the musculoskeletal system and the viscera is reflected in the musculoskeletal system. When the resulting dys function is severe and diffuse, motor activity and even mainte nance of posture are difficult or impossible and automatically imposed. The Musculos keletal System as Source of Adverse Influences on Other Systems

I n view of the rich afferent input of the musculoskeletal system into the central nervous system and its rich interchange of sub stances with other systems through the body fluids, it is inevitable that structural and functional disturbances in the musculoskeletal system will have repercussions elsewhere in the body. Such structural and functional disturbances may be of postu ral, traumatic, or behavioral origin (neglect, misuse, or abuse by the person). Further, it must be appreciated that the hu man framework is, compared with other (quadruped) mammals, uniquely unstable and vulnerable to compressive, torsional, and shearing forces, because of the vertical configuration, higher cen ter of gravity, and the comparatively small, bipedal base. The human musculoskeletal system, therefore, is the frequent source of aberrant afferent input to the central nervous system and its autonomic distribution, with at least potential consequences to visceral function. Which organs, blood vessels, etc. are at risk is determined by the site of the musculoskeletal dysfunction and the part(s) of the central nervous system, (e.g., spinal segments) into which it discharges its sensory impulses. When a dysfunction or pathology has developed in a visceral organ, that disturbance is reflected in segmentally related somatic tissues. Viscus and soma become l inked in a vicious circle of afferent and efferent impulses, which sustain and exacerbate the disturbance. Appropriate treatment of the somatic component reduces its input to the vicious circle and may even interrupt that circle with therapeutic effect. Importance of the Personal Conte xt

Whether or not visceral or vasomotor consequences of somatic dysfunction occur, and with what consequences to the person, depends on orner factors in the person's life, such as the genetic, nutritional, psychological, behavioral, sociocultural, and environ mental. As research has shown, however, the presence of somatic dysfunction and the accompanying reflex and neurotrophic ef fects exaggerate the impact of other detrimental factors on the


person's health. Effective neatmem of the musculoskeletal dys funC[ion shields the patiem by reducing the deleterious effects of the other factors. Such rreatmenr, therefore, has prevenrive as well as therapeutic benefits. Such rreatmenr di rected to the musculoskeletal system as sumes even greater and often crucial significance when it is rec ognized that the other kinds of harmful factors, such as those enumerated above, are not readily subject to change and may even require social or governmenral inrervenrion. The muscu loskeletal system, however, is readily accessible and responsive to osteopathic mani pulative rreatmenr. I view these considerations as the rationale for osteopathic manipulative treatmenr and i rs srrategic role in total health care. Finally, the osteopathic philosophy and the unity of the person concept enjoins the physician to rreat the patienr as a whole and not merely the affected partS. Hence, appropriate corrective attention should also be given to other significant risk factors that are subject to change by both patienr and physician.

15

tl'ations) and sustain ourselves with chemically diverse food and drink. But the cells of our body can function and survive only in the i nrernal environmenr of i n rerstitial fluids which main tain body functions within relatively narrow limits as regards variations in chemical composition, temperature, tissue, osmotic pressure, pH, etc. This phenomenon, called homeostasis, is based on thousands of simultaneously dynamic equilibria occurring throughout the body. Examples i nclude rates of energy consumption and replen ishmenr by the cells. Homeostasis constancy and quick restora tion of constancy must be accomplished regardless of the vari ations in the external environmenr, composition of food and drink, and the momenr-to-momenr activities of the person. [ t i s accomplished b y an enormously complex array of regulatory mechanisms that conrinually monitor and control respiratory, circulatory, digestive, renal, metabolic, and countless other func tions and processes. Mai ntenance of optimal environments for cellular funC[ion is essenrial to health. The homeostatic mecha n isms may, therefore, be viewed as the health maintenance system of the body.

OUR P ERSONAL H EALT H CAR E SYST E MS The Natural Healing Power

Commentary

Appreciation, even in ancienr times, of our inherenr recupera tive, restorative, and rehabilitative powers is reflected in the Latin phrase, vis medicatrix naturae (nature's healing force) . We recover from illnesses, fevers drop, blood clots and wounds heal, broken bones reunite, infections are overcome, skin eruptions clear up, and even cancers are known to occasionally undergo sponraneous remission. But miraculous as is the healing power (and appreci ated as it was until we became more impressed by human-made mi racles and breakthroughs) , the other, more recently revealed componenrs of the health care system with which each of us is endowed are no less marvelous.

These, then are the three major components of our indwelling health care system, each comprising numerous component sys tems. In the order in which humans became aware of them, they are (a) the healing (remedial, curative, palliative, recupera tive, rehabilitative) componenr; (b) the componenr that defends against threats from the external environment; and (c) the home ostatic, health-mainraining component. These major component systems, of course, share subcomponents and mechan isms. When the i n rernal health care system is perm itted to operate optimally, without impediment, its product is what we call health. Irs natural tendency is always toward health and the recovery of health. Indeed, the personal health care system is the very source of health, upon which all externally applied measures depend for thei r beneficial effects. The i n rernal health care system, in effect, makes its own diagnoses, issues its own prescri ptions, draws upon its own vast pharmacy, and in most situations, admin isters each dose without side effects. Health and heali ng, therefore, come from within. [t is the patient who gets well, and not the practitioner or the treatment that makes them well.

The Component System That Defends against Threats from Without

This componenr includes, among others, immune mechanisms that defend us against the enormous variety and potency of for eign organisms that invade our bodies, wreaking damage and even bringing death. These same immune mechanisms guard us agai nst those of our own cells that become foreign and mal ignant as the result of mutation. Included also are the mechanisms that defend against foreign and poisonous substances that we may take in with our food and drink or that enter through the skin and lungs, by disarming them , converting them to innocuous substances, and elimi nating them from the body. They defend us (unril overwhelmed) even against the toxic substances that we ourselves in troduce into the atmosphere, soil, water, or more directly into our own bodies. Mechanisms That Defend against Changes in the Internal Environment We humans are exposed to, and adapt to, wide variations in phys ical and chemical properties of our environmenr (e.g., temper ature, baromerric pressure, oxygen, and carbon dioxide concen-

T H E T HR E E PRINCIPL ES AS GUID ES TO M EDICAL PRACT IC E The Unity of the Person

[ n caring for the whole person, the well-grounded osteopathic physician goes beyond the presenting complaint, beyond relief of symptoms, beyond identification of the disease and rreatmenr of the impaired organ, malfunction, or pathology, important as they are to total care. The osteopathic physician also explores those factors i n the person and the person's life that may have conrributed to the illness and that, appropriately modified, com pensated, or eliminated, would favor recovery, prevenr recurrence, and improve health in general.

16


The physician then selects that factor or combination of fac tors that are readily subject to change and that would be of suf ficient impact to shift the balance toward recovery and enhance ment of heal th. The possible factors include such categories as the biological (e.g., genetic, nutrirional) , psychological, behav ioral (use, neglect, or abuse of body and mind; interpersonal rela tionships; habits; etc.), sociocultural, occupational, and environ mental. Some of these factors, especially some of the biological, are responsive to appropriate clin ical i ntervention, some are re sponsive only to social or governmental action, and still others re quire changes by patients themselves. Osteopathic whole-person care, therefore, is a collaborative relationship berween patient and physician. The Place of the Musculoskeletal System in Human Biology and Behavior : The Strategic Role of Osteopathic Manipulative Treatment

It is obvious that some of the most deleterious factors are difficult or impossible for patient and physician to change or elimi nate. These include (at least at present) genetic factors (although some inherited predispositions can be mitigated by lifestyle change) . They include also such items as social convention, lifelong habits (e.g., dietary and behavioral), widely shared beliefs, prejudices, misconceptions and cultural doctrines, attitudes, and values. Others, such as the quality of the physical or socioeconomic environments, may require concerted community, national, and even international action. Focus falls, therefore, upon those deleterious factors that are fa vorably modifiable by personal and professional action, and that, when appropriately modified or eliminated, mitigate the health impairing effects of the less changeable factors. Improvement of body mechanics by osteopathic manipulative treatment is a major consideration when dealing with these complex i n teractions.

OUR PERSONAL HEALT H CARE SYSTE MS

This pri nciple has important impl ications for the respective re sponsibilities of patient and physician and for their relationship. Si nce each person is the owner and hence the guardian of his or her own personal health care system, the ultimate source of health and healing, the primary responsibility for one's health is each individual's. That responsibility is met by the way the per son lives, thi nks, behaves, nourishes himself or herself, uses body and mind, relates to others, and the other factor usually called lifestyle. Each person must be taught and enabled to assume that responsibility. It is the physician's responsibility, while giving palliative and remedial attention to the patient's immediate problem, to support each patient's internal health care system, to remove impediments to its competence, and above all, to do it no harm. It is also the responsibility of physicians to i nstruct patients on how to do the same for themselves and to strive to motivate them to do so, especially by their own example. The relationship berween patient and osteopathic physician is therefore a collaborative one, a partnership, in maintaining and enhancing the competence of the patient's personal health care

system. The maintenance and enhancement of health is the most effective and comprehensive form of preventive medicine, for health is the best defense against disease. As stated by A.T. Still, "To find health should be the object of the doctor. Anyone can fi nd disease." Relevance to the Current and Future Health of the Nation

The preventive strategy of health maintenance and health en hancement, i nt ri nsic to the osteopathic philosophy, is urgently needed by our society today. One of the greatest burdens on the nation's health care system and on the national economy is in the care of victims of the chronic degenerative diseases, such as heart disease, cancer, stroke, and arthritis, which require long term care. The incidence of these diseases has increased and will con tinue to increase well into the next century as the average age of our population continues to increase. The widely accepted (but usually unspoken) assumption that guides current practice (and national policy) is that the chronic degenerative diseases are an inevitable aspect of the aging process; that is, that aging is itself pathological. It is now i ncreasingly apparent, however, that the i ncrease of their incidence with age is because the longer one lives, the greater the toll taken by minor, seemingly inconsequential, in conspicuous, treatable impairments and modifiable contributing factors in and around the person. They are, therefore, largely the natural culmination of less-than-favorable lifestyles, and, hence, they are largely preventable. The great national tragedy is that, while the nation's health care system is so extensively and expensively absorbed in the care of millions of older adult victims of chronic disease (at per capita cost 3.5 times that of persons under the age of 65 years), tens of millions of younger people and children are living on and embarlcing on life paths that will culmi nate in the same diseases. The health care system simply must move upstream to move people from pathogenic to salutary paths. And the osteopathic profession can show the way. The osteopathic profession has a historic opportunity to make an enormous contribution to the enhancement of the health of Out nation . It can do this by giving leadership in addressing this great tragedy by bringing its basic strategy of whole-person, health-oriented care to bear on the problem and demonstrating its effectiveness in practice. Having reviewed and enlarged on the principles of osteopathic medicine, their meaning, biological foundations, and clinical im plications, it seems appropriate to propose a definition ·of osteo pathic medicine. The author offers the following: Osteopathic medicine is a system of medicine that is based on the continually deepening and expanding understanding of (a) human nature; (b) those components of human biology that are centrally relevant to health, namely the i nherent regulatory, protective, regenerative, and recuperative biological mechan isms, whose combined effect is consistently in the direction of the maintenance, enhancement, and recovery of health; and (c) the factors in and around the per son that both favorably and unfavorably affect those mechanisms. The practice of osteopathic medicine is, essentially, the poten tiation of the intrinsic health-maintai ning and health-restoring

J. Osteopathic Philosophy

resources of the individual. The methods and agents employed are those that are effective in enhancing the favorable factors and diminishing or elimi nating the unfavorable factors affect ing each individual. Osteopathic medical practice necessarily in cludes the application of palliative and remedial measures, but always on the condition that they do no harm to the patient's own health-maintaining and health-restoring resources. This stipula tion governing the choice of methods and agents is based on the recogn ition that all therapeutic methods depend on the patient's own recuperative power for their effectiveness and are valueless without it and that health and the recovery of health come from within. The art and science of osteopathic medicine are expressed in the identification and selection of those factors in each individ ual that are accessible and amenable to change and that, when changed, would most decisively potentate the person on health supporting resources. Osteopathic physicians give special emphasis to factors origi nating in the musculoskeletal system, for the fol lowing reasons: 1.

The vertical human framework (a) is h ighly vulnerable to compressive (gravitational ) , torsional, and shearing forces, and (b) encases the entire central nervous system.

2. Since the massive, energy-demanding system has rich two-way communication with all other body systems, it is, because of its vulnerability, a common and frequent source of impediments to the functions of other systems. 3. These impediments exaggerate the physiological impact of other detrimental factors in the person's life, and, through the central nervous system, focus it on specific organs and tissues. 4. The musculoskeletal impediments (somatic dysfunctions) are readily accessible to the hands and responsive to the manipu lative and other methods developed and refined by the osteo pathic medical profession.

R EFER ENCES I . Trowbridge C . Andrew Taylor Still. Kirksville, MO: Thomas Jefferson University Press, Northeast M issouri State University; 1 99 1 :95- 1 40. 2. Still AT. Autobiograpby of Andrew T Still. Rev ed. K i rksville, M O : Published b y the author; 1 908. Distributed, Indianapolis: American Academy of Osteopathy. 3. Still AT. Osteopatby Researcb and Practice. Seattle, WA: Eastland Press; 1 992. Originally published by the author; 1 9 1 0. 4. Still CE Jr. Frontier Doctor Medical Pioneer. Kirksville, MO: Thomas Jefferson University Press, Northeast Missouri State Un iversity; 1 99 1 . 5 . Hildreth AG. The Lengthening Shadow ofDr. Andrew Taylor Still. Macon, MO: Privately publ ished, 1 942. Reprinred and distributed, Kirksville, Mo: Osteopath ic Enterprises, I nc. 6. Still AT. The Philosopby and Mechanical Principles ofOsteopathy. Original copyright by the author, Kirksville, Mo: 1 892. Then, Kansas City, Mo: 1 902. Reprinred, Kirksville, MO: Osteopathic Enterprises; 1 986. 7. Still AT. Philosophy of Osteopathy. K i rksville, MO: \ 899. Reprinted, Academy of Appl ied Osteopathy. Carmel, CA; 1 946. 8. Booth ER. Summation of causes in disease and death. J Am Osteopath Assoc. 1 902;2(2) :33-4 1 . 9. Lyne ST. Osteopathic phi losophy of the cause of disease. JAm Osteopath Assoc. 1 904;3 ( 1 2):395-403. Repri n ted in J Am Osteopath Assoc. 2000; 1 00(3) : 1 8 1 - 1 89.

17

1 0 . Littlejohn J M . Osteopathy: an independent system co-extensive with the science and art of healing. J Am Osteopath Assoc. 1 90 I ;vol I . Reprinted in J Am Osteopath Assoc. 2000; 1 00 ( 1 ) : 1 4-26. 1 1 . Lane MA. Dr. A. T Still. Founder of Osteopathy. Ch icago, I L: The Os teopathic Publishing Co; 1 9 1 8. 1 2 . Hulett GO. A Text Book ofthe Principles ofOsteopathy, 5th ed. Pasadena, Ck A.T. Still Research Insti tute; 1 922. 1 3 . Schnucker RV, ed. Early Osteopathy: In the Word< ofA. T Still. Kirksville, MO: Thomas Jefferson Un iversity Press, Northeast M issouri State Uni versity; 1 99 1 . 1 4. Littlejohn J M . The physiological basis of the therapeutic law. J Sci Os teopath. 1 902;3(4). 1 5 . Downing C H . Osteopathic Principles in DisfOse. Originally published, San Francisco, CA: Ricardo J . Orozco; 1 935. Reprinted and publ ished, Newark, O H : American Academy of Osteopathy; 1 988. 1 6. Page LE. Principles ofOsteopathy. Kansas Ci ty, MO: Academy of Applied Osteopathy; 1 9 52. 1 7. Korr 1M. The osteopathic role i n medical evolution. The DO. 1 973;(Nov). 1 8. Northup GW. Osteopathic Medicine; An American Reformation. Ch icago, IL: American Osteopathic Association; 1 979. 1 9. Hulen CMT. Relation of osteopathy ro other systems. J Am Osteopatb Assoc. 1 90 1 ; 1 : 227-233. 20. Schiotz, E H and Cyriax, J. Manipulation. Past and Presenl. London, England: William Heinemann Medical Books, Ltd; 1 975. 2 1 . Lomax E. Manipulative therapy: a historical perspective from ancient times to the modern era. In: Goldstein M, ed. The Research Status of Spinal Manipulative Therapy. Bethesda, M D: U.S. Dept. of Health, Ed ucation and Welfare; 1 97 5 : I 1 - 1 7. N I H publication 76-998. 22. Adams F. The Genuine Works of Hippocrates. First published his trans lation i n 1 849, then again in 1 886, and again in 1 929. However, the published editions that are usually available today were published in Philadelphia, PA: Will iams & Wilkins; 1 939. 23. Harris J 0, McPartland J M . H istorical perspectives of manual medicine. In: Stanton OF, Mein EA, eds. Physical Med Rehabil Clin North Am. 1 996;7(4) : 679-692. 24. Burns L. Pathogenesis of VisceraL Disease Following Vertebral Lesions. Chicago, l L: American Osteopathic Association; 1 948. 25. Beal MC, ed. The Cole Book ofPapers SeLected From the Writings and Lec tures ofWilbur V Cole, D. 0. , F.A.A. 0. Newark, O H : American Academy of Osteopathy; also see Hoag J M , Cole WV, Bradford SG, eds. Osteo pathic Medicine. New York, NY: McGraw- H i l i ; 1 969. 26. Beal MC, ed. Selected Papers ofJohn Stedman Denslow, DO. Indianapolis, I N : American Academy of Osteopathy; 1 993. 27. Korr 1 M . The Neurobiologic Mechanisms ofManipulative Therapy. New York, NY: Plenum Ptess; 1 977. 28. Peterson B, ed. The Collected Papers ofIrvin M. Karl'. Colorado Springs, CO: The American Academy of Osteopathy (currently i n I ndianapolis, I N ) ; 1 979. 29. Jones JM. Osteopathic philosophy. In: Gallagher RM, Humphrey FJ. eds. Osteopathic Medicine: A Reformation in Progress. New York, NY: Churchill Livingstone; 200 I . 30. McConnell Cp, Teall Cc. The Practice of Osteopathy, 3rd ed. Kirksville, MO: The Journal Printing Co, 1 906. 3 1 . Tasker D . Principles of Osteopathy. Los Angeles, CA: Baumgardt Pub lishing Co; 1 903. 32. Burns L. Studies in the Osteopathic Sciences; Basic Principles, Vol I . Los Angeles, CA: Occident Pri ntery; 1 907. 33. Downing CH. Principles and Practice of Osteopathy. Kansas Ci ty, MO: Williams Publishing Co; 1 923. 34. Barber E. Osteopathy Complete. Kansas City, MO: Hudson-Ki mberly Publishing; 1 898. 35. Booth ER. History ofOsteopathy and Twentieth Century Medical Practice. Cincinnati, O H : Jennings and Graham, 1 905. 36. H ildreth AG. The Lengthening Shadow ofAndrew Taylor Still. Macon, MO and Paw Paw, M I : Privately published by M rs. AG H i ldreth and Mrs. AE Van Vleck; 1 942. 37. College of Osteopathic Physician and Surgeons documents, 1 948. Uni versity of Cali fornia at I rvine, Library Archives, Special Collections. 38. Special Com m ittee on Osteopathic Princi ples and Osteopathic Technic,

18

39.

40. 4I . 42. 43.


Kirksville Col lege of Osteopathy and Surgery. An i nterpretation of the osteopathic concept. Tentative formulation of a teach ing guide for fac ulty, hospital staff and student body. J Osteopath. 1 953;60( 1 0) :7- 1 0. Felton DL. Neural influence on i m m une responses: underlying suppo sitions and basic principles of neural-immune signaling. Prog Brain Res. 2000( 1 22), Ch. 27. Pert CB. Molecules ofEmotion: The Science Behind Mind-Body Medicine. New York, NY: Touchstone, Simon and Schuster; 1 997. Damasio A. The Feeling of What Happens: Body and Emotion in the Making of Consciousness. New York, NY: Harcourt; 1 999. Dossey L. Prayer Is Good Medicine: How to Reap the Healing Benefits of Prayer. San Francisco, CA: HarperColl ins; 1 996. Scffinger MA. Development of osteopathic philosophy. I n Ward RC,

44.

45. 46.

47.

exec ed. Foundations for Osteopathic Medicine. Baltimore: Williams & Wilkins; 1 997:3-7. Korr 1M. An explication of osteopathic principles. In Ward RC, exec ed. Foundations for Osteopathic Medicine. Baltimore: Will iams & Wilkins; 1 997:7- 1 2. Ward R, Sprafka S. Glossary of osteopathic terminology. J Am Osteo-' pathic Assoc. 1 98 1 ;80(8) : 5 52-567. Rogets FJ, D'Alonzo G E, Glover J , Kort 1 M , et al. Proposed tenets of osteopathic medicine and princi ples for patienr care. J Am Osteopad) Assoc. 2002; 1 02(2):63-65. Educational Council on Osteopathic Principles. Core Curriculum Out l i ne. Washi ngton, DC: American Association of Col leges of Osteopathic Medicine; 1 987.

MAJOR EVENTS IN OSTEOPATHIC HISTORY BARBARA E. PETERSON

Andrew Still had the sketchy education of a frontier child (3), KEY CONCEPTS • Beginnings of osteopathic medicine • Growth of the osteopathic profession • Educational issues • Areas of conflict and agreement with allopathic medicine • Osteopathic professional organizations • Recognition by state and federal governments • Role in specialties, hospitals, and primary care

but he was an inventive person, and he liked to read. Eventually he would become familiar with many of the major practical and ideological trends of his time. But learning to survive had to come first; Missouri and Kansas were true frontiers. The Stills first eked out a living by hunting for food and making some of their clothes from animal skins. The family also plowed their land claim and established a farm while the father rode a circuit among scattered settlers, ministering to minds and bodies. It was a lifesryle that gave substance to the word "survivor" (7). Andrew Still would later say how important animal dissection had been as a preparation for study of human anatomy. He also recorded another prophetic childhood experience in his Autobi

Osteopathic medicine has from its beginning been a profession based on ideas, tenets that have lasted through all sorts of adversiry and have been credited with bringing the profession to its present

ography. One day, when about ten years old, I suffered from a headache.

I made a swing of my father's plow-line between two trees; but my

level of success. T he previous chapter outlines in some detail the

head hurt toO much to make swinging comfortable, so I let the rope

growth of these ideas. It is perhaps significant that the profession's

down to about eight or ten inches of the ground, threw the end of a

founder never wrote clinical manuals, only books of philosophy

blanket on it, and I lay down on the ground and used the rope for

(1--4). It is striking that these ideas, still quoted extensively today (5), came not from universities or medical centers, but from the creative problem solving of an informally educated American frontier doctor named Andrew Taylor Still. Looking back more than a century, it seems surprising that his ideas were so contro versial when first put forward. But perhaps history has caught up with this eccentric, inventive man. The story of Andrew Taylor Still is worth knowing in detail but must be told superficially.

a swinging pillow. Thus I lay stretched on my back, with my neck actoss the rope. Soon I became easy and went to sleep, got up in a little while with the headache gone. As I knew nothing of anatomy at this time, I took no thought of how a rope could stop headache and the sick stomach which accompanied it. After that discovery 1 roped my neck whenever I felt one of those spells coming on

(3).

To the end of his life, Still continued to "rope his neck" (see Fig. 1.1). In his old age he would lie down daily with his neck on a version of a Chinese pillow, known among country folk as a "saint's rest"-a wooden frame with a leather strap suspended

He was born in a log cabin in Virginia in 1828, the year

across it-giving the same effect as a plow rope suspended be

Andrew Jackson was elected president. Still's family were farmers,

tween two trees. In his middle years he discovered other crude

as most people were then; his father was also a Methodist circuit

but effective methods for self-treatment, notably a croquet ball,

rider who preached and treated people's ills. He later would teach

upon which he lay down at the correct point when the problem

his five sons to be doctors in the usual frontier apprentice system

was in his back rather than his neck (8).

of the time.

In the 1840s the issue of slavery divided the Methodist church,

Still's mother came from a family that was nearly all wiped

and the Stills stayed with the northern (abolitionist) branch. By

out by a Shawnee Indian massacre (6), and it must have seemed

the early 1850s, most of the family had moved to Kansas, in

a supreme irony when in 1851 she and her husband moved

cluding Andrew and his young wife. At that time Andrew began

to Kansas as missionaries to the descendants of these same

seriously to read and practice medicine with his father. T hey gave

Indians. However, the family course first took them to Tennessee

the Indians "such drugs as white men used [and] cured most of

and then to Missouri, where they also were frontier missionaries.

the cases [they] met" (3).

20


In 1855 the government forced the Shawnees further west, and Kansas became a virtual war zone, as both abolitionist and pro-slavery settlers rushed in. The fate of Kansas as a free state depended on a popular vote. The Stills chose ro be active aboli tionists. Still recalled: I could not do otherwise, For no man can have delegated to him by statute a just right to any man's liberty, either on account of race or color. With these truths before me I entered all combats For the abolition of slavery at home and abroad, and soon had a host of bitter political enemies, which resulted in many thrilling and curious adventures (3).

The Stills met John Brown and fought under the command of Jim Lane, twO of the abolitionist leaders active on the western frontier. There are numerous srories of "abolitionist encounters" during the pre-Civil War days (9-11). The Struggle lasted, said Still, until Abraham Lincoln "wrote the golden words: 'Forever free, without regard ro race or color.' I will add-or sex" (3). The terrirorial political situation was volatile and confusing, with even the elections seemingly decided by gun barrles. There are many accounts of "bloody Kansas" in the pre-Civil War pe riod, including those in early osteopathic writings. But somehow a free-state legislature was elected in 1857, and Andrew Still was a proud member of that group (12). Andrew Still's first wife, nee Mary Margaret Vaughn, died in 1859, leaving three children. [n late 1860 Still married a young schoolteacher, who had learned ro mix prescriptions for her physi cian father and who was prepared by her background ro accept Still's medical and spiritual speculations (9). Ir was a most im portant partnership; Mary Elvira Turner Still was ro support her husband and family through the long period of doubt and dis grace that preceded successful establishment of the osteopathic profession, and again through the heady days of unexpected suc cess. But all this was in the future. When the Civil War officially began, Andrew Still enlisted first in a cavalry division of a force assigned ro Jim Lane. Later he organized a company of Kansas militia, which was in turn consolidated with other militia barralions. He was commissioned a major and saw active combat; some experiences are recounted in his Autobiography (3). He also served as a military surgeon, though he had been listed as a hospital steward on the official record (13). His unit was disbanded in Ocrober 1864, and Still went home ro resume normal civilian life. It was not exactly a joyful homecoming. In February 1864 three Still children had died of cerebrospinal meningitis, despite the best efforts of the physicians called ro help. All around him, Still saw people who had become addicted ro alcohol or mor phine, and he considered that these were "habits, cusroms, and traditions no better than slavery in its worst days" (3). Mainstream Civil War medicine still depended heavily on purging, bloodletting, and an armamentarium of medicines that could only be characterized as violent. On both sides there were many more casualties from sickness than from battle injuries (14). A hisrory of American medicine recounts: Even the most erudite and experienced physician had Few effective medicines at his command. Some of those which were effective were unknown to the poorly educated practitioner; others he knew not how to use. The short list of effective agents in the 1870s included

the anesthetics (ether, chloroform, and nitrous oxide); opium and its alkaloids (morphine was first used extensively during the Civil War to ease the pain of the wounded); digitaIis, which was used chieAy for cardiac edema [congestive heart failure]; ergot, to stimulate uter ine contractions and to control postpartum hemorrhage; mercury in the Form of an inunction For syphilis and in the Form of calomel to purge and salivate; various cathartics of botanical origin; iron, usually in the form of Blaud's pills For anemia; quinine For malaria; amyl nitrite, which was first recommended For the relief of angina pectoris by Sir Thomas Lauder Brunton in 1867 but was still not well known in 1876; sulfur ointment For rhe itch (scabies); green vegetables or citrus Fruit For the prevention or treatment of scurvy. These various medicines were adminisrered eirher by mouth, by rec tum, by inhalarion, or by application to the skin. The hypodermic syringe had been introduced by the French surgeon Pravaz in 1851. He employed ir to i'iject "chloride of iron" into vascular rumors to coagulate their contents. Although it was subsequently used For other restricted purposes, rhe danger of infection limited its use until the physician had learned how to prevent infections by the preparation of sterile solurions (15).

This description of the best of the armamentarium available was recorded about a decade after the Civil War. The urban populations certainly benefited most from these breakthroughs; frontier docrors and their patients were very much worse off. Still agonized over the situation: My sleep was well nigh ruined; by day and night I saw legions of men and women staggering to and Fro, all over the land, crying for Freedom From habits of drugs and drink .... I dreamed of the dead and dying who were and had been slaves of habit. I soughr to know rhe cause of so much dearh, bondage, and distress among my race.... I who had had some experience in alleviating pain found medicine a Failure. Since my early life I had been a student of nature's book. In my early days in windswept Kansas I had devoted my attention to the study of anatomy. I became a robber in the name of science. Indian graves were desecrated and the bodies of the sleeping dead exhumed in the name of science. Yes, I grew to be one of those vultures with rhe scalpel, and studied the dead that rhe living might be benefited. I had printed books, but went back to the great book of nature as my chief study (3).

He also wrote that he attended a course of lectures at a Kansas City medical school that was long defunct at the time of writing (16). The next decade of Still's life was devoted ro a search for a better way. He farmed, and he invented a butter churn and a version of a grain reaper. More children were born, the sons and daughter who would eventually become prominent in the profession their father was soon ro found. The search for a better way had many potential bypaths. The post-Civil War period was a time of great diversity in the healing professions, both in terms of how one became identified as a physician and how one approached the practice (17). In the mid19th century there were no licensing boards and only scattered state laws governing medical practice. There were a few medical schools, but there were no standard curricula. Most physicians, especially on the frontiers, were trained as apprentices, doing some reading and serving as a physician's assistant for an unstated length of time. A majority of physicians followed a standard parrern, heavily inAuenced by the "heroic medicine" of Benjamin Rush, who

2. Major Events in Osteopathic History

said that "there is but one disease in the world," and that it was treatable by "depletion," which translated as blood-letting, blistering, and purging. One influential textbook writer, John Esten Cooke, wrote that: AJI diseases, particularly fevers, arose from cold or malaria, which weakened the heart and thus produced an accumulation of blood in the vena cavae and in the adjoining large veins of the liver. Conse quently, calomel and other cathartics which acted on that organ were the cure. "If calomel did not salivate and opium did not constipate, there is no telling what we could do in the practice of physic" (18).

Calomel-and other mercury compounds were still listed as late as 1899 in the first Merck's manual, along with opium and mor phine and many alcohol-based compounds (19). The practice of "heroic" dosing was well established and well defended. By the time of the Civil War, the system was also called "allopathy," now defined as "that system of therapeutics in which diseases are treated by producing a condition incompatible with or antago nistic to the condition to be cured or alleviated" (20). The damage caused by the "heroic" techniques was obvious to thinkers before Still, and there were alternative systems of medicine available for consideration. Home remedies and Indian herbal preparations were a basic choice, and this lore was sub stantial and widely used (J 8). Numerous resources for botanic preparations were available as well; many of these manuals were widely circulated. Homeopathy was a major influence in the 19th century. Ar ticulated by Samuel Hahnemann (1755-1843), it was a system of therapy in which "diseases are treated by drugs which are ca pable of producing in healthy persons symptoms like those of the disease to be treated, the drug being administered in minute doses" (20,21). Eclecticism was another choice, described as "a once popular system of medicine which treats diseases by the application of single remedies to known pathologic conditions, without reference to nosology, special attention being given to developing indigenous plant remedies" (J 7). Magnetic healing, which "combined spiritualism and healing by seeking to restore the balance of an invisible magnetic fluid circulating throughout the body" (17), and its variants that attempted to use electrical . current to restore health were employed. The water cure, move ments emphasizing hygiene, anti-alcoholism or temperance, fresh air and sunlight, nutritional -programs, and physical education, and popular versions of mental healing, including hypnotism, spiritualism (table rapping), and phrenology were additional al ternatives. And, there were the bone-setters. At least two of these methods attracted A.T. Still and he linked his name to each for a time. A professional card in the Still Mu seum in Kirksville, Missouri, identifies Still as a "lightning bone setter." In 1874 he advertised himself in Kirksville as a "magnetic healer, " possibly because he was persuaded by "the metaphor of the harmonious balance of the interaction of body parts and the unobstructed flow of body fluids" (17). After a decade of study, in 1874, Still "flung to the breeze the banner of osteopathy" (3). He did not say precisely what that meant-perhaps a decision, perhaps a sudden coming together of creative thought-but it was followed by attempts to present his findings at Baker University, an institution his family had helped to found (22). He could not get a hearing. Further, he was

21

ejected from the Methodist church on the basis that only Christ was allowed to heal by the laying of hands. Still's description of that experience makes it clear that his "laying on of hands" was therapeutic manipulation. During the next year Still spent some time with his brother, who had become addicted to morphine through medical treat ment. This experience, added to the uselessness of medications in saving his family and others, roused in Still a hatred for the drugs of the day. This enmity sometimes appeared to be nearly abso lute, even when the armamentarium of drugs began to move from harmful toward helpful (1-4,23). However, there is evidence in his own writings that he sometimes used topical medications. For example, for snakebites, he washed the wounds with spirits of ammonia, and washed areas bitten by a dog with hydrophobia/ rabies with a diluted sulfuric acid solution, and used alcohol ro wash a spasmodic tetanic joint (4). Late in 1875 Stili moved from Kansas to Kirksville, Missouri, where he spent the rest of his life. For several years Still used Kirksville as a base to conduct a marginal itinerant practice (24). H is practice evolved as he gained experience, so that the main treatment modality became manipulation. AJthough this treat ment included some of the traditions of magnetic healing and bone setting, it emphasized detailed knowledge of anatomy and body mechanics so that treatment could be said to restore normal function. He held that the body is an efficient chemical labora tory that, in health, makes all the "drugs" it naturally needs. The object of treatment was to discover what caused the sickness and remove the interference so that the body could heal itself (2). By 1887 enough patients came to Kirksville so that Still could stop his itinerant practice. Word of dramatic successful outcomes began to spread via the newspapers and word of mouth, and once that happened, the burden of practice quickly became heavy. Still began to think about teaching others his methods; unlike many alternative practitioners of his day, he never intended to keep therapeutic secrets to himself or to grow rich from his methods. There were abortive attempts first to train apprentices and then to teach a class of operators to assist in the practice of osteopathy. The attempts were unsuccessful largely because the students lacked Still's detailed knowledge of anatomy and bodily function. The term "osteopathy" was coined by Still in about 1889. The story is told (25) that when challenged because this word was not in the dictionary, Still replied, "We are going to put it there." The word became for Still and his followers a symbol for medical reform, for a science that would refocus medicine on the restoration of normal function. Osteopathy aimed to work with and facilitate the natural machinery of the body for normal and reparative function, rather than working against it, as seemed to be the case with purgatives, emetics, bloodletting, and addictive drugs.

PROFESSIONAL EDUCATION AND GROWTH First School

The first successful school where osteopathy was taught, the American School of Osteopathy, was chartered in May 1892 and opened that fall with a class of about 21 men and women, in cluding members of Still's family and other local people. The

22


faculty consisted of Still and Dr. W illiam Smith, a physician trained in Edinburgh, Scotland, who taught anatomy in ex change for learning osteopathy. The goal, as stated in the revised (1894) charter for the school, was "to improve our present sys tem of surgery, obstetrics, and treatment of diseases generally, and [to] place the same on a more rational and scientific basis, and to impart information to the medical profession." The charter would have permitted granting the doctor of medicine (MD) de gree, but Still insisted on a distinctive recognition for graduates, DO, for diplomate in osteopathy (later doctor of osteopathy) (26). The first course was just a few months long; most of the stu dents voluntarily returned for a second year of additional train ing. By 1894 the course was 2 years long, two terms of 5 months each. In addition to their study of anatomy, students worked in the clinic under experienced operators, at first only under Still but later under graduates as well. Duri ng the last 5 years of the 19rh century the growth of both clinic and school were spectacular. Patients came from near and distant places, having heard by word of mouth or by printed ac counts of near-miraculous cures. There were enough of such "mir acles" that the osteopathic profession was widely promoted by grateful patients. A significant number of early DOs were either former patients or family members of patients who came to their studies with a kind of evangelical fervor. The town of Kirksville prospered and came to regard Still, who once was ridiculed, as a citizen of immense importance. He was lavishly praised, and he lived to see his statue, with the inscription "Demonstrate the Vision," erected in the town square (27,28). Data on numbers of enrolled students illustrate the school's dramatic growth. I n October 1895 there were 28 students. By the following summer there were 102. By 1900, there were over 700 students, with a faculty of 18 (26). By the turn of the century there were also more than a dozen "daughter" schools founded by graduates of the original school (29). Some of the schools were well organized under the model established by Still; others were established as diploma mills with the anticipation of generating large incomes for the persons establishing them. Still considered many of these to be for training "engine wipers" who were in capable or inexperienced in the practice of osteopathy. Many of these closed as standards were established by the American Os teopathic Association and by state licensure; by 1910, only eight remained. Conflict with the American Medical Association

Medical education in the late 19th century was not well regu lated. Many schools, allopathic, eclectic, homeopathic, and os teopathic, had virtually no entrance requirements except tuition payments, and many schools were for-profit institutions. Licens ing laws had not yet reached a stage where they were effective in setting educational standards. The American Medical Association (AMA) , founded in 1847, later a powerful influence on raising educational standards, was, in the 1890s, weak and in need of reorganization. A new, reorganized AMA, observing that there were too many doctors, made its first order of business, under a revised constitu-

tion, the regulation of medical education. Its Council on Medical Education was formed in 1904, with a charge (among others) to improve the academic requirements for medical schools. This was fulfilled by rating all medical schools as class A (approved), B (pro bation), or C (unapproved), and making the findings available to state licensing boards (30). Even before the AMA formed its Council on Medical Educa tion, the young American Osteopathic Association ( AOA) had adopted standards of its own for approval of osteopathic colleges (1902) and began inspections (1903) (31). This caused many small osteopathic colleges to close or merge with larger institu tions. Osteopathic schools were not included in the first AMA sur vey, but they were included in the influential Flexner Report, published in 1910 (32). After this report, which harshly con demned osteopathic schools along with many medical schools, more marginal schools closed, and the surviving ones converted to a not-for-profit status. Few of the schools established for teach ing black physicians survived this period (33), and all but two or three of the schools for women closed (34,35). State licens ing boards began to enforce stricter requirements; this prob ably was a more decisive influence than the Flexner Report (17,36). Curricul um

Many medical schools formed affiliations with universities; by doing so, they gained both experienced science faculty and stable funding. This was not an option for osteopathic institutions at that time, and they faced a difficult dilemma: raise entry stan dards and lose major portions of tuition payments, which rep resented their only income, or adopt a "go slow" attitude. They chose the latter, which meant that they were perhaps two decades behind in the educational reforms that many agreed were de sirable (37). AOA standards did increase the required length of osteopathic curricula, to 3 years in 1905 and to 4 years in 1915 (31). The profession responded officially to external criticism by pointing out the differences between osteopathic and orthodox medical education. However, when there was an opportunity to raise general standards, as came about in the 1930s, the profession did so. By the mid-1930s, osteopathic colleges were requiring at least 2 years of college before matriculation; in 1954,3 years were required; by 1960, over 70% of students had either baccalaureate or advanced degrees prior to entry (37). At present, virtually all students enter colleges of osteopathy with at least baccalaureate degrees; many have advanced degrees as well. Curriculum content similarly grew and changed with the times. An 1899-1900 Kirksville catalogue describes the school's course of study as follows (38): The course of srudy extends over two years, and is divided into four terms of five months each. The first term is devoted to Descriptive Anatomy, including Oste ology, Syndesmology and Myology; lectures on Histology illustrated by micro-stereopticon; the principles of General Inorganic Chem istry, Physics and Toxicology. The second term includes Descriptive and Regional Anatomy with demonstrations; didactic and laboratory work in Histology;


Physiology and physiological demonstrations; Physiological Chem istry and Urinalysis; Principles of Osteopathy; Clinical Demonstra tions in Osteopathy. The third term includes Demonstrations in Regional Anatomy; Physiology and physiological demonstrations; lectures on Pathology illusnated by micro-stereopticon; Symptomatology; Bacteriology; Physiological Psychology; clinical demonstrations in Osteopathy and Osteopathic diagnosis and therapeutics. The fourth term includes Symptomatology; Surgery; didactic and laboratory work in Pathology; Psycho-Pathology and Psycho Therapeutics; Gynecology; Obstetrics; Hygiene and Public Health; Venereal Diseases; Medical Jurisprudence; Dietetics; clinical demon strations; Osteopathic and Operative clinics.

The major difference between this 1899-1900 curriculum and that of an allopathic medical school of the same period, in addition to the distinctive osteopathic content, was the exclusion of materia medica (pharmacology). Early in osteopathic history a difference appeared between so called lesion osteopaths and btoad osteopaths: those who limited their therapeutic practice essentially to manipulation, and those who used all the tools available to medicine, including materia medica.

Andrew Taylor Still practiced midwifery (obstetrics) and surgery; both were taught under his guidance. I ndeed, when the issue of surgery became controversial among later DOs, Still's son provided an affidavit concerning his father's practice (39). As al ready noted, A.T. Still remained skeptical about using or teaching any form of pharmaceutical therapy. Still's general opposition to drugs did not prevent some early DOs from using them for treatment. Quite a few had been trained as MDs before they came to osteopathic schools; others went on to earn MD degrees after they became DOs; still others simply de cided to use all the adjunctive treatments available. Most "broad" osteopaths felt that after new safer medications were developed it was consistent with being a completely trained physician to in corporate them into osteopathic practice. The most direct early confrontation came in 1897 when a DO-MD opened the short lived Columbian School of Osteopathy in Kirksville, with the an nounced intention of offering DO and MD degrees upon gradu ation from a course in manipulation, surgery, and materia medica. The competitive and personal issues in this case extended beyond the academic questions, and the school closed after graduating only three classes (26). The issue was professionally divisive for many years thereafter. Adjunctive treatments became a major subject of debate within the AOA and the Associated Colleges of Osteopathy (now the American Association of Colleges of Osteopathic Medicine) for many years. The question finally was resolved in favor of the "broad" osteopaths, not by consensus over the idea but by recognizing that state licensing laws required fuller training. I n 1916, against the direct protest of Still (40), the trustees revoked a previous year's action condemning individuals and colleges that taught drug therapy, effectively opening the way for the colleges to form their own curricula. The profession's great success in using manipulative treatment during the 1918 influenza epi demic (41) probably slowed the integration of materia medica into the osteopathic curriculum. However, by the late 1920s it became officially permissible to institute courses in "comparative

23

therapeutics," of which pharmacology was one subheading (37). By the mid-1930s the integration was complete. The change was validated as drugs were greatly improved, making it possi ble to offer pharmaceutical treatment where benefits outweighed risks. Curricular improvement continued as clinical teaching facili ties grew and as budgets permitted the hiring of full-time faculty, particularly in the basic sciences. W hile instruction by physicians in active practice was an advantage for students who were de veloping clinical skills, the basic sciences and laboratory-based research required faculty who could give these interests their full anention. All the colleges had full-time basic science faculty by the time the first osteopathic medical school became affiliated with a major American university; such affiliations had been the route by which allopathic schools had strengthened their basic science teaching earlier in the 20th century. One other curricular improvement deserves mention. For many years, teachers of osteopathic principles and practice de veloped courses in their area of expertise as traditions within their individual schools, sometimes jealously guarded and always zealously defended. In 1968, a small intercollegiate group of os teopathic principles professors met for the first time. The initial agenda was a response to the new initiative of uniform medical coding, in light of a movement to change the term "osteopathic lesion" to "somatic dysfunction." This change had to be discussed and agreed upon as part of preparation for diagnostic coding. The group continued to meet, and it became known as the Educa tional Council on Osteopathic Principles, and later it became affiliated with the American Association of Colleges of Osteo pathic Medicine. Irs agenda grew to include a uniform glossary of osteopathic terminology (a current edition is included at the back of this text), systematic development of agreement about the content of a multidisciplinary-oriented osteopathic princi ples curriculum, and finally this textbook, Foundationsfor Osteo pathic Medicine. Its continuing role also includes development of osteopathic-oriented questions for national board/licensure and specialty board examinations. Research

On one level, since its earliest days, osteopathic medicine has been a profession based on a research question: "Can we find a bener way?" Osteopathic manipulation developed as an experi mental approach to clinical conditions that did not respond to the conventional treatmen:s of the time, and its practical success became the empirical research results that led to another level: the questions of "why" and "what if " appropriate to laboratory study. Medical research, in parallel with medical education, un derwent a process of developing new traditions and controls, as well as bener equipment, all of which would shape future clinical studies. Laboratory studies began among osteopathic physicians al most as soon as there was an organized osteopathic school (42). Study of the scientific questions raised by osteopathic manipula tive practice has never been easy; the difficulty can be illustrated by one obvious clinical question: "What is a manipulative placebo?" I n spite of these and other difficulties, a number of significant accomplishments have been recorded (43). Section V I I I of this

24

J. Osteopathic Philosophy and History

book offers an extensive survey of osteopathic research efforts from past to present. Growth of the Profession's Schools

Enthusiastic graduates of the first osteopathic college-for rea sons evangelistic or pecuniary-quickly began to establish new schools throughout the country. Some of these were short-lived because they were unable to meet rhe rising srandards of the AOA. Orhers merged with stronger institutions and survived in a new organizarion. Srill others strengrhened rheir posirions and survived. This was rhe general rrend for medical educarion in rhe 19th cenrury, and the smaller schools, wherher alloparhic, osreo parhic, or homeoparhic, had similar closures, consolidarions, or rebuilding. As nored previously, by 1910 only eight of the early osreoparhic schools were srill in operarion. Six of these have survived into the new millennium; all have had complicated histories of name changes, relocations, charter changes, mergers, and affiliarions with orher educational institutions. The five original schools still accredited (29) are: Kirksville College of Osteopathic Medicine, successor to the first school (1892); Philadelphia College of Osteopathic Medicine (1898); Chicago College of Osteopathic Medicine at Midwestern Uni versity (1900); University of Health Sciences, College of Osteopathic Medicine, Kansas City (1916)-there had been an osteopathic college in Kansas City as early as 1895; and Des Moines University, College of Osteopathic Medicine and Surgery (1905)-there had been a school in Des Moines as early as 1898. One school, the College of Osteopathic Physicians and Sur geons, Los Angeles, has survived as a medical school (University of California at Irvine). The California conflict and merger in the 1960s, described briefly under "State Licensure," resulted not only in the change of an osteopathic college to an allopathic college, but in a revival of interest in osteopathic education in the profession. The first new educational focus was in Michigan, and ir began nor only a new tradition in osreoparhic educarion bur became an imperus for narionwide growrh rhar continues to rhis day. In 1964, the Michigan Associarion of Osteoparhic Physicians and Surgeons commirred irself to develop a new, independently funded college of osteopathic medicine. This initiarive occurred because more than 1,000 osteopathic physicians practiced in the state, representing about 5% of the state's physician total and providing care for about 20% of the state's patients. None of these DOs had received their education in the state. In 1969, 18 students enrolled in the first class at a new campus in Pontiac, Michigan. Within 2 years, it was clear that a program of such complexity could not survive financially as a freestanding insti tution. A number of strong supporters in the Michigan legis lature, and Michigan's governor, were willing to support a bill for state funding with one major stipularion: rhe college had to be integrated with an exisring, accredited university program. After complex negoriarions, rhe program rransferred to the cam-

pus of Michigan Srare University in 1971, where ir became rhe first university-based osteoparhic college. Afrer rhis affiliation proved successful, 13 more osreopathic schools (some public, some private) were developed over rhe nexr 25 years. In 2002, 19 colleges were accredired by rhe AOA for predoctoral osteopathic education (29). In addition to rhe "sur viving five," they are: Michigan State University College of Osteopathic Medicine (1964) University of North Texas Health Science Center ar Fort Worth, Texas College of Osteopathic Medicine (1966) Oklahoma State University College of Osteopathic Medicine (1974) West Virginia School of Osreopathic Medicine (1974) Ohio University College of Osreopathic Medicine (1975) University of Medicine and Denristry of New Jersey, School of Osteopathic Medicine (1976) University of New England, College of Osteopathic Medicine (1976) Western University of Health Sciences, College of Osteoparhic Medicine of the Pacific (1977) New York College of Osteopathic Medicine (1977) Nova Southeastern University College of Osteopathic Medicine (1981) Lake Erie College of Osteopathic Medicine (1992) Arizona College of Osteopathic Medicine (1995) Pikeville College, School of Osteopathic Medicine (1997) Touro University, College of Osteopathic Medicine (1997) As of 2002, a 20th school, Edward Via Virginia College of Osteopathic Medicine, was undergoing provisional accrediration and planning to admit its first class in fall of 2003.

STATE LICENSURE

Closely related to the issue of educarional standards was licensure under increasingly strict state laws. The first legislative recognition of osteopathic pracrice came from Vermont in 1896 (44), where graduates of rhe American School of Osteopathy, Kirksville, were accorded rhe right to prac rice in rhar stare. Missouri had a successful bill as early as 1895, bur it was vetoed by rhe governor; whar was hailed as a berrer bill was passed and signed into law in March 1897 (23,45). Such laws as rhese, greered wirh much rejoicing, made tremen dous growrh possible in rhe osreoparhic profession in stares where legislarion provided a friendly welcome. Osreoparhic history in cludes numerous stories abour legal acrion againsr DOs for prac ricing wirhour a valid license, David-and-Goliarh encounters of DOs with MD-dominated legislatures, and testimony or influ ence offered by prominent people who were osteopathic patienrs. These colorful rales were the war stories of an energetic firsr gen erarion of DOs, who managed to secure legislative righrs to ar least limited practice in a majority of states. Registrarion and licensure were related, bur ofren differenr, marrers. Some stares provided for the formarion of separare os teoparhic licensing boards; some permirted rhe addition of an osteopathic represenrative to an existing or composire board; and


a few permitted DOs to apply through a medical board without osteopathic representation. The toles of these boards were not immediately clear at the time of their formation. There was opposition on ideological grounds even to the idea oflicensure. Some populists, not partisan to either osteopathic or allopathic physicians, said that medical licensure was in itself discriminatory. Others said that licensing would interfere with freedom of medical research. Some social Darwinists went so far as to say that if the poor died of their own foolishness in choosing bad medical practitioners, the species would improve (33). By 1901, however, every state had some form of legislation requiring at least registration, with a diploma ftom an accepted school, or a state examination of some type. When the Missouri board began to function in 1903, the first certificate it issued was to A.T. Still (46). Licensure to practice a full scope of medicine was another matter, and in most places it was related first to the content of the osteopathic curriculum and later to the results of examina tions. Again using Missouri as an example, by 1897 the subjects taught had expanded to include anatomy, physiology, surgery, midwifery, histology, chemistry, urinalysis, toxicology, pathology, and symptomatology. Everything was included except materia medica and academic consciences were temporarily satisfied. By 1937, however, only 26 states had any provision to provide un limited licenses to DOs. In some states DOs were ineligible to apply because their edu cation did not meet specific criteria. As late as 1937, osteopathic srandards did not meet pre-professional college requirements in 16 states; in 8 states, a year's internship was needed. Originally, DOs who took examinations under medical or composite boards showed a much lower pass rate. Whether this was a difference in osteopathic curricula or an educational deficiency, as it was argued, in due course, the curricula were altered and the pass rates increased. The major changes were addition of more basic science courses, more faculty, and larger clinical facilities (37). After World War I I, a major effort was made to change the old limited practice laws. These efforts, along with major changes in osteopathic education, enabled the enactment of new practice laws for all 50 states (47). A final dramatic chapter in the American licensing story of the osteopathic professional came when the California Osteopathic Association agreed in 196 1 to merge with the California Medical Association, and the College of Osteopathic Physicians and Sur geons, Los Angeles, became the California College of Medicine. Consenting DOs were given MD degrees as a preparation for a referendum approved by voters in 1962, which discontinued licensure of DOs in that state (37). A new state osteopathic group, Osteopathic Physicians and Surgeons of California, was chartered by the AOA. This group fought against the referendum but lost; they then began a long legal batrle that culminated in a 1974 decision by the California Supreme Court that licensure of DOs must be resumed (48). A new college was chartered in that state, and professional conti nuity was restored. By the end ofthe 20th century, state licensure could be attained in various ways: through the standard national osteopathic licens ing examination and/or through the standard national medical

25

licensing examination, depending on state requirements. Some states maintained separate osteopathic and allopathic licensing boards; many were composite boards. Graduate education re quired for new licenses still varied from state to state. In every state, however, as well as in a number of foreign countries, it was possible for DOs to be licensed for unlimited practice.

OSTEOPATHIC ORGANIZATION

The AOA began as a student organization in Kirksville, under the name American Association for the Advancemen t of Osteopathy, in 1897. Its present name was adopted in 1 901 (49). The sec ond national association was the Associated Colleges of Osteopa thy (now the American Association of Colleges of Osteopathic Medicine), formed in 1898. Both groups sought to protect and raise standards for education and practice of DOs. The AOA be came the regulatory group, no longer under student control; the Associated Colleges became a discussion and consensus group for faculty and officers of the schools. In 1907 the first organization devoted to osteopathic research began, though the first recorded osteopathic research was done almost a decade earlier (42). The AOA played a vital role in encouraging and supporting osteopathic research. Money for re search has never been plentiful; a major portion of the support for osteopathic research, especially in earlier days, has come from financial contributions by DOs themselves. More recently quali fied researchers have been recipients ofpublic grant funds, but the role of AOA-affiliated research organizations has been essential for start-up projects. State (divisional) and local (district) osteopathic organizations were established to serve DOs in their own localities. W hen the AOA grew too large for general membership meetings, state so cieties began (in 1 920) to name representatives to serve in an AOA House of Delegates. That body thereafter became the chief policy-making group for the osteopathic profession. A board of trustees, elected by the house, oversaw the implementation of those policies, a role it still fills. Students participate as voting members of delegations from the states in which their schools are located, are appointed to AOA boards, bureaus, and committees; and they have a number of organizations of their own. A major early effort of the AOA was to produce a code of ethics; this was accomplished in 1904. A participant in those deliberations observed that the problem was not because any one really wished to practice unethically, but rather that on some points it was difficult to agree upon what was ethical (50). To put this in perspective: the issue of advertising was a hard-fought question among all professionals at that time. The question was resolved by declaring advertising unethical except for brief profes sional card listings. By the 1990s advertising by professionals was ultimately considered ethical, though not of course to condone unfounded claims. Over time many osteopathic organizations grew, from start ing points as various as special tasks, geographic or school affinity, and practice interest. A current guide to all AOA-recognized os teopathic organizations is available online (51). The AOA has always been the umbrella group that recognizes and coordinates its efforts on behalf of the profession. The AOA

26


itself has many imporranr functions. Through its bureaus, coun cils, and commi[[ees, it is the osteopathic accrediting organization for undergraduate, graduate, and continuing medical education and for health care facilities. It certifies specialists in all fields, through a network of specialty boards and its own cenual bu reau. Research granrs and related projects, as well as educational meetings, are arranged through AOA bureaus and councils. Staff, directed by elected officers and trustees, provide pro fessional services, including: mainrenance of central records on all DOs, public and legislative education, member services, ed ucational activities including publications and conventions, and coordinated special efforrs on a variety of concerns. Position pa pers on various topics are approved by the House of Delegates and presenred as the profession's position on questions of public health and professional interest. In addition to activities of the AOA itself, a network of divi sional and affiliate societies is recognized by the AOA. Certain major "sub-umbrella" organizations have networks of their own: the associations of osteopathic colleges, health care organizations, licensing groups, and foundations. Specialty colleges, distinct from the certifYing boards, conduct educational affairs and recognize their own members' achieve menrs through fellowships and other awards. State (divisional) and local (district) societies typically deal with state legislative and regulatory affairs, conduct educational programs, and pro vide a variety of member services. Colleges typically have studenr and alumni groups, studenr chapters of certain specialty organizations, fraternities and soror ities, and a variety of special interest groups. Many of the physi cians' and students' organizations have auxiliary organizations for spouses. All organizations recognized by the AOA accept such ongo ing controls as approval of any changes in basic documents and designation of how many represenratives (if any) are senr to the AOA House of Delegates for voice and vote in professional policy affairs.

FEDERAL GOVERNMENT RECOGNITION

The first major attempt by the AOA to obtain federal govern ment recognition was during World War 1, when it tried to gain commissions for DOs as military physicians (41). This effort was unsuccessful, in spite of active support by such prominenr ad vocates as the former presidenr of the United States, Theodore Roosevelt (52). At that time, an examination was set, and it was understood that if DOs (along with MDs) took this and passed it, they could be commissioned as medical officers. About 25 DOs rook the examination and were recommended for commissions. The Sur geon General unilaterally ruled that only MDs were eligible. Bills were then introduced (1917) in both the House of Representa tives and the Senate to correct this inequity. The bills were referred to the Military Affairs Commi[[ees, and hearings were held. The committee then referred the issue ro the Surgeon General, who in his statement of opposition claimed that regular physicians would withhold their services if DOs were allowed to serve. The bills remained in committee without resolution unril the end of

the war. Meanwhile, DOs served as regular soldiers, unable to use their medical training. The situation remained uncorrected when World War I I be gan. Again there were efforts to obtain commissions for DOs, this time emphasizing regulatory rather than legislative barriers (41,53). DOs were deferred rather than drafted, waiting for the possibility to serve in a medical capacity that never came. Ironi cally, the DOs left behind became family physicians to the thou sands of the patients left by the MDs in military service, which enhanced the public's view of DOs as full-service physicians. The pressure for federal recognition conrinued after World War I I ended, and in 1956 a new law specifically provided for the appoinrmenr of DOs as commissioned officers in the nation's military medical corps. However, implementation of that law was blocked for another 10 years, unril the Vietnam conAicr created another special need for military physicians. The first DO was finally commissioned in May 1966. The next year the AMA withdrew its long-standing opposition, and DOs were included in the doctor draft. It was another 20 years, in 1983, before the first DO was promoted to be a Aag officer in the U.S. military medical corps (31). Acceptance of DOs as medical officers in the U.S. Civil Service was accomplished in 1963. Careers in this field became possible after that date. Nearly every federal recognition for DOs came after a long and difficult fight. Among the important federal recognitions were the following (31,37): 1951: The U.S. Public Health Service first awarded renewable teaching grants to each of the six osteopathic colleges. 1957: The AOA was recognized by the U.S. Office of Educa rion, Departmenr of Healrh, Education and Welfare ( D H EW), as the accrediting body for osteopathic education. 1963: The Health Professions Educational Assistance Act in cluded a provision for matching construction grants for osteo pathic colleges and loans to osteopathic students. 1966: The AOA was designated by the D H EW (now the Department of Health and Human Services [ D H H S ) ) as the official accrediting body for hospitals under Medicare. 1967: The AOA was recognized by the National Commission on Accrediting as the accrediting agency for all facets of osteo pathic education. 1983: The first osteopathic Aag officer in the U.S. military was appointed. 1997: The first osteopathic surgeon-general of the army was appointed. The AOA continues to maintain a presence in Washingcon, D.C., where it attempts to ensure inclusion of DOs and osteo pathic institutions as active partners in all legislative and regula cory 1 I1ltlatIves. Specialties

Perhaps the first osteopathic activity in what now is called a med ical specialty began only 3 years after Wilhelm Roentgen an nounced the discovery of radiographs. The second x-ray machine west of the Mississippi was installed in Kirksville in 1898. With it, Dr. William Smith formulated a method to inject a radiopaque


substance in cadaveric veins and arteries to demonstrate the nor mal panern of circulation. Two arricles were published late that year, one in the Journal o/Osteopathy, a Kirksville journal associ ated with the American School of Osteopathy, and the other in the fledgling American X-Ray Journal. These were reprinted for modern reference in AOA publications in 1 974 (54). When for mal cerrifying boards for osteopathic specialties were organized, radiology was first ( 1 939) (3 1 ). Along with these events came the long story of the develop ment of osteopathic hospitals, internships, residencies, specialry organizations, specialry standards, examinations, and recognition for those standards. By the 1 990s a full complement of specialties, training programs, and cerrifying boards were well established in the osteopathic profession, including a board recognizing osteopathic manipulative medicine, now referred ro as neuro musculoskeletal medicine. At the same time, the profession was unknowingly developing what would come ro be the most needed rype of practice for the 1 990s: primary care. Throughout its history, osteopathic clinical education has taken place in primary care settings: communiry hospitals and clinics. The profession has supported very few academic medical centers. By the 1 990s, this disadvantage became an advantage because of the profession's success in producing primary care physicians, including many willing to work in underserved com munities. Many factors have been cited as influential in the choice of practice rype and venue, but the chief ones seem to be under graduate experiences and role models (55). Students trained in academic medical centers tend to have only subspecialists as role models and their clinical contacts tend to be cases rypically re ferred to tertiary medical centers. Meanwhile, osteopathic stu dents have continued to have regular contact with communiry clinics and hospitals and have many faculry role models who are primary care physicians. For instance, rural clinics, long a mainstay of clinical education for the Kirksville college and later for other osteopathic schools, have become a model for primary care education (56). In the last decade of the 20th century, the osteopathic profession found itself in the enviable role of advisor on how to replicate its educational processes in other places.

HOSPITALS As with medicine in general, hospitals had their share of devel opmental problems in the 1 9th century. Inadequate facilities and staff, infection, disagreement over who should get patient fees, social stigma, and hospital ownership all entered the picture. By about 1 900, however, with the growth of an educated nursing profession and a new sense of sanitation, hospitals began to be at the very least-safe. Many small institutions were privately owned by surgeons who furnished hotel services and nursing for their own patients. New general hospitals began to appeal to pa tients other than the poor, and patient fees began to help with hospital development (36). There were osteopathic hospitals early in the 20th century; at the time of Flexner's inspection, Kirksville had the largest, with 54 beds. Chicago had 20 beds; the Pacific College, 1 5; Boston,

27

1 0; and Philadelphia, 3. No others were listed in that report (37). Eventually the numbers and size of osteopathic hospitals grew, but few reached the size and diversiry of specialties that charac terized the academic medical centers associated with universiry medical schools. However, the osteopathic profession did set hos pital standards, first for the training of interns and residents, and then for accreditation of the institutions themselves. The growth of osteopathic hospitals was especially marked in the period during and after World War I I, when MD-run hospitals did not permit DOs to join their medical staffs. When U.S. government programs were approved to help with construc tion of hospitals, osteopathic institutions participated along with MD-run institutions. Many communiry teaching hospitals were constructed during those years. In 1 954, a landmark court decision in Audrain Counry, Mis souri, made it illegal for public hospitals to deny staff membership and admining privileges to qualified DOs. This initiated a series of changes in areas outside California, where for many years DOs had been in charge of half the Los Angeles Counry Hospital. By the 1 960s, most public hospitals were open to DOs; by the 1 980s most private hospitals were open as well. By the 1 990s, with medical residencies open to both MDs and DOs, the need for a network of osteopathic hospitals for training purposes was much reduced. Mechanisms were adopted to recognize training that took place in allopathic institutions as acceptable for osteopathic board certification. This is now possi ble either by affiliation of the MD institution with an accredited osteopathic college or by direct AOA accreditation of the training institution (5 1 ). By 1 999, osteopathic graduate training institutes (OPTIs), were the standard, linking resources through hospital college consortiums. Reorganization of the health care system itself made these changes necessary. Payment mechanisms led to the formation of large networks of health care providers, including hospitals, out patient facilities, home care, extended and long-term care, and multiple independent contractors and physician organizations. Conimuniry hospitals, including many osteopathic insritutions, were merged with larger groups or simply closed. The lines be tween osteopathic and allopathic hospitals blurred, as both came under the umbrella of managed care organizations. In a case of history repeating itself, economic factors control health care delivery, and the profit motive is once again a re spectable part of medical practice. This is placed against a call for serious reform of medical education and bener distribution of primary care physicians. The goal is to provide excellence in patient care and in physician education, while seeking through corporate management tools the funds to survive in a competitive environment.

CONCLUSION

At the start of the 2 1 st century, the "parallel and distinctive" os teopathic profession is respected in many quarters for a variery of reasons. First and foremost is the osteopathic emphasis on pri mary care. This arose not only from the earlier circumstances of training opportunities and role models but also from the profes sion's traditional whole-person philosophy.

28


Additionally, there has been a rebirth of i nterest in manual medicine and other osteopathic methods. In most osteopathic colleges and graduate education programs, there is increased em phasis on historic tenets and clinical skills. The profession's hori zons have been expanded by a global emphasis of its own and an interest in international groups devoted to manual medicine (57-60). Osteopathic physicians have gained a positive voice in public affairs. In the public arena, DOs are regarded as "parallel and dis tinctive" in regulatory and legislative affairs, and the profession is consulted on most matters of public health policy. The profession has also launched clinical initiatives in such categories as women's health, minority health care, and pediatric end-of-life care. Con tinued emphasis on preventive care and health maintenance is i n line with traditional osteopathic values. An ambitious strategic plan launched in 200 1 by the AOA formalized some of these emphases and added others, including international recognition of U.S.-rrained DOs, an AOA Center for International Affairs, and a new World Osteopathic Medical Association (6 1 ). One of the dedicatees of this volume, George W. Northup, wrote in 1988:

218 and 1 8:299-302, Feb 1919; 18:335-338 and 18:351-368, Mar 1919; 18:396-398 and 1 8:415-418, Apr 1919. A lso: An attempt was made by the editors of the publication Osteopathic Physician to quantifY treatment results. See OP 34:1-2, Dec 1918 and 36: 1, jul 1919. Some suggestive details on type oftreatment also were published and reprinted in Time Capsule. The DO 1980;(Jan):31-36. See also Booth ER: H istory of Osteopathy and Twentieth Century Medical Practice, 1 924 edition. 1 . Still AT. The Philosophy and Mechanical Principles of Osteopathy. Kansas City. MO: Hudson-Kimberly Publishing Co; 1 892 and 1 902. 2. Still AT. Philosophy of osteopathy. Publ ished by the author. Kirksvi lle. M O ; 1 899. 3. Still AT. A utobiography ofAndrew T Still with a History ofthe Discovery

and Development of the Science of Osteopathy. Rev ed. Published by the author, K irksville, MO; 1 908. 4 . Still AT. Osteopathy. Research and Practice. Published by the author. K i rksville, MO; 1 9 1 0. 5. Tenets

l i g h t o f a fundamental p h ilosophy. I t needs to recognize the action and explore new fron tiers founded o n the osteopath i c profession's basic p h ilosophy . . . . Dr S t i l l d i d not say he was givi ng the world a phi losophy that should act as a guide to t h e future. Rather, in h is book, The Philosophy of Osteopathy, he stated h i s desi re was " . . . to give the world a start in a p h i l osophy that may be a guide to the

7. 8. 9. 1 0. 1 1. 1 2.

1 3. 1 4. 1 5. 1 6. 1 7.

1 8. 1 9.

ACKNOWLEDGMENTS

Appreciation is expressed to the following, who contributed sub stantively to the current version of this chapter: Dr. G. D'Alonzo, Dr. E. DiGiovanna, Dr. D. Dowling, Dr. N. Gevitz, Ms. P. Grauer, Dr. M. Kuchera, Dr. G. Osborn, Dr. D. Ward, and Dr. R. Ward.

REFERENCES

20. 21. 22. 23.

24. 25.

Note: Concerning reflrence 3: There is a typographic error on page 18 of the edition currently in print, concerning the date of the Stitt's move to Missouri: The dnte should be 1831, not 1827. Concerning reforences 41 and 52: A number ofinteresting anecdotal accounts were published in JAOA by various authors: 18:241-248, jan 1 919; 18:211-

American

Osteopathic Associa

cessed April 1 5 . 2002.

future" ( 6 2 ) .

The purpose of medical history has long been a subject for discussion. At its best and fullest, it can be said to "provide a wonderful schooling in prudence" (63). The caution follows that the historical record must be "considered in terms of its own cir cumstances and standards. This demands insight into the view points, thoughts, emotions, reactions, likes and dislikes of people of the pasr." Such insight requires a more thorough study than an introductory chapter can offer. Some care has been taken to offer to the i nterested studenr a list of references that can facilitate deepened insights. But beyond these readings, there is much more to explore and understand.

medicine,

6. Brown ]M, Woodworth RB. The Captives ofAbb's Valley; a Legend of

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of osteopathic

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26.

Frontier Lifo. New ed. Staunton, VA: Printed for the author by the McClure Co; 1 942. Dick E. The Sod-House Frontier. Lincoln. N E : Johnsen Publishing Co; 1 9 54. Personal communication: Mrs. J . S . Denslow (Dr. Still's granddaughter); 1 972. Trowbridge C. Andrew Taylor Still. 1828-1917. Ki rksvil le, M 0: Thomas Jefferson Universiry Press. Northeast Missouri Srate Un iversity; 1 99 1 . Thomas J L. ed. Slavery A ttacked' The Abolitionist Crusade. Englewood Cliffs, N): Prentice-H a l l ; 1 965. Monaghan J . Civil war on the Western Border, 1854-1865. New York, NY: Bonanza Books; 1 965. Eldridge SW. First free-stare legislarure. I n : Recollections ofEarly Days in Kansas; Publications ofthe Kansas State Historical Society. Vol 1 1 . Topeka, KS: Kansas Srare Printing Plant; 1 920: 1 4 9- 1 5 8 . A.T. S t i l l Pension F i l e . S r i l l Narional Osreopath ic Museum. Kirksv ille, MO. Duffy). From Humors to Medical Science; A History ofA merican Medicine. 2nd ed. Urbana, I L: University of I ll i nois Press; 1 993. Bordley J , Hatvey A M . Two Centuries ofAmerican. Medicine. 1176-1 916. Phi ladelphia, PA: WE Saunders Co; 1 976:97. Laughl i n GM. Asks if A.T. Srili was ever a doctor. Osteopathic Physician. 1 909; 1 5 (Jan ) : 8 . Osborn G G . T h e begin n ing: ni nereenth century medical sectarianism. In: H u mphrey RM, Gallagher F), eds. Osteopathic Medicine: A Ref ormation in Progress. London. England: Churchill Livingsrone; 200 1 : 3-26. Pickard M E. Buley RC. The Midwest Pioneer; His Ills. Cures & Doctors. Crawfordsv i lle, I N : R.E. Banta; 1 94 5 . Merck's 1899 Manual of the Materia Medica. Together with a Summary of Therapeutic Indications and a Classification ofMedicaments; a Ready Reforence Pocket Book for the Practicing Physician. New York, NY: Merck & Co; 1 899. Reprinred in facsimile by Merck & Co; 1 999. Dorland's fllustrated Medical Dictionary. 26th ed. Philadelphia. PA: WB Saunders Co; 1 98 1 . Danciger E . The Emergence of Homeopathy; Alchemy into ' Medicille. London. England: Century Hutchi nson Ltd; 1 987. Ebright HK. The History ofBaker University. Baldwin, KS: Published by the Universiry; 1 9 5 1 . Schnucker RV. ed. Early Osteopathy in the Wouls ofA. T Still. Ki rksv i lle, M O : Thomas Jefferson University Press, Northeast Missouri Srate Uni versity; 1 99 1 . Srill CEo A.T. Still: the itinerant years. I n : From the Archives. The DO. 1 97 5 ; ( Mar):27-30. Riley Gw. Following osteopathic principles. I n : H i ldrerh AG. ed. The Lengthening Shadow ofDr. Andrew Taylor Stilt. Published by the au thor. Macon. M O ; 1 938:4 1 1 -435. Walter GW The First School ofOsteopathic Medicin.e; A Chronicle. 18921992. Kirksvil le. MO: Thomas Jefferson University Press. Northeast M issouri Stare Un iversity; 1 992.


27. Violene EM. History ofAdair County. K i rksville, M O : Denslow H isrory Co; 1 9 1 1 :253. 28. Srill CE J r. Frontier Doctor, Medical Pioneer; The Lift and Times ofA. T.

29

45. H ildrerh AG. The Lengthening Shadow of Dr A ndrew Taylor Still. Pub lished by rhe author, Macon, MO; 1 938. 46. The Old Doctor gers first certificate. j Osteopathy 1 904; 1 1 (Jan) : 2 8 .

Still and His Family. Kirksville, MO: Thomas Jefferson University Press, Northeasr M issouri Srare University; 1 99 1 . Hisroric reference of osreoparh ic colleges. American Osreoparhic Associ arion. Available ar: hnp:llwww.aoa-ner.org/Education/collegehist.hrm. Accessed. Johnson V, Weiskorren H G . A HistolY ofthe Council on Medical Edu cation and Hospitals ofthe A merican Medical Association. Ch icago, I L: American Medical Associarion; 1 960. I mportanr dares in osreoparhic hisrory. American Osreoparhic Associ arion. Available at: hnp:1Ilwww.aoa-ner.org/Publ ications/yearbookroc. hrm. Accessed April 1 5 , 2002. Flexner A. Medical Education in the United States and Canada; a Report

47. Years srares passed u n l i m i ted pracrice laws. American Osreoparhic As

to the Carnegie Foundationfor the Advancement of Teaching. Bosron, MA: Merrymou nt Press; 1 9 1 0. 33. Morais H M . The hisrory of the Negro in medicine. I n : International Library of Negro Lift and History. Vol 4. The Association for rhe Study

52. They passed rhe exam, bur rhey could nor serve: rhe DO doughboys.

29.

30.

31.

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of Negro Life and H isrory. New York, NY: Publ ishers Co; 1 968. 34. Lopare C. Women in Medicine. Publ ished for rhe Josiah Macy, J r. Foun dation. Balrimore, M D: Johns Hopkins Press; 1 968. 35. Walsh M R. Doctors Wanted, No Women Need Apply; Sexual Barriers in

the Medical Profession. New Haven, CT: Yale Un iversity Press; 1 977. 36. Srarr I� The Social Transformation ofA merican Medicine. New York, NY: Basic Books; 1 982. 37. Gevirz N . The D.O.s: Osteopathic Medicine in America. Balrimore, M D : Johns Hopkins University Press; 1 982:75-87. 38. Catalogue of the American School of Osteopathy. Session of 1899-1 900. Kirksville, MO; sevenrh annual announcemenr. 39. The memoirs of Dr. Charles Sri l l ; I V. A posrscripr. In: From rhe Archives.

The DO. 1 97 5 ; (Jun): 25-26. 40. Boorh ER. History ofOsteopathy and Twentieth-Century Medical Practice. Cincinnari, O H : Prinred for rhe aurhor by rhe Caxron Press; 1 924. 4 1 . Gevirz N. The sword and rhe scalpel: rhe osreoparhic 'war' to enter the Milirary Medical Corps, 1 9 1 6- 1 966. jA OA. I 998(May);279-286. 42. Pererson B. How old is osreoparhic research) I n : Time Capsule. The DO.

I 978 ; ( Dec): 24-26. 43. Cole WV. Historical basis for osreoparh ic rheory and pracrice. I n : Northup GW, e d . Osteopathic Research: Growth and Development. Chicago, I L: American Osreoparhic Associarion; 1 987:57. 44. A Vermont story and Contacrs wirh rhe law. I n : From rhe Archives. The

DO. I 972;(Nov):46-50.

sociation. Available at: h rrp:1 Iwww.aoa-net.org/Recognirionllaws.htm. Accessed. 4 8 . Fryman V M . Alexander Tobin, 1 92 1 - 1 992. I n : The Collected Papers

of Viola M. Frymann, DO. I ndianapolis, I N : American Academy of Osreoparhy; 1 996. 49. Students form association. American Osreoparhic Associarion. Available at: hrrp:1 Iwww.aoa-ner.org/Assocarion/aoa.hrm. Accessed. 50. Evans AL. The beginnings of rhe AOA ( 1 928 manuscripr). I n : From rhe Archives. The DO. 1 972; (Sep):34-38. 5 1 . American Osreoparh i c Associarion. Available ar: hrrp:llwww.aoa-ner.

Q!g, Accessed April 1 5 , 2002. I n : From rhe Archives. The DO. 1 97 5 ; (Aug):39-46. 53. How DOs gained commissions. I n: Time Capsule. The DO. 1 980;(Apr): 25-32. 54. 1 898: Radiology in Kirksville. In: Time Capsule. jA OA. 1 974;74(Oct): 1 67- 1 72. 5 5 . Rodos Jj , Pererson B . Proposed Strategiesfor Fulfilling Primary Care Man

power Needs; a White Paper Preparedfor the National Advisory Counci/, National Health Service Corps, u. s. Public Health Service. Rockville, M D: Narional Healrh Service Corps; 1 990. 56. Blondell RD, S m i th l], Byrne ME, H iggins Cw. Rural heald1, family pracrice, and area healrh educarion centers: a national study. Fam Med I 989;3(May-Jun): 1 83- 1 86. 57. Svoboda J. Cmon, rake your medici ne-global. The DO. 2000(Dec): 56-58. 58. V i tucci N . Healing hands around rhe world. The DO. 2002(Mar): 36-40. 59. Vitucci N. Finding common ground. The DO. 2002(Mar): 42-45. 60. Kuchera M L. Global all iances: advancing research and rhe evidence base.

jA OA. 2002; 1 02:5-7. 6 1 . AO!\s ann ual report: 2000-0 I and beyond. The DO. 200 I ;(Sep):6570. 62. Northup Gw. Mission accomplished) jA OA. I 988;9(Sep). Reprinted in Beal MC, ed. 1 995-96 Yearbook: Osteopathic Vision. I ndianapolis, I N : American Academy o f Osreoparhy; 1 996: 1 24. 63. Rosen G. Purposes and values of medical histo ry. I n : Galdsron I, ed. On

the Utility ofMedical History. New York, NY: I nternarional Un iversities Press; 1 9 57: 1 1 - 1 9.


S

E

C

T

I

O

N

OSTEOPATHIC CONSIDERATIONS IN THE BASIC SCIENCES

INTRODUCTION MICHAEL M. PATTERSON

Osteopathic medical practice is built on the foundation of

becoming increasingly difficult for any one person to have even

both scientific knowledge and a medical philosophy that guides

a basic understanding of all the fields of medical knowledge, let

the application of facts within the art of treatment. Too often,

alone a mastery of them. Rather than decreasing the need for a

in the practice of medicine, we overlook the fact that medical

philosophic basis for medical practice, the increasing knowledge

knowledge must be delivered in the context of a philosophy of

base makes it even more important to have a means of organizing

how life, health, and disease processes function. The interaction

the vast numbers of facts and theories to make a coherent medical

between physician and patient then flows from that philosophy

practice. Without such a philosophy, the practitioner is prone

and directly affects the patient's response.

being whipsawed by the medical treatment dujour and hence not

to

serving the patient well. It is the purpose of this section to present ways to look at and

OSTEOPATHIC PHILOSOPHY

organize various areas of knowledge in the basic sciences for the

The philosophy of osteopathic medicine was initially formulated

of osteopathic philosophy; the integration of function. Ir is not

student of osteopathic medicine, in light of an important part by Andrew Taylor Still, MD, DO and has been elaborated by

possible for one or often even a series of texts to present all the

leaders of the profession for almost 110 years. Still's initial for

knowledge of the various scientific areas underlying biomedical

mulations had their roots in the earliest of medical thought and

science. Some physiology texts alone are longer than this book

practice. To these ideas, Still added important insights and un

and the same holds true for most of the other basic sciences.

derstandings gained from his own experience and knowledge.

This section is meant to serve as material to supplement the ba

As new medical knowledge and understandings of human func

sic science training of the osteopathic student or to refresh and

tion have been discovered, the philosophy has been refined and

enhance the practicing osteopathic clinician's knowledge. Chap

its implications better elucidated. However, its basic tenets have

ters in this section provide information and knowledge in these

remained as fundamental guides for osteopathic physicians, sci

areas in terms of integration of function and, in some cases, ways

entists, and teachers in optimizing health and diminishing dis

in which the lack of integration, or disintegration, can occur.

ease processes in their patients, guiding the scientific process in

Some of the chapters present information or syntheses of areas

formulating new knowledge, and passing the profession to new

not readily available elsewhere, but that are important to inter

generations.

preting osteopathic clinical practice. T hus, the chapters do not

Within osteopathic philosophy, one of the most important

attempt to cover all areas of basic science or even to summarize

aspects is that for optimal function, there must be integration of

the current knowledge in these areas, but rarher provide ways

the various constituent functional levels, from the subcellular to

of conceptualizing areas within an osteopathic understanding of

organ systems to the psychological. When a breakdown in the

health and loss of health.

integration of these functions develops, the individual can no longer maintain the best level of health, and disease symptoms are increasingly likely. This leads to another of the basic tenets of the profession, that the underlying cause of disease is distur

Anatomy The first three chapters of the section deal with the very important

bance of function; homeostatic mechanisms can no longer ward

area of anatomy and build on each other. T he study of anatomy is

off invasions of bacteria or viruses or contain the degeneration

of utmost importance to the osteopathic student. Without a thor

of aging or use. Osteopathic philosophy suggests that one of the

ough understanding of not only the structures of the body, but

most important things for the osteopathic physician to under

also how the structures provide function, the osteopathic physi

stand is how body functions are integrated, how that integration

cian will be unable to best use the basic principles of palpation

can be degraded, and how it can be restored.

and manipulation. In Chapter 3, "Rules of Anatomy," Towns uses

The amount of knowledge available to the student of human

his years of experience in teaching anatomy to draw attention to

function is not beyond the wildest dreams of those in the field

some of the important ways to view the body's structures and the

only a few years ago. Information of human function is increasing

principles that combine these structures with function. He points

at an astounding rate, and all indications are that it will continue

out that it is important for the osteopathic physician

to compound even more rapidly in the years ahead. The Human

to visualize the true relationships between structures, not only

Genome Project alone promises to provide insights into the basic

to understand their function, but also to know when they are

nature of human disease that is beyond our comprehension. It is

not functioning correctly and how to use the best manipulative

to

be able

Introduction

33

techniques to improve functional capacity. How Auids move into

tems as they relate to the integration of body function. While

and out of an area is vital to understanding normal and abnormal

obviously not separate from the autonomic nervous system, the

function. This includes not only the arterial and venous supply,

information in these two chapters focuses on the organization of

but also lymph movement and drainage. Improper Auid move

the somatovisceral and viscerosomatic interactions of the body

ment is a vital and primary cause of loss of integrated function.

and the functional changes brought about by afferent input

Knowledge of what is connected to what and how pain can be

to these systems. In Chapter 7, Patterson and Wurster review

used or misunderstood is a vital part of understanding anatomy.

the structural basis for somatovisceral and viscerosomatic in

It contributes to a physician's ability to help the patient. These

teractions and present an example of these pathways. The four

topics are discussed here.

stages of reflex alterations, from short-term to permanent alter

Chapter 4, by Jacobs and Falls, provides an overview of the

ations in reflex function are reviewed and some of their impli

concepts of anatomy. The authors point out that a thorough un

cations for function are outlined. The authors then review the

derstanding not only of anatomic structutes but of how they in

evidence for axoplasmic or nonimpulse-based actions of nerves

terrelate is key to understanding the basis of healrh. They discuss

on end organs and the implications for function of this neural

the often overlooked, all-encompassing fascial tissues as impor

actiVIty.

tant contributors to continuity throughout the body. They also

In Chapter 8, Willard presents the neurochemical basis for

emphasize the importance of myofascial continuity throughout

reflex change and reviews the implications of nociceptive activity

the body as a means to understanding the disparate effects of

for higher neural or brain function. The results of pain inputs

disturbances in an often-distant structure.

for psychological and immune function are given, along with a

Chapter 5, by Wells, completes this trilogy with a presentation

basic outline of the brain processes involved. Willard presents a

of biomechanics. This chapter brings together the basic concepts

model for interpreting aspects of the somatic dysfunction in terms

of the Chapters 3 and 4 into a functional whole. Many of the

of these changes, and provides good evidence for an organized

concepts presented here are necessary to interpret the findings of

dysfunctional pattern that evolves from abnormal responses to

palpatory diagnosis and to determine the best means of treatment

pall1 ll1puts.

of biomechanical problems. Key elements include the idea of

The coordinated picture emerging from various areas of neu

constant remodeling of tissues, including bone, functional stress,

rophysiology and neuropsychology fully supports the clinical ob

the changes of these properties with age, and the storing of energy

servations of the osteopathic profession regarding the integrated

during movement by elastic properties of tissues.

nature of physiological and psychological function. The effects

These three chapters provide the student of osteopathic

of pain inputs have consequences for reflex function at the spinal

medicine with an excellent introduction to the important issues

cord level that were seen by Denslow and Korr in their studies of

in anatomy. They should supplement well the basic knowledge

the 1940s and 1950s. It is now becoming clear that these types

gained in the anatomy laboratory and during the study of palpa

of alterations that disrupt normal function also occur at higher

tion and manipulation.

centers and cause psychological, immune, and adaptive dysfunc tion. By understanding these sequences of change and how to

Autonomic Nervous System The autonomic nervous system is one of the most important,

minimize, reverse, or enable adaptation to them, the osteopathic physician will be much better able to help a wide spectrum of patients once thought to be intractable to health restoration.

and yet one of the mosr poorly understood, systems of rhe body. Usually thought of as a rather dull and even uninteresting part of the nervous system, dealing with only visceral functions, it is ac tually one of the most important of the integrating systems. The

Respiration/Circulation The topic of respiration and circulation was one of the most

sympathetic nerves actually innervate almost all body structures

important issues in the thinking of Still and early osteopathic

and have tremendous inAuence over the body's immune function.

practitioners. The Aow of Auids and the proper balance of res

In Chapter 6, Willard provides a glimpse of the vast complexity

piratory products in the tissues were vitally important in the

of rhis system as it inAuences all body function. He examines

maintenance of proper function. While the nerves controlled the

not only the structure of the system, but outlines many of the

flow of blood, the arteries supplied the route and means for the

neurochemical aspects of this great integrating system, and the

Auids to reach the tissues and the veins and lymphatics allowed

complexity of the process involved. He emphasizes the impor

for the return and purification of blood and extracellular fluids.

tance of this system in coordinating the activities of the visceral

Any disruption of these flows was looked on as the moment of

systems to meet the demands imposed by the musculoskeletal

the start of disease, or dysfunction. When discussing respiration,

system. An understanding of the autonomic system is vital to the

Still generally meant respiration at a cellular level, and the Auid

osteopathic physician's understanding of rotal body integration,

circulation was the key to that process.

and to the often confusing and seemingly contradictory symp toms that are produced when the system malfunctions.

Chapter 9, by Sparks, begins by acknowledging this fact, that the circulation is the cell's connection to the outside world. The chapter reviews the cellular requirements for activity and how the

Neurophysiology

basic cellular processes require regulated energy resources. From there, the author advances to the regulation of tissue circulation at

Chapter 7, by Patterson and Wurster, and Chapter 8, by Willard,

the local and regional levels. The coronary circulation is used as an

present a picture of the workings of the neurophysiological sys-

example of the interactions between local and neural circulatory

34

II. Osteopathic Considerations in the Basic Sciences

regulation. Finally, he discusses blood flow regulation in the skin. Thus, the contrasts between skin and coronary blood flow regu lation show the differences in regulation in vital versus nonvital organs. This discussion of blood flow regulation and circulatory demands should allow the student to begin to see the complexity of cellular respiration and circulation and how the requirements differ in various tissues, as well as how the moment-to-moment circulatory requirements and flows directly affect cellular func tion and, hence, health.

Endocrinology The endocrine sysrem is treared uniquely by Porranova in Chap rer 11. As with all other systems discussed in this secrion, the author has room only to provide an overview of rhe endocrine system as ir applies to rhe concepr of funcrional inregration. Por tanova uses rhe complexity and ubiquity of endocrine function to illusrrare rhe beauty of inreracrions at every level of function. He points out rhar, while rhe level of knowledge in Srill's rime was very rudimenrary (bur then, what will our grandchildren say of our understanding?), the concepts of funcrional inregrarion held

Microbiology The area of microbiology is one that was in its infancy at the time the osteopathic profession was founded. Still clearly recognized the role of the microbe as a pathological process affecting human morbidity and mortality. The germ theory of disease was well de lineated by the time Still founded his school, and he referred to it often. While recognizing the role of microorganisms in patho logic processes of illness, Still also recognized that in many, if not all cases, in order to have symptomatic consequences for the human being, the microorganism must have a fertile ground in which to grow. Under normal function, the pathological organ ism would be kept in check by the host. When the circulatory

by Still are beaurifully shown by the control loops and feedback pathways within the endocrine system. Indeed, Portanova uses several of the basic tenets of the osreoparhic philosophy as reners of endocrine function. This allows rhe reader to see rhe appli cation of these conceprs at a systems level. Indeed, the author points out thar rhe osteopathic philosophy is so "deeply rooted in the fabric of life" rhat even knowledge gained in the future will be embraced by rhis philosophy. Perhaps rhis is one of the beauries of Still's philosophy and conceptualization of funcrion. Certainly, the reader will gain a new and deeper appreciarion for borh the osteopathic philosophy and rhe endocrine system while reading this chapter.

or other functions were disturbed, the often naturally occurring organism could produce illness or death. Thus, for Still, the pri mary cause of disease was not the microorganism, but the lack of proper function. Indeed this is a very important distincrion to make. Thus, the root cause of a disease process is function, not a mIcroorganism. In Chapter 10, the Jensens masterfully outline the background of microbiology and the germ theory of disease. They point out just what the constraints of this theory are and how osteopathic philosophy recognized the theory within its own framework. The chapter introduces the student to the concepts of virulence and virulence factors as they affect the operation of pathogenic organ isms. The role of the hosr is identified and discussed. The authors outline the factors that affect the success of microbes in their as sault on rhe human, and the various countermeasures humans have evolved to thwart microbial assaulr. They show rhe reader rhe important role of nutrition, fever, and immune mechanisms in discouraging microbial pathology. Of particular imporrance is rhe discussion of the role and pitfalls of antibiotics in medical practice. This should be read by all osteopathic medical students, as should the discussion of hygiene and vaccinarions. The dis tinction rhe Jensens make between a microbe and a parhogen at rhe end of Chapter lOis very importanr. Many microbes co exisr peacefully wirh every human being until rhe controlling mechanisms of the host human are compromised, allowing the microbe to change to a pathogen, somerimes killing the host. It is this principle that was recognized by Still and that must be

Pharmacology In the early days of rhe osteopathic profession, drug use was looked upon with great suspicion. In fact, Still forbade rhe use of drugs and the teaching of pharmacology in his school. In ret rospecr, it is easy to see why Still took this artirude. Mosr, if nor all, common drugs of the time were detrimental to function and health, or were used in harmful ways. It was common to use mer cury in sufficienr amounts to cause teerh to fall our. Now, rhe use of P harmacopoeia is common and viewed as a necessary adjuncr for complete medical practice. There is lirrle doubr, however, that drugs are often overprescribed, incorrectly used, and abused. In Chapter 12, Theobald presents parallels between rhe concepts of osreopathic medicine and the use of modern pharmacologic agenrs. He points out rhar the rarional use of any pharmacologic agenr necessitares understanding that each individual is unique. Chemical agents used properly can help rhe body regain con trol of sysrems rhat are functioning improperly and help redress balance of function. The aurhor's description of the treatment of hyperrension with pharmacologic agenrs using the principles of integration is a wonderful example of how endogenous agents can help rhe body restore properly integrated function. There can be lirtle doubr rhat Srill's attitude, were he alive today, would be somewhat different raward the proper use of some pharmacologic agents, although jusr as surely, not appreciaring the widespread and profligate use seen in many medical practices raday.

reemphasized today. In most cases, the proper function of rhe hosr is sufficient untO itself to control rhe microbe. When rhe host's function is compromised, the pathogenic properries of the

CONCLUSION

microbe are allowed to be manifesr. The major problem is not rhe microbe, bur in rhe host's function, and that is where major

The chaprers of this section show various levels of inregration

restorative efforts must be directed. Too ofren in medicine today,

within and between various body systems and units. In addirion,

the only effort is to externally control the microbe and rhe role

the correspondence of the osteopathic philosophy wirh princi

of the host is forgotten.

ples used in human funcrion is evident. These examples provide

Introduction

35

a basis for understanding ways in which structure and function

losophy is admirably demonstrated in these chapters, with the

are interrelated. The interrelatedness of structure with function

authors showing the fit between the emerging scientific under

provides an integration that is the hallmark of health. The exam

standing of human function and osteopathic philosophy. T hus,

ples used in many of the chapters show how the integration of

the authors have provided a means for a deeper understanding of

health can become disrupted, producing the first and necessary

the application of osteopathic philosophy to the optimization of

cause of disease, but as an effect, not a cause. Osteopathic phi-

human health.


RULES OF ANATOMY LEX C. TOWNS

indeed, faculty at each school will add or subrracr as they see fit. KEY CONCEPTS

Seven "rules" of anatomy will help guide the study and use of anatomy in medical practice: • Understanding three-dimensional relationships is funda

Nevertheless rhese rules are intended to illusrrate rhat attention to fundamental concepts of anatomy will assisr rhe srudent in learning anatomy and, hopefully, will also convince rhe student that effecrive osteoparhic medical rreatment proceeds from an accurare understanding of strucrure.

mental to using anatomy. • Knowing what things do is the companion goal of knowing

their location. • The integrity of arteries and nerves is essential to health . • Healthy homeostasis requires that fluid entering be drained

away, too. • Pain is almost always an anatomic symptom. • No organ or organ system exists in isolation in the body. • Each person has a different anatomy.

RULE 1: RULE OF PROXIMITY Undersranding spatial relarionships forms the essence of the use of anatomy in medical practice. The most usable admonirion is also rhe mosr obvious: in any particular part of the body, you musr know the sparial arrangement of all rhe organs and rissues. Knowledge of spatial relations, gained from lectures, readings, and dissections, allows one to mentally reconstrucr the entire anatomy of an area when only limited cues are available. For example, when palparing rhe abdomen, rhe physician must be able to accurarely place rhe entire abdominal contents based

An understanding of anatomy is fundamental to the rational

on a few large organs or surface landmarks that can be seen

practice of medicine. To assess health and disease, physicians must

or felr manually. Another example: when casting a limb, the

have a derailed knowledge of rhe srrucrures of rhe body wirh which

physician musr understand the placement of important arter

rhey deal. The detailed anatomic knowledge of many physicians

ies, veins, and nerves to avoid the disastrous consequences that

may be restricted to rhe particular body area or functional sys

would result from compromise to these vital structures, the loca

rem that rhey use in a specialized practice. However, effective

rions of which are inferable only from bony or muscular surface

physicians, even rhose in specialized pracrices, need and use a

landmarks.

working knowledge of rhe reciprocal, interactive narure of the

A necessary first step is often to learn basic facts of anatomy,

body's structure and function. Osteopathic physicians need suf

such as: What is the attachment of the biceps brachii? What are

ficienr knowledge of body srructure and function to understand

rhe branches of the femoral artery? How is the brachial plexus

how focal desrrucrive causes may not only lead to localized effects

formed and what are its branches? However, rhe more important

bur may also contribute to more subtle, widespread, or distant

rask is to place those isolated facts into a larger morphologic

degenerative, morbid events. The payoff for mastering anatomy

context. For example, a student might initially memorize the

is to develop the ability to practice medicine-especially osteo

layout of the brachial plexus; but the brachial plexus is spatially

pathic medicine-in a more intelligent, predictable, and effective

related to other crucial srructures in the arm, axilla, and root of

manner.

the neck. The ventral rami of spinal nerves that form rhe brachial

This chapter does not attempt to thoroughly review anatomy.

plexus pass through and among the scalene muscles of the neck;

Numetous excellent books and programs are available on human

the cords of rhe brachial plexus surround the brachial artery; and

anatomy, and the effective methods of teaching anatomy vary

the nerves derived from the cords pass around and among the

from school to school. The purpose of this chapter is to pro

muscles of the arm. Without rhis subsequent understanding, the

vide the beginning student with some conceptual bases to guide

memorization is largely a wasted effort.

the study of anatomy and thereby to help maximize the posi

With the advent of powerful new imaging technologies, some

tive impact of anatomic knowledge on the eventual osteopathic

might assume that the eventual rask of the practicing physician

medical practice. These concepts are sketched here as a series of

would be greatly simplified, that the study of relarional anatomy

"rules." These "rules" are not mutually exclusive or exhaustive;

would become unnecessary. In fact, a new level of complexity

38

If

Osteopathic Considerations in the Basic Sciences

is added by the ready availability of computerized tomogra

testinal tract is to digest and absorb nutrients and water. Details

phy (CT), magnetic resonance imaging (MRI), and other mod

of these functions are left to the other basic sciences, which in

ern imaging technologies. Recognizing and reconstructing whole

turn assume an understanding of gross structure. Nevertheless

anatomic structures on the basis of their sectional representation

it remains important to grasp the intimate relationship of struc

is not an inconsequential mental task. Most teaching programs

ture and function. The human organism is a complex, unified

of anaromy now emphasize how the three-dimensional morphol

organism; relating structure and function is one basic and nec

ogy seen in dissection and represented in textbooks and aclases

essary strategy to understand the functioning, integrated, whole

appears when imaged via various technologies. Physicians must

human being.

now be conversant with the contemporary images of structure,

The musculoskeletal system is approximately 75% of the body

and they must also become facile at translating these static or dy

mass; this vast system gives stability in health, provide clues to dys

namic images inro complete, inclusive, three-dimensional living

function and disease, and offers a mode of treatment to suppOrt

patients. Realistically, the advent of modern imaging technology

the patient who is diseased or stressed. Osteopathic physicians

has replaced the need ro infer deep anaromy from subcle surface

must understand well the function of the individual components

landmarks. However, the clarity with which previously unview

of the musculoskeletal system. This function is seen from two fun

able structures can now be seen is offset by the necessity to men

damental, complementary perspectives: What action or function

tally reconstruct whole regions of the body three-dimensionally

does a muscle (joint, bone, ligament, etc.) produce? And, Which

from slices. AJso, despite the power of these remarkable new tools, many

muscle (joint, bone, ligament, etc.) produces a specific action or function?

important small structures are not visualized. Physicians must

In a clinical evaluation, the physician may be presented with

still rely on a detailed knowledge of relational anatomy in order

a patient who has, among other symptoms, a weakness in ab

to be able to place small nerves and vessels into the context of

ducting the arm. Abducting the arm-that is, moving the upper

structures seen on CT or MRI images. For example, the esoph

limb from aside the body to a position overhead-requires the

agus is easily visualized in CT or MRI, and many pathological

coordinated, sequential action of several muscles. A small muscle

conditions (i.e., esophageal cancer) would be readily detected.

attached to the scapula (the supraspinatus) initiates abduction.

The esophageal plexus, on the other hand, would not be visual

Movement of the arm to a horizontal position is accomplished

ized. This plexus of nerves, embedded in the external fascia of the

by contraction of the deltoid, the large muscle making up the

esophagus, is the sole source of parasympathetic fibers to many

rounded point of the shoulder. For the arm to be raised over

abdominal organs and contains important sensory fibers as well.

head, the scapula has to be rotated by muscles that attach the

Thus, the knowledgeable physician would want to be attentive to

scapula to the spine (principally the trapezius).

the possibility of symptoms that would result from destruction of the esophageal plexus as a result of esophageal disease.

Working from the complaint or observation, the physician must recall which muscle(s) produces the action and then assess

The rule of proximity is also powerfully applied with the re

the strength of each in its various movements. Let's assume in this

construction of spatial relations as osteopathic physicians use

scenario that the physician has demonstrated a weakness of the

the most distinctive features of their practice: palpatory diagno

deltoid muscle. The physician must then use his or her knowledge

sis and musculoskeletal manipulative therapy. The osteopathic

of anatomy to move to the question of why the deltoid is weak.

physician must have a clear comprehension of the anatomic re

First, the physician must recall the innervation of the muscle

lationships of muscles, muscle attachments, and bones to each

(the axillary nerve) and assess the strength of other muscles (teres

other and to vessels, nerves, lymphatics, fascia, and organs. This

minor) innervated by that nerve. The axillary nerve also provides

is prerequisite to most osteopathic diagnostic and therapeutic

sensory fibers to the point of the shoulder; thus, the physician

strategies. Together, palpation and manipulation can be thought

would want to examine sensation to the area. Working proximally

of as anatomy in practice. This mental reconstruction of the

up the brachial plexus, the physician then checks the function of

anatomic structure of a region proceeds from only a few palpable

muscles that, like the deltoid via the axillary nerve, receive their

or visible superficial landmarks.

motor supply from branches of the posterior cord of the brachial

The accurate diagnosis and treatment of many conditions and

plexus (this would be all the extensor muscles of the upper limb).

diseases proceeds from knowing where things are located. Virtu

More proximally still, the innervation of the deltoid muscle is

ally all the utilization of anatomy in a clinical setting, as well as

principally from the fifth cervical spinal nerve. From this cervical

all of the other rules described in this chapter, are based on the

spinal segment also arises some of the motor fibers that innervate

rule of proximity.

the thoracic diaphragm. Thus, starting with a relatively simple functional loss in the deltoid muscle, the physician looks for answers to the following questions: Does teres minor contract

RULE 2: RULE OF FUNCTION

properly? Is sensory loss evident over the point of the shoulder? Are the extensor muscles of the upper limb weak? Is there any

Most gross anatomy courses appropriately limit the discussion of

compromise in respiratory function?

function for many of the structures, organs, or organ systems.

The physician may then proceed to enlarge the domain of the

For example, the function of the lung is to provide gas exchange

functional examination. What postural or functional compensa

between the air and the blood; the function of the kidneys is to

tion has the patient made for weakness of the deltoid? Is weakness

filter the blood and excrete urine; and the function of the gastroin-

of abduction unrelated to the deltoid and simply a function of

3. RuLes ofAnatomy pain in the shoulder; that is, does the parient not raise the arm

As do arteries, nerves also supply vital components

39

to

every

because it hurrs to do so? Is the pain in the joint itself or does it

porrion of the body. Nerves supply control; they are a major

resulr from disease of some internal organ?

component of the body's homeostatic mechanisms. Nerve cell

Understanding the rule of function in the musculoskeletal

bodies in the central nervous system (CNS) send nerve fibers to

system leads inevitably to a series of questions predicated on more

control contraction of smooth (involuntary) muscles and skele

complex structural and functional interrelationships: How might

ral (voluntary) muscles and to control secretion of glands. Nerves

dysfunction of the muscle (or other musculoskeletal component)

also provide sensory input; they convey either exteroceptive input

affect total body efficiency and health? How might dysfunction

concerning physical forces thar impinge on the body or intero

of some visceral element degrade the structural or functional

ceptive feedback about the status of the internal milieu. Nerve

integrity of the musculoskeletal system? These questions fOfm

fibers also supply chemical materials from the CNS to rhe pe

the core of some of the following rules.

riphery and vice versa. Through rhe mechanism of axoplasmic transport, rrophic (growth promoting) chemicals are manufac tured in the neuron cell body and carried to rarget muscles or

RULE 3: RULE OF SUPPLY

organs where, after release into the synaptic space, they are taken intO rhe targer rissue to promore healthy function. Passing in

Two structural entities, arteries and nerves, are important for the

the opposite direction, chemicals from the muscle or organ can

health and maintenance of any organ or area. Arteries supply nu

cross the synapse, be taken up, and be transported retrogradely

trients, oxygen, and a variety of hormonal regulatory substances

to the neuron cell bodies where the chemicals can then alter basic

to the area of their distriburion. Nerves provide ongoing neural

neuronal function.

control of skeletal and smooth muscle and glandular tissue and

Individual peripheral nerves have specific segmental relation

deliver trophic or regulatOry factOrs to the muscles or organs that

ship to the CNS and, therefore, to the entire body. The segmental

rhey innervate. The rule of supply illustrates a major source for

origin of nerves is pertinent to three general targets of innerva

maintenance of health or, conversely, origin of pathology when

tion: skin, muscles, and internal organs. The dermatOmai (skin)

disrupted.

innervarion parrern is relarively straightforward. Pain or sensory

Few statements are more cogent than A.T. Still's insightful dic

loss over some specific dermatomal zone leads the knowledgeable

tum: "The rule of the artery is supreme" (1). An adequate blood

physician to inferences abour the integrity of resrricred areas of

supply during varying physiologic conditions is a prerequisite for

rhe CNS or nerves near rheir origin. Innervation of rhe skin of

health of an organ or region. Conversely, compromise to the blood

rhe limbs becomes a bir more complicated because the sensory

supply often leads to functional capaciry being diminished, cas

nerves from specific spinal cord segments are drawn together into

cading, in rurn, toward disease. The osteopathic physician must

specific curaneous nerves that contain sensory fibers from more

work to ensure continued blood supply in the healthy stare and,

than one segment. A specific peripheral nerve (e.g., the medial

when treating injury or disease, should attempt to enhance arterial

cutaneous nerve of the forearm) will contain fibers from two or

supply ro affected regions. One important condition of compro

more segments (in this case C8 and Tl), alrhough those fibers

mise is bleeding due to trauma or disease. The physician must

will distribute at their termination in the skin in a dermaromal

have sufficient understanding of anatOmy to be able to halt hem

pattern. Here the notion is that the examining physician must

orrhage quickly and subsequently restore adequate blood flow to

have sufficient understanding of anatOmy to be able to differenti

ischemic areas. Bur the physician must also be able to recognize

ate sensory disturbances that arise in a particular peripheral nerve

the clinical signs of ischemia due to blockage of arterial supply

as opposed to an entire segmental level.

and work to relieve the blockage.

The innervarion parrern of muscles is particularly pertinent

To optimize strategies that continue arterial supply (and vigor)

to osteopathic medicine because changes in rhe tone, texrure, or

in the healthy state, and to use appropriate therapeutic interven

function of a muscle may be related to rhe segmental source of

rions in disease or injury to restOre adequare blood supply, a

nerve supply to that muscle. The innervation of muscles of rhe

physician must have an accurare knowledge of the arterial supply

trunk is relarively simple and follows a partern similar to that

to an area. Consisrenr with rule 1, as previously outlined, it is not

of the dermatomes. Nerve fibers to the muscles of rhe limbs,

sufficienr simply to know rhe name of rhe artery rhar provides

on the other hand, arise from the spinal cord and are woven

supply; rather, the passage of the arterial supply must be placed in

through complex networks (the brachial plexus and lumbosacral

rhe contexr of surrounding muscles, bones, organs, lympharics,

plexus) that combine fibers from several spinal cord segments intO

fascia, and so forrh.

motOr nerves that typically serve functional groups of muscles.

One of rhe goals of an osteopathic approach to medical rreat

A physician must understand innervation of limb muscles well

ment is, firsr, to recognize which piece of surrounding tissue

enough to reconstruct rhose nerve fibers from their termination,

mighr be compressing an artery and, having visualized rhe me

rhrough the plexus to their spinal cord origin. As with the sensory

chanical impediment to blood flow, adopr appropriare rherapies

nerves, the goal for the physician is to be able to differentiare

to relieve rhe compression and rhereby restore normal flow. Sim

motOr losses due to compromise of a distal, peripheral nerve

ilarly, rhe osteopathic physician works to recognize in the healthy

versus losses associated with a lesion of one or more spinal cord

individual rhose areas or organs that mighr be at risk for reduced

segments or associated spinal nerves.

blood flow caused by lifestyle, activities, posrure, obesity, and so

The internal viscera receive abundant autOnomic nerve sup

on, and adopr a rrearment plan to maintain health in zones at risk.

ply, and the sensory innervation to the internal viscera that signals

40

II.


functional stacus, distemion, and pain cypically accompanies the

indicate a pathologic condition. Most venous blood from the

auconomic innervation co the target organ. The panern by which

gastrointestinal system, for example, is drained through the por

this auconomic and sensory nerve supply arises from the spinal

tal venous system co the liver. But most of the blood from the

cord or brainstem and passes co target tissue is schematicalJy sim

lower half of the body walJ and lower limbs drains into the in

ple but anacomically complex; as such, its panern will not be

ferior vena cava. Some small, usually insignificant anastomoses

summarized here. The key poim co be made, however, is that be

between these twO major venous channels do exist. However,

cause of developmemal and maturational evems, the segmemal

when large amounts of blood are shunted from the porral sys

origin of auconomic and sensory innervation of a specific or

tem to the caval system, these anasromotic vessels become en

gan may be relatively distant from that particular viscus. As a

larged. Internal anal hemorrhoids or esophageal varices are en

result, changes in a particular visceral organ may appear as pain

gorgements of these anastomotic vessels and indicate shunting

or changes in muscle texcure some distance from the organ. On

of blood from the portal venous system to the vena caval system

the other hand, localized musculoskeletal misalignmem may pro

and may, therefore, indicate blockage of venous drainage to the

duce alteration in auconomic outflow from the related segmemal

liver-so-calJed portal hypertension-that results when the liver

zone of the spinal cord and may discurb function in an inter

is diseased.

nal organ some distance away from that segment. The physician

The rule of venous drainage is to know by which veins an area

must understand both the general segmental origin and anacomic

is cypically drained of blood, by what routes blood drains if the

pathway by which auconomic nerve fibers and the accompanying

cypical route is blocked, and where the veins lie relative to the

sensory nerve fibers pass co the various imernal organs.

surtounding structures.

Nerves supply important functional and trophic control co

Lymphatic channels are cypically even more variable than veins

all parts of the body. An importam aspect of osteopathic medical

in their gross morphology; knowing general patterns and spatial

practice is co recognize and treat conditions that alter nerve supply

relations of lymph drainage is usually sufficient. Although they

co a region or organ. The success of palpation and treatments

are less well defined anatomically, they are important to under

in recognizing and relieving compression or irritation to nerves

stand . As with venous return, selecting osteopathic approaches

and the effectiveness of maintenance of nerve traffic by healthy

to treatment of edema assumes a working knowledge of the lo

lifescyles depend directly on how well the physician understands

cation of lymph channels and how to augment lymphatic flow.

the route that nerves take from their origin co their destination.

Lymph colJects into blind-ended endothelial mbes in the periph ery. These channels merge into ever-larger channels throughout the body, are filtered at predictable intervals by lymph nodes,

RULE 4: RULE OF DRAINAGE

and finally converge on (usually) two large lymphatic ducts in the root of the neck. These two lymphatic ducts then empcy into

While the arterial supply is the only means by which fluid and

the venous system near the heart.

blood cellular components are taken ro an area, two pathways

As the lymphatic system has no intrinsic pump, fluid is moved

remove fluids and blood cells from a region. The venous net

from peripheral to central regions by osmotic pressure, muscu

work collects the deoxygenated blood from the capillary bed; the

lar contractions, external pressure, and pressure differences be

lymphatic channels drain the relatively cell-free extracellular fluid

tween the thorax and the abdomen. There are various techniques

that accumulates outside the vascular system. Compromising ei

to increase lymphatic remrn. When using techniques of mus

ther of these return channels leads co edema in the affected area:

cle contraction or applying local pressure or lymphatic pump

more fluid goes in than comes out.

mechanisms, one needs prerequisite knowledge of the anatomy

To alleviate edema, the osteopathic physician may choose to

of lymphatic flow.

use protocols to enhance venous and/or lymphatic remrn. The

In addition to returning extracellular fluid to the general cir

strategy selected depends, of course, on the medical condition of

culation, the lymphatic system and the lymph nodes are often

the patient as well as on a thorough knowledge of the anatomy

indicators of disease. The lymphoid system houses important

of the venous and lymphatic systems. As with the arterial system,

cells of the immune system. As a result of infection, lymphocytes

the knowledge of anacomy places venous and lymphatic channels

proliferate and are sequestered in lymph nodes, where they attack

inco the context of surrounding organs, muscles, bones, fascia,

pathogens (bacteria, viruses, etc.) in the lymph. Because of this

and so forth, usually by appreciating those structures on the basis

important immune function, lymph nodes draining an infected

of subtle palpable or surface landmarks.

area are often swollen and palpable.

Peripheral venous channels tend co be somewhat variable, with

Cancer in an organ will often metastasize to adjacent lymph

considerable anascomoses. For general medical application, it is

nodes and will also cause node enlargement. It is therefore cru

acceptable co understand the overall panern of peripheral ve

cial that the examining physician understand the potential sig

nous drainage and concentrate one's effort on the larger, more

nificance of enlarged lymph nodes. For example, breast cancer

predictable central veins. Understanding the anastomoses of pe

may metastasize to the lymph nodes on the lateral thoracic wall

ripheral venous channels is useful in the treatment of the ve

or in the axilla that drain lymph from the breast. Or, illustrating

nous system. For example, venous anascomoses offer therapeutic

a less obvious anatomic relationship, an enlarged node above the

strategies for the physician as alternate routes of venous drainage

clavicle in the root of the neck may indicate disease of the stom

are established. Understanding the routes of venous anastomoses

ach. When enlarged lymph nodes are detected, the examining

is vital co also correctly diagnose pathology, as significant ve

physician can use knowledge of the anatomic panern by which

nous blood flow through some anastomoses is unusual and may

lymph drains to infer the source of a disease process.

3. Rufes ofAnatomy

41

Physicians must also be alert to referred pain (i.e., when an

RULE 5: RULE OF PAIN

organ or structure is diseased or damaged but the pain is felt Pain brings more people to the physician than any other single

somewhere else). The most coherent hypothesis of referred pain

complaint. Because of the prevalence of pain as a symptom, it

postulates that individual pain transmission neurons in the spinal

is imporrant to understand the anatomy of pain. Pain is almost

cord receive afferents from both somatic pain fibers from the body

always a symptom, not the disease or disturbance itself.

wall and visceral pain fibers from deep organs. Individual pain

Pain-whether sharp or dull, constant or intermittent, recent

transmission cells are almost always stimulated by somatic pain;

or long-standing-can usually be localized by the patient. Where

higher somatosensory centers thus come to interpret that cell's

the pain is easily attributed to an identifiable injury, the physi

firing as localized to a somatic site. In the rare circumstance that

cian's use of anatomy is somewhat simplified; the pain is generally

a pain transmission cell in the spinal cord is stimulated by vis

alleviated by administering analgesics and adopting therapies to

ceral pain afferems, the pain is nevertheless imerpreted by higher

support wound healing. Even in these cases, however, a working

centers as originating at the somatic site.

knowledge of the anatomy of the damaged area is a useful tool

Referred pain is often difficult to localize and may move as

in the treatment of pain resulting from injury. The structural

the state of the disease progresses. Initially, pain may be vague

and functional imegrity of the arterial supply, venous and lym

and gnawing, and felt in the midline of the body. Later, pain may

phatic drainage, and nerve supply to the wounded area must be

become paravertebral and then follow a segmental or dermatomal

optimized to treat pain caused by a localized wound.

pattern. Examples of referred pain are numerous. The following

A common medical scenario, however, is of a patiem who has

are [wo examples: Damage to heart tissue invokes a sensation

a symptom of localized pain, yet no superficial tissue damage

of pain in the left arm, shoulder, neck, and jaw; or gallbladder

is visible. Swelling or redness may help direct the examination,

irritation causes referred pain in the right Rank.

but often the complail1[ is without an obvious external physical

Physicians recognize referred pain by experience and further

manifestarion. Whether local signs are presem or not, the physi

understand its significance in a patient. The osteopathic physician

cian must be able to appreciate the structures in that area and

should be particularly attentive to pathways of sensory innerva

their spatial relationships. Using this mental map of the area,

tion and pain innervation. The somatic innervation to the body

and guided by the history, the physician gently palpates in an

wall and limbs is via spinal nerves, while the pain innervation

effort to more clearly identify the source of the pain. Such palpa

of thoracic, abdominal, and pelvic viscera is via peripheral pro

tory examinations are of limited use without an understanding of

cesses of dorsal root ganglia cells that generally accompany the

anatomy and, indeed, proceeding in ignorance may risk further

distribution of autonomic fibers.

II1Jury.

Pain is the most anatomic of symptoms. The proper localiza

The task of inferring anatomy from surface palpation is some

tion and identification of the source of pain, whether superficial

what simpler in the limbs. These areas are not intrinsically easier

or deep, direct or referred, is essential to understanding the signif

(some of the most complex spatial relationships of structure are

icance of the pain and a necessary prerequisite

associated wirh the limbs), but a proportionally greater amount

treatment of the underlying condition.

to

comprehensive

of the limbs are available for direct visual inspection and pal pation. Similarly, much of rhe superficial neck anatomy can be assessed with palpation, but deep prevertebral structures are inac

RULE 6: RULE OF CONNECTE DNESS

cessible to palpation. The walls of the thorax, abdomen, or pelvis are readily palpated; superficial pain in these walls can often be

It has not been customary in modern medicine to poim out

assessed with limited necessity

recall deep anatomy. However,

that the human is a complex, unified organism made up of

to address a patient's pain inside the thorax, abdomen, or pelvis,

many overlapping, interconnected systems. Recently, conven

to

one must know the normal anatomy of the affected region. Pre

tional medicine has attempted to reassemble its various specialties

liminary judgme,m of the size, integrity, and health of the viscera

and subspecialties, each focused on a body region or functional

are based on superficial cues.

system, into a holistic understanding of health and disease. Nev

In most medical environments, the initial visual or palpatory

ertheless, the structure of medicine retains much of its compart

inference of anatomy may be rapidly checked with one or more

mentalization; it is difficult for even the most thoughtful physi

medical imaging modalities, such as plane radiographic films,

cian, particularly those in a demanding specialty practice, to step

CT, MRl, or ultrasound. The information given the physician is

back routinely and holistically assess a patient.

anatomically more concrete, but in some cases requires an even

A physician's understanding of body unity and the propensity

more sophisticated level of anatomic knowledge. The examining

to view the patient holistically is heightened by remembering a

physician must call on a detailed mental image of the anatomy

basic unifying principle: although the body is made up of many

of an area during initial examination. The physician must rhen

structurally and functionally discrete elements, the elements are

reconstrucr three-dimensional spatial relarions from CT or MRl

linked together by a number of connectors. These connectors,

sections, inferring placement of structures from shades of gray in

or the connectedness of the body, make up a significant portion

a radiograph, or visualizing unseen structures in the shadows of

of the study of medicine in general and the study of anatomy in

an ultrasound secror, which also requires a detailed knowledge of

particular.

anatomy. Ir is difficult to localize and interpret the source of that

Some of the connectors are easily listed and we have already

most common symptom, pain, without an accurate understand

touched on their importance. The circulatory system obviously

ing of the anatomy of a region.

connects distant body parts and, among other things, serves as a

42

II.


means of communication and connection. The nervous system,

Many of the layers of fascia, whether subcutaneous or invest

although traditionally divided into component parts (central, pe

ing, merge together and/or have common points of attachment.

ripheral, autonomic, and enteric), is one continuous, functional

The fasciae that separate and ensheathe the external and internal

entity. The nervous system constantly receives external and in

abdominal oblique muscles merge posteriorly. They also merge

ternal stimuli filters, sorts and integrates those stimuli, and then

with the thick connective tissue, thoracolumbar fascia, which

produces the coordinated contraction of muscles and/or secre

continues upward, encasing and separating the erector spinae,

tion of glands in response to those stimuli. The nervous system

the deep muscles of the back. Anteriorly the fasciae of the ab

can even impel muscular contraction and/or glandular secretion

dominal muscles merge, split, and are reAected to contribute to

independent of external stimulation. The endocrine and immune

the inguinal anatomy and abdominal aponeurosis. These fasciae

systems, interconnected to each other and to the nervous systems,

are continuous with connective tissue sheets that Aow over the

are also major connectors, serving to bring tissues distant from

crest of the pelvis and become the fascia lata of the thigh. The

each other under unified, coordinated control. One class of connectors is connective tissue in general, and

fascia of the thigh is continuous, in turn, with the crural Fascia of the leg. As a consequence of the widespread continuity of fascia,

Fascia in particular. Connective tissue binds organ to organ, mus

distortion or damage to fascia in one area can have effects in a

cle to bone, and bone to bone, and literally is the fundamental

distant, seemingly unrelated area.

con nector that allows strucmral and functional systems to be

The subcutaneous fasciae are also continuous from one body

physically grouped inro a unified package. Without connective

region to another. The deep layer of superficial fascia of the ab

tissue, the body is a dissociated mass of dying cells. It is the con

domen (Scarpa's Fascia) defines a space that is more or less contin

nective tissue, most of it a proteinaceous extracellular matrix, that

uous from the Aank onto the abdominal wall. It continues inFe

enforces Form and thereby permits Function. Connective tissue

riorly into the perineum, where it is the superficial perineal space

plays a critical role in body health and disease, but ironically it is

(bounded by Colles' and dartos fasciae, continuations of Scarpa's

so pervasive that it is easily overlooked in the study of anatomy,

fascia). Fluid or inFection in the abdominal subcutaneous space

in the maintenance of health, and in the diagnosis and treatment

can, thus, spread to the lumbar area or into the perineum.

of disease. Fascia is one component of body connective tissue that is read

The importance of the two-faceted aspect of fascia, that it at once not only separates and segregates but is also continuous

ily identified in gross anatomy. Fasciae are sheets of connective

structure-to-structure and area-to-area, should not be overlooked.

tissue that envelop specific structures and segregate one structure,

This pervasive connector (along with muscle and bone) helps to

organ, or area From another. For example, each individual muscle

regionalize the body and also connects region-to-region. Such

is wrapped in a layer of tightly investing connective fascia. Groups

a dualism is apparent in many physical manifestations of both

of muscle of similar location and function are Further ensheathed

health and disease.

in an enveloping Fascia.

The body, so often represented as a group of discrete regions or

At a basic anatomic level, these fasciae define the individual

functional systems, is in reality an integrated whole. The integra

muscles and muscle groups. For example, each of the muscles in

tion of the body region-to-region and system-to-system is accom

the anterior compartment of the leg has its own investing fascia.

plished by a series of connectors. Some of these connectors, the

The entire group is bounded laterally by a wall of fascia, the ante

endocrine and immune systems, are more commonly included

rior crural septum, medially by fascia that is continuous with the

in the context of physiology, biochemistry, or immunology. The

periosteum of the tibia, and anteriorly by the encasing deep Fascia

nervous system, the vascular system, and the lymphatics are also

of the leg. As is typical, the blood and nervous supply to these

important connectors, the structural components of which are

muscles, as well as venous and lymphatic return, are principally

part of anatomic disciplines. Finally, the visible connective tis

contained within this fascial compartment. These fasciae collec

sues of the body, and particularly the fascia, are great physical

tively define the anterior compartment. More important, they

connectors that bind organs or muscles into larger groups.

enhance the extensor functions of the muscles, while simultane

Coherent medical practice requires attention to the connected

ously providing protection, support, and separation from other

nature of the unified human organism. Typically, one disturbing

muscle groups. The fasciae define the normal, healthy limit of

force (a localized injury, lesion, or infection) causes a cascade of

the group; they tend to constrain destructive states and prevent

altered structural and Functional changes in other areas or systems.

the spread of bleeding, infection, mmor growth, and so forrh,

Similarly, the treatment of localized disease or injury must be not

into adjacent compartments.

only localized but must also attempt to bring the whole organism

Fascial compartments also separate muscles of the trunk. For

into healthy equilibrium. Planned treatments must account for

example, the muscles of the anterior abdominal wall are easily

not only the effect of the treatment protocol on the target site or

divided into planes and groups by tough, enveloping fascia. The

organ system, but also the so-called side-effect alterations brought

external oblique, internal oblique, transversus abdominis, and

about in distant, relatively healthy systems by the treatment.

rectus abdominis are delineable as a group and from one another

Observe the obvious examples of body unity. Take time to

not only by their attachments and orientations but also by the

appreciate the connected nature of the body. For didactic rea

tight-fitting sheets of fascia that enclose them. Planes of fascia

sons the body is traditionally disassembled into component partS

are also Found in the subcutaneous space, external to the deep

or regions such as bones, muscles, vessels, nerves, thorax, gas

Fascia that bounds the surfaces of the muscles. Understanding

trointestinal system, or upper limb. Yet it is important to be able

the placement of these fasciae is important in a variety of medical

mentally to reconstruct the intact specimen. The Fundamental

and surgical settings.

idea of holistic medicine is predicated on this.

3. Rules ofAnatomy

43

RULE 7: RULE OF DIFFERENCE

characterize the physical, human condition. The strucrural out

The human body is not always built the way it is "supposed"

gastrointestinal, musculoskeletal, or other, are often visible in the

co be: Sometimes it does not look like the picrure in the arlas.

morphologic condition of those organs.

come of systemic disorders, be they cardiovascular, pulmonary,

The imporrant rule co be stated is, again, the most obvious: The

The cadavers availabl e for teaching anacomy are usually of

srructure of each human body is different from all others. As

older individuals and, in addition co the types of systemic pathol

our faces differ person-co-person, so, coo, does the rest of our

ogy outlined previously, these bodies also show the struccural

anacomy. There are cwo reasons for variation of human form:

changes caused by the wear and tear of seven or eight decades.

developmenral and hiscorical. Variation in srructure may be based

One can find arthritic j oints, muscles wirhered by disuse, worn

on either or both.

or infected teeth, or resorbed bones of the jaw when teeth are

During developmenr and maruration of the human form, each

missing . The list of the normal alterations of anacomy that ac

person's gehetic information, along with extrinsic influences, de

company aging is lengthy; these are imporranr consequences of

termines their ulrimate form. Developmental deviations of struc

each person's life history. Many patients show morphologic evi

cure are so common that descriptions of normal anacorny can

dence of age-related deterioration, and the physician can benefit

more usefully be rranslated as usual anacomy, with variations as

from recollecting the texrure and appearance of those changes

sumed. For example, the pattern of venous drainage of surface

first seen in cadaver dissection.

srructures (the limbs and neck are all good examples) is so vari able that only a general plan can be described, and even with the propensity of anacomists co name everything, only the larger elements can typically be idenrified. Similar normal variation is common in arrerial supply. The branching of the celiac trunk co supply the scomach, liver, pancreas, spleen, and duodenum fol lows a general parre rn, bur there are numerous deviations. How ever, deviation of srructure from the "norm" does not necessarily imply a pathologic condition. As you continue the study of anacomy, you will also see how

CONCLUSION The rules that have been outlined here are, for rhe mosr part, self evident. Anatomy is the srudy of srrucrure and general function. It is imperative co learn where things are, what they do, how they are connected, how they influence each other, and how they change with time and life's experience.

each individual 's anacomy has been altered by injury or disease that is parr of their life hiscory. Virtually every cadaver has lo calized and/or widespread, visible, pathologic alteration of srruc ture, caused by ravages of atherosclerotic disease, metastatic car cinoma, prolapsed reccum or uterus, arrhritic changes, or any of the nearly endless list of diseases, injuries, or dysfunctions that

REFERENCE 1 . Sri II AT. Autobiography ofA. T. Stili. Published by rhe aurhor, K i rksville, MO; 1 897:2 1 9.

ANATOMY ALLEN W. JACOBS WILLIAM M. FALLS

KEY CONCEPTS • How the full y developed h u m an body's segmental ner

• •

• • • •

•

vous system is d irectly related t o embryological growth patterns Differences among major types of c onnective t issue, t he constit uents of each, an d t heir funct ion al significance Differences between synov ial and n onsyn ovial j o in ts; joint play and its s ignificance in t he diagnosis of j oint- related dysfunct i on s St ruct ures i n synov ial j oints and t hei r functi on al basis E xamples ofnonsyn ov ial j o in ts and t he differences between fi b rous and c art ilagin ous types Anat o m y oft he m uscle-t en don c o m p lex and its function al sign ificance How t he innerv ati on fro m spinal segments is dist ribut ed t h roughout t he body an d how the lim bs are supplied fro m t his sourc e St ruct ural i m pl ic at i on s of myofascial continuity and its i m pact on t he osteopat hic diagn osis an d t reat m ent of m usc u loskeletal dysfunct ion

A fun dam ent al un derstandin g of basic human an atomy forms t he foun dat i on of ost eopat h ic medic in e. T he em bryologic devel opment ofthe neu rom usc uloskelet al system prov ides t he basis for un derstandin g the segmental dermatomal representation of t he nervous system as well as the dist ribut ion of somat ic an d v isceral nerve supply t o the enti re body. The microsc opic st ruct ure of c onnective t i ssue is a key ele ment in un derstan ding myofasc ial contin u ity of the body. The gross st ructu re of t he m usc uloskelet al system is based on the m ic roscopic st ructural an d funct ion al com ponents of c onnec t ive t issue an d their interrelat ionship with skelet al m uscle. The ability of the t issues of t he musc uloskeletal system t o heal and repair following in j ury is d i rec dy related to t heir cell ular c on t en t an d m ic rosc opic struct ure. At t he m ac roscopic level t he ar rangement of neurov asc ular bun d les, whic h supply somat ic t is sue, is int imately related to c onnect ive t issue spaces an d fasc i al planes.

T he funct ion al un its oft he m usc uloskeletal system are the syn ov ial joint , m uscle-ten don complex, an d fasc ial elements, which support skelet al muscles an d their n eurovasc ular supply. At t he macroscopic level, t he em bryologic segmental orga nizat ion of t he body is represented in t he axial skeleton . The arran gement of n erve an d arterial supply, as well as venous an d lymphat ic d rainage, is repeated segmentally t hroughout the axial skeleton an d is modified to serve t he upper an d lower limbs. An un derst an d ing oft h is segmental organ izat ion is essential for diag n osis an d t reat m ent ofn eurom usc uloskeletal system dysfunct ion an d disorders. The functional adaptat ion of t he l i m bs is best un derstood t hrough t he conc ept of myofasc ial con t in uity. Posture, balance, an d st ability during dynamic act ivity are direc dy related to t he funct ional capac it y an d adaprability of t he myofasc ial elements of t he body. The discussion oft he em bryologic development, m ic roscopic an at omy, funct ion al un its, an d segm ental organ izat ion ofthe neu romusc u loskeletal system is based on an an at om ic un derst anding t hat c an be obtained by st udying t he detail presented in ma j o r an atomy textbooks ( 1 -8 ) . The applicat ion of t h is kn owledge an d an un derst anding of myofasc ial cont in uity are the foun da t ions of osteopat h ic medicine, whic h are ut ilized in the diag n osis an d t reat ment of neuro musc uloskeletal dysfunct ions and disorders. NEUROMUSCULOSKELETAL EMBRYOLOGY

T he emb ryologic developmen t of t he neurom usc uloskeletal sys tem exem plifies t he segment al organ izat ion oft he body. The for m ation of somites in t he developing em bryo, c om posed of em b ryon ic mesoderm ( m esenc hyme), is spec i fic al ly related to t he segmentat ion of t he neural tube. E ac h som ite differenti ates into two part s: a sclerotome an d a dermomyotome ( Fig. 4.1). As the m esenchyme m igrates from t hese parts of t he som ites during development t o form t he segmen tal elem ents of the axial skele t on (e.g. , vertebral column an d ribs from t he scleroto me; deep bac k m uscles an d interc ost al m usc les from t he myotome), seg mental nerve (spinal nerve) supply from the developing neural tube (spinal cord) is main tained (Figs. 4.2 an d 4.3). E ac h my ot ome divides into an epimere innervated by the posterior pri mary ram us of a spinal nerve an d a hypomere inn ervated by the

4. Anatomy

45

Dermomyotome Neural groove

In tr a-

B Notochord

Dorsal aorta

FIGURE 4.1. A a n d B: Tra nsverse sections showing differ entiation of a somite in relation to development of neural tube.

Condensation of sclerotome cells

Myotome

Nephrotome Intraembryonic coelom Splanchnic mesoderm layer

Spinal gangllon

B

-�WfQ,�:X'I

FIGURE 4.2. A a n d B: Transverse sections showing mi gration of cells from sclerotome a n d myotome d u r i n g development.

Outer,

intermediate, and inner muscular

layer of ypomere as found in wall of thorax and

Ventral primary ramus

abdomen

Co el om i c c avi

Rectus col umn

A

-;4jIlJ!�\liiii!llP'

FIGURE 4.3. A and B: Transverse sections showing seg mental nerve from develop i n g s p i nal cord i n nervati n g developing musculature o f thorax a n d a bdomen.

46

11.

Osteopathic Considerations in the Basic Sciences T he segment ally organ ized ner vous s ystem provides t he lin k between t he somat ic t iss ue an d t he viscer a, whic h deve lop in ternally in a si m il ar segment al manner. T herefore , t hrough t he segment a l organ izat ion of t he nervous s ystem t here is a struc t ural re lat ions hip between t he nerve s upply t o t he somat ic t iss ue and t he autOno m ic viscer al nerve s upply of e ac h segment of t he deve loping e mbryo.

MUSCULOSKELETAL MICROSCOPIC ANATOMY

FIGURE 4.4. Transverse section showing that m u scles (as well as bone and connective tissues) of developing l i m bs m a i n t a i n segmental i n ner vation from developing spinal cord.

anterior pr i mar y ramus of a s pin al nerve ( Fig. 4.3). T his segmen t at ion in t he axial s ke leton is s ustained in t he adult . T he mes enchymal cells in t he e pi mere become t he deep bac k m usc les in t he adult , while t he mesenc hymal ce l ls in t he hypo mere beco me t he m usc les of t he anterolateral wall of t he t hor ax an d abdomen ( Fig. 4.3). With t he deve lopment of t he upper and lower l imbs t he mes enc hyme , whic h for ms bone , c onnect ive t issue, an d m usc le ( de r ive d fr om t he hypomere) maint ains segment al c onnect ions wit h t he deve lo p ing s pinal cord t hrough t he anter ior pr i mar y rami of spinal ner ves growing into r he developing limbs ( Fig. 4.4). How e ver, t hrough d ifferential li mb growt h an d development (e .g. , mesenc hymal ce lls fr om d ifferent se gments c ombining t o for m a s ingle m uscle in t he adult) t he in it ial segmental re presentat ion of t he e m br yo is modified in t he adult .

Collagenous flbers

T he c onnect ive t iss ues oft he body are der ived fr om mesenchyme. T hese developing t iss ues (connect ive t issue, bone , and cart ilage ) contain cel ls (fi broblasts , osteoblasts , and c hon droblasts) t h at pr oduce a matr ix of gr oun d s ubst ance an d fi bers s urrounding rhe ce l ls . E ac h type of c onnect ive t iss ue has a unique arr ange ment of ce l l types (fibr ocytes , osteocyres , an d c hon dr oc ytes) wit h in a s pecific matrix of groun d s ubst ance an d fibers . By c hanging t hese t hree ele ments (ce l ls , ground s ubstance , and fibers ) t he var i able composit ion and cons istency of e ac h t ype of connec t ive tiss ue in t he musculoskeletal s yste m is pr oduced. Connect ive t iss ue is c lass ified on t he basis of rhe arr an ge ment of t hese t hree ele ments.

Connectiv e Tissue

Loose c onnective t issue for ms an open meshwork of ce lls ( fi brocytes , fi br oblasts) and fi bers (collagen , elastic , ret icular ) with a large amount of fat cel ls an d ground subst ance in between . Loose c onnective tiss ue also s urroun ds ne urovasc ular bundles an d fi l ls t he spaces between individual muscles an d fasc ial planes ( Fig. 4.5).

FIGURE 4.5. Cellular elements of loose connective tissue.

4. Anatomy

47

Dense fi b rous conne ct ive t issue is class i fied on t he basis oft he dense, regular arrange ment of t he predominant collagen fibe r bun dles , which run in t he s ame direction . This t iss ue forms t he substan ce of pe rioste um, ten dons , ligaments , an d dee p fascia. It is common l y described as regular or i rregular (e .g., pe rios te um and dee p fascia) depen ding upon t he arran ge ment of t he close ly packe d collagen fi be r bun d les (e .g., ten dons an d l iga ments) ( Fig. 4.6). Cartilage and Bone

FIGURE 4.6. Cellular elements of dense, regular fibrous connective tis sue. Dark fibroblast nuclei lie between bundles of regularly arranged collagen fibers.

Perichondrium

Nucleus or corli/oge cell

Interferritorio/ motrix

Cart i lage an d bone are highly s pecialized conne ct ive t iss ues in which t he groun d substance of t he matrix is pre domin an t ove r t he ce l lular an d fibrous e le ments . The chon d roblast is respons ible for producing t he ground substan ce an d fibe rs of t he t h ree t ypes of cartilage: hyal ine (ar t icular; foun d in synovial join ts ) , e l ast ic (found in t he extern al e ar, auditory tube, l arynx, an d e pigl ott is ) , an d fibrous ( found in inte rve rte bral discs ) . These t h ree cart i lage types vary in h istologic makeup on t he basis of t hei r ground subst an ce an d predominan t fibe r type (collagen or e last in) an d are avascu lar (Figs . 4.7-4.9 ) . The oste ocytes o fbone are maintained in a rigid matrix, which is calcified an d re in fo rced by conne ct ive t iss ue fibe rs , which are produced by t he osteoblasts . The st ruct ural unit of bone , t he os teon ( have rs ian syste m ) , is formed by concent ri c lame l lae of bone s urroun ding a microscopic neur ovascular bundle in t he have rs ian can al . The osteocytes are located wit h in microscopic s paces (la cunae) between t he concent ric bone mat rix lame llae an d extend processes int o t he m at rix ( Fig. 4. 1 0) .

Territorio/ matrix

FIGURE 4.7. Cellular elements of hyaline (articular) carti lage .

48

If.


Territorial matrix

Capsule Elastic Abers

.. ---"' ..1.l��-....tt"

Elastic Abers

Cartilage cells

Capsules

Collagenous Fibers (cross section)

Capsule

Surlace 01 territorial matrix

Perichondrium

Collagenous Flb.ers (long. sec. I

FIGURE 4.8. Cellular elements of elastic cartilage.

Cortiloge cell

Territorial hyalIne matrix

FIGURE 4.9. Cellular elements of fibrocartilage.

4. Anatomy

Canaliculi

Haversian canal

Lacuna

49

Interstitial lamellae

FIGURE 4.10. Transverse section show i n g ce"ular ele ments of compact bone.

Skeletal Muscle

S keletal muscle tissue is also derived from mesenchyme and i s modi fied for r h e speci fic function of contracrion. T h e i ndividual skeletal muscle cells (fibers) are arranged in a regular, system aric manner to faci litate contraction when stimulated by a nerve impulse. The microscopic appearance of skeleral muscle presents a classic b anding parrern, which represents the i n ternal organization of the protei n contracti le elements in each muscle fiber ( Fig. 4. 1 I ).

The articular surfaces of rhe [wo bones, which form rhe joi n r, are covered by hyali ne (articular) carri lage, which is speci fically modi fi ed for rhe funcri o n of arri cular morion. The [wo arricular surfaces are separared by a monolayer of synovial Auid in the joinr cavi ty. The j oi n t capsule is com posed of two layers. The fibrous outer layer is in conti nuity wi th rhe periosreum of the proxi mal

Response to Injury

The i n herent capaci ty of the musculoskeletal system to heal and repai r followi ng inj ur y i s a di rect reAecrion of the histologi c orga nization of connective tissue. At the macroscopic level connective ti ssue i nvests the neurovascular b undles, which supply speci fic parts of the body. At the microscopic level the capi llary beds are located wi thi n the open meshwork of loose connective tissue and nourish the cellular e l ements of the tissue. These cel ls, in turn , produce the ground subsrance and fibers o f the connecrive ris sue. Followi ng inju ry a complex biochemical reacrion resulrs i n sti mulari ng the i n herent capacity o f heali ng and repai r.

FUNCTIONAL MUSCULOSKELETAL CONCEPTS Synovial and Nonsynovial Joints

Al l synovial joi nrs of rhe body are freely movable and si mi lar i n s tr ucrure. The " typical" synovial joi n r i s exemplified i n Fig. 4. 1 2.

FIGURE 4. 1 1 . Long it u d i n a l section of skeletal muscle show i n g classic b a n d i n g pattern found i n i nd i v i d u a l fi bers.

50

[1.


Articular cartilage �t��uV�1 Fibrous stratum

1

Articular

capsule

A FIGURE 4.1 2. Typical synovial joint.

and dist al bones, which form t he synovial j o i nt, and it i s classified as dense, irregular fi brous con nect ive t issue. At t he point where t he art icular hyal ine cart i lage ends t he bone t issue is covered by t he periosteum. The fibrous outer layer oft he j o i nt capsule could be described as t he free periosteum, which envelops the freely movable joint and con nects t he prox i mal and d istal bones at t he art iculat ion. The unique i n ner l ayer is t he synovial membrane, which li nes the fibrous outer layer. Th is membrane secretes t he synovial Auid, which lubricates t he i nternal j o i nt surfaces and t he articular hyal ine cart i lage. The uniqueness of t h is membrane is t hat ir is derived from mesenchyme. However, m icroscopically and funct ionally t h is t issue is similar ro epit helial t issue, which is an ecrodermal derivat ive. Each synovial j o i nt is st abilized by specific l igament s. L i ga ments may be classified as capsular or accessory. A capsular l ig ament is a part of t he fibrous outer layer of the joint capsule, while accessory ligaments are either located wit h i n the j o i nt cav ity (intracapsular) or outside t h e j o i nt capsule, separated from t he fibro us outer layer (ext racapsular). AJ l ligaments are h isrolog ically com posed of dense, regular fi brous con nective t issue and have microscopic, st ructural, and fu nct ional cont i n uity with the periosteum of adjacent bone. The t emporo mandibular, sternoclavicular, ulnomeniscotri quet ral , and knee j oi nts are highly special ized types of synovial joint s. These joints have t he un ique feat ure of either a disc or meniscus ( i ncomplete d isc) wit h i n t he j o i nt cavity ( Fig. 4.13). The fib rocart i laginous disc provides for addit ional support and stability as it separates the rwo hyal ine cart i lage art icular surfaces. Peri pherally discs are con nected to t h e fibrous outer layer of t he

Synovial stratum

B

c

FIGURE 4. 1 4. Motion at a synovial joint. A: Spin.

B: Rol l . C: S l ide.

j o i nt capsule. A disc ex tends across a synovial joint, dividing it st ruct urally and functionally i nto rwo sy'hovial cavit ies. The d isc, which is derived from mesoderm, represents a h ighly specialized form of connect ive t issue, which is dist i nct in t hat t he fibrous ele ment oft he matrix predominates. A synovial j o i n t wit h a fibrocar tilaginous disc displays a st ruct ur e similar to the embryologically developing synovial joint. This type of synovial j oi nt maintains t h e fi brocart i l aginous element, which is development ally lost in t he "typical" synovial j o i nt . Synovial joints are commonly classified according t o t he shape of t h e articular surfaces and/or the movements perm itted. None oft he art icular sur faces are t ruly A at. Biomechanically t hese joint surfaces perm it mot ion, which is described as spin, rol l , or slide (Fig. 4.14). S pin represents rot ation about the longitu d i nal ax is of a bone. Roll is t he re sult of decreasing and increasi ng the angle berween t h e rwo bones at an articulation. S l ide is t he resulr of a t ranslat ory mot ion of one bone gliding/sliding on rhe ot her ar t he joint. S pecific detai ls regard ing t he classification system and individual synovial j o i nt s can be found in any anato my tex rbook (1,2,4,5,7,8). N onsynovial j o i nts are subdivided int o fibro us and cart i lagi nous types. These joints, where the art iculat i ng bones are di rect ly con nect ed by eit her fibrous t issue or cart i lage, have no free surface for movement , but provide for sr rengt h and srability berween adj acent bones. The fi brous joi nts include rhe sut ures of t he skull ( Fig. 4.15), teet h in t he mandible and max illa, and the distal t ibiofibular joint. The fibrocart ilaginous intervertebral discs berween adjacent vertebral bodies and the pubic symphysis ( Fig. 4.16) are examples of cart i laginous joint s. The sut u res oft he skull provide a classic ex ample of rhe i nter relat ionship ber ween structur e and fu nct ion. Each surure (joi nt) berween adj acent cran ial bones un iquely provides support and mobility. Unlike the freely moveable synovial joint s, the sutures are highly rest ricted to sl ight glid i ng mot ion. H owever, mot ion loss/rest rict ion is t he clin ically signi ficant facto r in describing so mat ic dysfunct ion of the joint .

Sutural ligament

FIGURE 4. 13. Synovial joint with an articular d isc.

FIGURE 4.15. A suture is an exam ple of a fibrous joint.

4. Anatomy Ligament Disc of fibrocanilage Anicular canilage FIGURE 4. 1 6. A symphysis is an example of a cartilaginous joint.

Cranial bone motion is also i n fl uenced by the tens ion of the cranial dura mater, which covers the bra i n and forms the imernal li ning of the s kull. Cranial dura mater consists of two layers: periosteal and meningeal. The periosteal layer is the perios teal l in ing of the cranium and there is h is tologic com inuity of this layer with the fibrous tissue (sutural ligamem) at each cranial suture. The meningeal layer of cranial dura mater has com in u i ty

with the s pi nal dura mater (thecal sac) at the foramen magn u m of the occipital bone (Fig. 4.17). The d i rect effect of these connective tiss ues on cranial bone motion has been described by Sutherland (9 ) as the reciprocal tens i o n membrane. I n s u mmary, synovial and nonsynovial joims exemplifY the os teopathic concept of the i nterrelations h i p between s tructure and function . S ynovial joims, which are freely moveable, allow for the body to have mobility and greater range of motio n . The nonsynovial joints (fibrous and cartilaginous) provide s t rength and s tabil i ty within a l i mited range of motion.

Joint Play

The volumary movemem of synovial joims is accommodated by joi m play as described by Mennell (10). J o in t play is defi ned as a

into cerebral veins

First cervical nerve First denticulate lig. Post. info cerebellar a. Second denticulate lig.

Ligamentum flavum

Duro mater -t-......,_

51

Dorsal ro ot gong I ion

Trunk of cervical nerve

fourth

FIGURE 4. 1 7 . Area of foramen magnum. Cranial dura mater lines the internal surface of cranium, is continuous with fibrous tissue of sutures, and is continuous with spinal dura mater of foramen magnum.

52

If.


small but precise amou nt of movement (less than one- eight h of an i nch), which is i ndependent of t he act io n of voluntary muscle fu nct ion. The normal, easy, volu ntary range of act ive mot ion at a synovial joint is dependent u pon t h e i ntegrity of j o i n t play. J o i nt play is o n ly present in t he l iving synovial joint . The movement of joint play can only be demonst rated by passive exami natio n . E ach synovial joint h a s one or more j oi nt play movements. Joint dysfu nct ion is defi ned as t h e loss of j oi nt play and t herefore a l i m it at ion of the volu ntary range of mot io n at a synovial j oi nt . Joint dysfu nct ion i s a component o f somat ic dysfu nct ion (acute or chro n ic) which is diagnosed in the evalu at ion of the neu ro musculoskeletal system. The resrorat ion of joint play appears ro be the b asis for t he success of synovial joint mob i l izat ion u s i ng d i rect or i nd i rect act ion t reat ment techni ques i n osteopat hic ma n i pu l at i o n .

Muscle-Tend on Complex

A del icate network of fine con nect ive t issu e su rrou nds individual skeletal muscle fibers. At each end of t he muscle this conn ect ive t issue forms a tendon composed of dense, regu lar fibrous connec t ive tissue. The tendon is attached ro bone t h rough a m icroscopi c interlacing o f its con nect ive t issue wit h the periosteal connect ive t issue covering t he bone (Fig. 4.18). E ach muscle has two pans: a predominant con nect ive t issue at its ends t h at att aches ro b ones and a predominance of muscle t issue in its fu nct ional contract ile bel ly. The change ro connect ive t issue at its ends provides the mu scle a fi rm att ach ment ro bone. The muscu lotendinou s junc t ion re presents t he point at which t here is a significant change in t he h isrologic composit ion of skeletal muscle fro m predom inantly muscle fibers ro predominantly collagen fibers. Muscle contract ion exerts force on t he mu scu lot endinou s ju nct ion and t hen the tendon, which moves a bone at a j o i nt .

,,,'-- 5up�rf'icia.l fa.",cia.

I T'\.tG�rmu!>cul

5em.i.�pinc.li& Capit is

Tra p ezius

FIGURE 4.31. Suboccipital region. Suboccipital muscles (obliquus capitis superior and rectus capitis pos terior minor) provide myofascial continuity between the cranium and C 1 /atlas.

muscle then provides functional and structural continuity be tween the upper limb, spine (thoracic, lumbar, and sacral) , ribs, and pelvis through an attachment to the crest of the ilium and pelvis. Dysfunction of the latissim us dorsi muscle can therefore have a d i rect effect on the glenohumeral joint, scapulothoracic articulation, acromioclavicular j o i n t , thoracic facet joints, cos tovertebral joi nts, lumbar facet j o i n ts, and stabil i ty of the pelvis at the sacroil iac j o i n t. MyoFascial con tinuity From one region of the body to another can best be understood through consideration of the regional structure of the body which i ncludes the cranium, cervical spine and upper limb, thoracic spine and trunk, l u mbosacral spine, and the pelvis and lower l i m b ( Fig. 4 .30) . The myofascial conti n u i ty of the cranium is best u nderstood by studying the i nternal and external structure of the skull as i t articulates with t h e fi rs t cervical vertebra ( C l /adas). Suboccipital muscles (obliquus capitis superior and rectus capi tis posterior minor) provide For t h is conti n uity (Fig. 4.3 1 ) . The meningeal layer of cranial dura mater is continuous with the spinal d ura at the occipital foramen magnum (Fig. 4 . 1 7) . The spinal dura surrounding a n d supporting t h e spinal cord is Free with i n the vertebral canal. The i n ferior aspect of the spinal dura mater at the S 2 vertebral level is attached to the coccyx by the coccygeal l i gament ( Fig. 4.32). Through the dura mater there is a d i rect con nection between the i n ternal aspect of the neurocranium and the i n ferior aspect of the vertebral column.

The bones of the face (viscerocranium) and the cranial vault (neurocranium) are covered externally by a thin layer of con nective tissue periosteum. Th is periosteum provides a protective covering of each bone and a mechanism For attachment of specific muscles (e.g., muscles of Facial expression; Fig. 4.33). I t is important to understand the concept of myoFascial con tinuity and the fact that many muscles in the body cross more than one joint and exert their actions on those joi nts, as well as diFFerent areas of the body. Because of this, the physician should always examine joints and muscle groups well removed from an area of d iscomfort in order to d iscover the true source of inj ury or dysfunction.

D E D I C ATION

Allen W jacobs, DO, PhD, a nationally recognized leader in osteo pathic medicine, dean ofthe Michigan State University College of Osteopathic Medicine, and co-author ofthis chapter, died unexpect edly on December 2, 2001. The thing that J remember most about Al was his great compassion and love for his fomily, the college, the osteopathic proftssion, and the discipline ofanatomy. This chapter reflects his beliefthat a solid understanding ofanatomic principles is the foundation ofosteopathic medicine. [ honor his passing by ded icating this chapter to keeping alive the beliefthat he so devoutly expounded. William M. Falls, PhD

Spinal cord

I.,Irp..�f--

Arachnoid mater

J

r--- Denticu late l igaments Thoracic

XII --�iI

]

Spinal c o rd

Filum terminale Conus m e d u l laris

L1

S u ba rachnoid space, conta i n i n g cerebrosp i n a l f l u i d a n d n e rve roots

D o rsal root fila

L2

F i l u m terminale

Dorsal root Ventral root L3

Cauda eQuina

Subarac h n o i d space

L4

�-- Pedicle of vertebra L5

.;-+'.,.... - Superior a rticular

p rocess of sacrum

FIGURE 4.32. Lower end of the s p i n a l cord, i n c l u d i n g c a u d a e q u i n a , a n d i t s coverings. Inferior e n d o f d u ra mater at S2 is attached to coccyx by coccygea l l ig a ment. D u ra mater provides a d i rect connection from the internal s u rface of the cra n i u m to the coccyx.

Procerus Frontalis

Corrugator

Camp. naris Orbic. oculi --;----r, Dilatornaris depr. sept i

L.L.SAN .

&

Lev. ang. oris

Lev. I. super. -----'.�"!"

Buccinator Zyg. minor Zyg. major

s

R i ori u s

Dep. ang. oris

�VJ·ff+f---

Facial a.

==== Mentalis ::: � I -] � � � \�

Dep . lab. in f r.

FIGURE 4.33. Muscles of facial express i o n . Periosteum covering bones of viscerocra n i u m provides attachment for these muscles i nserting into s k i n .

62

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REFERENCES I . Basmajian J V, Sionecker CEo Grant's Method ofAnatomy, I I th cd. Balti more, MO: Williams & Wilkins; 1 989.

2 . Clemente CO. Gray's Anatomy of the Human Body (American ed.), 3rd ed. P h i ladelphia, PA: Lea & Febiger; 1 98 5 . 3. Copenhaver WM, B u nge RP, Bu nge M B . Bailey's Textbook ofHistology, 1 6th ed. Balti more, M O: Will iams & Wilki ns; 1 97 1 . 4 . Holl inshead WH, Rosse C. Textbook ofAnatomy. 4th ed. Philadelphia, PA: Harper & Row; 1 985 . 5 . Moore K L.

Clinically Oriented Anatomy. 3rd ed. Baltimore, M O :

Wi ll i ams & Wi l ki ns; 1 992.

6. Sadler TW. Langman's Medical Embryology, 6th ed. Baltimore, MO: Williams & Wilkins; 1 990. 7. Williams PL, Warwick R, Oyson M , Bannister LH. Gray's Anatomy (Bri tish ed.),

37th

cd.

London, England: Church i l l

Livi ngstone;

1 989. 8 . Woodburne RT, Burkel WE. Essentials ofHuman Anatomy, 9th ed. New York, NY: Oxford Un iversiry Press; 1 994. 9. Magoun H I . Osteopathy. In: The Cranial Field, 3rd cd. K irksville, M O : T h e Journal Printing Company; 1 976. 1 0. Mennell J. joint Pain. Boston, MA: Little, Brown and Company; 1 964.

I 1 . Towns LC. Rules of anatomy. I n : FOllndations for Osteopathic Medicine, 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2002.

BIOMECHANICS: AN OSTEOPATHIC PERSPECTIVE MICHAEL R. WELLS

KEY CONCEPTS

• Biomechanics describes the relationship between structure

and function.

• Motion and forces i n three-dimensional space can be • •

• • • • • • • •

•

divided into components with a magnitude of action i n each dimension. Stress, strain, and force moments are terms used to describe how forces act o n objects and how objects respond to those forces. The biomaterial properties of tissues such as bone, cartilage, muscles, tendons, and l igaments, are based o n a hierarchy of biomechanical properties from the molecular, cellular, tissue, and gross anatomic levels. Tissues are constantly remodel ing in response to the stresses placed upon them. Excessive stresses or inadequate responses to them (loss of homeostasis) result i n i nj ury or disease in tissues. The basic biomaterial properties and remodeli ng capacity (adaptabi lity) of tissues change with age, generally to render them more vulnerable to stresses and injury. The gross biomechanical properties of the skeleton are defined by bony structure and the attachment of muscles and tendons which produce forces across j o ints. The primary motions at the surfaces of articulations are gliding (translation), rotation, roll ing, compression, and distraction. Basic properties of joint kinetics can be described by measuring the forces produced by m uscles and the length of moment arms acting across joints. The elastic properties of muscles, tendons, and l igaments allow them to store energy in some phases of movements for release d uri ng others. Normal movement in the spinal column is a composite of smaller motions of individual vertebrae. Restrictions of movement in one area can result in a compensatory increased mobi l i ty in others. The orientation of intervertebral joint facets in the spine, i n association with the direction of spinal muscle

contraction, produces a motion coupl i ng of vertebral movement. These coupling relationships differ over areas of the spine. • It is necessary to consider the biomechanical relationships of the body as a whole when attempting to define the consequences of i n j ury or altered function of a body segment.

BIOMECHANICS DESCRIBES THE RELATIONSHIP BE TWEEN STRUCTURE AND FUNCTION

The interrelationship of structure and function in the body is one of the basic principles of osteopathy. The science of biomechan ics is dedicated to describing this relationship more generally in biologic systems. This can apply to the organism as a whole (as with kinesiology) or even on a subcellular level (as with micro tubular transport mechanisms). The approach to the mechanics of biologic systems is similar to the mechanics of i nan imate ob jects, and consists largely of how they respond to forces applied to them. When struck with a hammer, an object may shatter or absorb the force and be accelerated i nto movement. The response will depend upon a variety of factors including the material com prising the object, the object's shape, internal structure, where and how the force is applied, and so forth. The response of the h uman body to either externally or i nternally applied forces can be described similarly, as i t must obey the same basic laws of physics. However, the human body and other biologic systems have extremely intricate structural arrangements of highly vari able materials down to the molecular level. This can make the accu rate biomechan ical modeling of even si mpie movements very challenging. Additionally, the body also has the essential biologic abiliry to adapt and structurally remodel i tself accord i ng to the s tresses placed upon it. Some of these adaptations, as in the me chanical properties of tissues, can occur relatively rapidly. Th is "moving target" property can add an additional layer of difficulty for accurate description.

64

fl.


The capacity of the body to adapt appropriately to environ mental stress will make the difference between health and dis ease. The goal of the osteopathic physician is to assist the body i n regaining a balance with the stressors of the patient's environ ment, usually at multiple levels of consideration. From a biome chanical standpoint, this may involve the correction of somatic dysfunctions or to break cycles of inappropriate responses that have produced them. In doing so, the primary biomechanical considerations for the osteopath ic physician m ust incl ude broad characteristics encompassing both biomaterial characteristics of tissues and the primary mechanical operation of the body as a unit. As opposed to other medical disciplines, this m ust i nclude a l i teral "feel" for the characteristics of tissues i n add i tion to fig urative "feel" for the u n derstanding of body mechanics derived from a knowledge of anatomy. The primary goal of this chap ter is to assist the reader in obtaining this latter knowledge. For this reason, an emphasis will be placed on basic biomaterial and biomechanical concepts rather than mathematical modeling of properties. As with other chapters in this volume, this chapter is i ntended to be a summary of biomechanical concepts that are of particular relevance to those who study osteopathic medicine. More comprehensive discussions may be readily obtained from texts on particular topics. It will be assumed that the reader has a basic working knowledge of gross anatomy and the concepts relating anatomy to function. Motion and Forces Can Be Described as Components With a Magnitude in Each Dimension of Three-Dimensional Space

The strategy for describing the mechanics of biologic materials begins wi th the same terms and methods employed to describe inanimate objects. The process of i nterest is broken down i n to components that can be measured and characterized. These com ponents and their properties are then incorporated i n to models (often mathematical) that can be used to describe the system and predict i ts reaction to defined stresses. The terminology used is common to areas of mechanical sciences, and can be categorized i nto terms related to:

A.

c.

B.

D.

FIGURE 5. 1 . A: An object in three-dimensional space (axes) can be de scribed by the length vectors (height [hl. width [wl. depth [d]). B: The motion of an object can be described as three separate primary vectors of velocity. The actual movement of the object is represented by the resultant vector (r). C: A force (F) that is applied to an object may also be represented by separate force vectors in each dimension directed into the object. The object may be moved in a direction (v) by the force. D: If one component of the accelerating force is resisted, the object will move in a new direction (0), determined by the magnitude of the remaining vector components.

an axis system (Fig. 5 . 1 ) that is used to model three-dimensional space. By describing the vectors of movement i n each of these three dimensions, the motion of the object can be characterized. The actual path of the object is referred to as the resultant veloc ity vector. Biomechanical analysis uses simi lar vector systems to describe most parameters in space, such as velocity, acceleration, and pressure. Beyond simple models, the properties of each component of a resultant vector can become increasingly complex. For exam ple, an object of irregular shape will require more than a simple length measurement in each dimension to describe it. Similarly, an object moving i n space may also rotate about an axis. Be cause of this, even relatively s imple movements of body segments may require sophisticated mathematical modeling to describe the movement.

1 . D imensions and movement in three-dimensional space 2. The nature of applied forces

3. Properties of biomaterials

Objects and Movements in Three-Dimensional Space Can Be Described as Components in Each of the Three Dimensions

An object can be described by the magni tude of i ts size in each

of i ts dimensions (length, width, height; Fig. 5 . 1 ) . Similarly, s i m ple movement (translation) of an object i n three-d imensional space can be described as three different components (vectors) of movement (up/down, back and forth, in and out relative to the page) that can occur simultaneously. Vectors will have a mag n i tude and direction similar to describing the dimensions of an object, except that the magnitude of movement is expressed as velocity (meters per second) . Vector components are shown on

Applied Forces Can Also B e Expressed as Three-Dimensional Vectors

Applied forces, such as a manipulative thrust, are essentially pres sure (force per unit area) applied to an object. By definition, forces act to accelerate an object of a given mass. Accordi ngly, an ob ject at rest m ust have a force applied to it in order to achieve movement through acceleration. An object moving at a constant velocity will require no forces to sustai n movement, unless other forces (e.g., friction) are acting to resist the movement. The ob j ect's resistance to change of velocity ( inertia) is also described as the force required to accelerate it from rest (zero veloci ty) or to decelerate it from movement. The magnitude of forces and associated force vectors are used to describe external pressures appl ied to the body and internal forces l ike those generated in muscles to achieve limb movement. Force magnitudes are expressed as the mass of the object times

5. Biomechanics the acceleration (F mal. The metric unit of force is a newton (N) or I kilogram accelerated to a velociry of I meter per second each second (kg x m/s2). Like velocity, forces are characterized as a combi nation of vector components of a certa i n magni tude i n each o f the three axes defin i ng space ( Fig. 5. 1 ). The resultantforce is the sum of the individual force vectors. The manner i n which the object might be moved or mobilized by the force will depend upon which of the vector components are resisted and which are not ( Fig. 5 .1). Similarly, a resultant force vector arising fro m a manipulative thrust would be characterized by describing force components not only directly i n to the body, but also in lateral directions (rostral, caudal, medial, or lateral) as well as rotational components. Mobil ization of body segments by the force will depend upon which components of the thrust meet with direct resistance and obviously how the body is positioned. In biome chanics, it is important to characterize the different components that a force may have in order to understand the ensuing reaction of the material or body structures. =

Moments Are Forces that Act at a Distance and/or Produce Rotation of an Object

Forces that act to produce rotation of an object about an axis, or in two-dimensional models, a center point (Fig. 5 .2), are called force moments (also momentor torque). The magnirude of a force moment is the product of the force applied and the distance of appl ication from the center of rotation (force x distance). The latter distance is referred to as the moment arm. This is esse ntially a process of using a lever to produce rotation about an axis. Because of this relationship, i t is important to note that moments of the same magnitude may be produced by i ncreasi n g the force applied while proportionately reducing the moment arm or vice versa ( Fig. 5 .2). A common example of the properties of force

A. C

B.

:i ..

moments can be obtained from pus h i ng open a door (Fig. 5 .2). Pushing the door open at the handle usually is relatively easy (low force), because of the long d istance (moment arm) between the handle and the center of rotation at the h inge. Note, h owever, that opening the door at the handle requires a relatively large d istance of movement (large d isplacement). Attempti ng to push the door open at a poi n t near the h i nge (short moment arm) is m uch more difficult (greater force), but requires less displacement to open the door. Note also that the direction or angle at wh ich the push is applied to the door will determine how m uch of the force applied is acrually used to push rhe door open ( Fig. 5 . 2 ). This rotation component of the applied force is at a right angle to the surface of the door (directly i n to the door) at any i nstant. The rema i n i ng force component will be i n a direction along the surface of the door. For the same openi ng force to be maintained , t h e direction of t h e applied force m ust change constantly t o move in a circle with the door. The strategy of changing the force or the length of the mo ment arm and the direction at which forces are applied is often employed i n body mechanics and in manipulation techniques, depending upon the need for more or less force at the cost of greater or lesser displacement. Moments are used i n the b iomechanical modeling of body motion because most movements are composi tes of rotational movemenrs of individual body segments around j o i nr s . Force moments are generated from the contracrion of muscles attached between two body segments causi ng the movemenr of the more mobile segment around a center of rotation (Fig. 5 . 2). The center of rotation is usually near the articulation surface in the less mo bile segment. The moment arm of the contracting force is related to the distance of the m uscle insertion on the mobile segment from the cenrer of rotation. In simple biomechanical models of body movement, this center of rotation i n the joint is usually shown as i mmobile. I n actual movements, both segments may be mobile and motions within the joint may also occur ro change the center of rotation.

...

...

,\

Stresses Are Forces Applied to Objects in Various Orientations

'rna

. -- ,

� C.

D.

65

f

rn

pr

"-', \

�

f

cj

(f) applied at a distance (moment arm, rna) in the middle of the door can produce rotation (dotted arrow) around a center or axis (c) located at the hinge. The moment is the force applied times the distance (d) from the center (f x d). A smaller force acting on a longer moment arm at the doorknob (B) will produce the same moment (f x d). C: If the force is applied in a direction other than directly against the moment arm, only part (pr) of the force will be used to produce the rotation. D: In the body, force moments are generated by muscle contraction forces (m) that produce rotation of a mobile body segment about a center in the joint (CJ)' FIGURE 5.2. Force moments on an object such as a door. A: A force

The characteristics of forces applied to an object are described as stresses (Fig. 5.3). The magnitude of basic stresses is described as force applied over a defined u n i t of object surface area or pressure. This may be described as pou n ds per square i nch (psi) or in the metric form, pascals ( N per square m). Particular rypes of stresses are identified to describe their relationship ro the object acted upon ( Fig. 5.3). For convenience, stresses are usually described for an object that is i mmobilized or constrained, such that the object m ust resist the stress and not undergo acceleration or movement other than deformation (see "Strai n Is Deformation Produced by Stress," later in the chapter). Tension is a force applied perpen dicularly outward from the surface of an object (pull), such that the object would be elongated or stretched. Compression stress is a force applied perpendicularly inward (push) to the surface of an object, such that the object would be shortened or compressed. Shear stresses are forces applied parallel to the surface of an object. Torsion stresses are rotation-like forces, which on a constrained object, act to twist it about a neutral axis (that is, an axis that

66

I!.

A.


B.

c.

t

D.

E.

F.

B.

A.

c c

a

FIGURE 5.4. A: Bending strain produces tensile stress (t) on one side of

an object and compressive stress (c) on the other. B:This same principle applies directly to biologic materials, such as spinal discs. FIGURE 5.3. A: Stresses are forces acting from various orientations rel ative to the object. Stresses are named according to their action upon the object. B: Tensile stresses act to stretch an object. C: Compressive stresses compact the object. D: Shear stresses act parallel to the sur face of an object. E: Bending stress acts to fold an object about an axis. F: Torsion stresses twist an object about an axis.

would not be translated or moved by the force) . Bending is also technically a rotation-like force (or coupled coactive forces) that acts to fold or bend an appropriately constrained object along a neutral axis. The sum of all stresses on an object is termed Load.

BEHAVIOR OF MATERIALS SUBJECTED TO FORCES The Behavior of an Object or Material May Be Isotropic or Anisotropic

While stresses may originate from external forces applied to an object's surfaces, they are also rransmirred from the area of contact rhrough the en tire substance comprising the objecr. The primary factors affecting the rransmission of forces through an object are its shape and material composition including infrastructure. The characteristics of the material composition of the object will de termine if the object can be accelerated or rotated by a stress of sufficient magn i tude or physically broken by ir. The s hape of an object may dramatically affect the manner i n which it responds to similar stresses exerted in different places on the objecr. An ob ject, such as a sphere of homogenous composition, will respond in the same way to a particular type and magnitude of stress ap plied to any point on its surface. This type of object is referred to as isotropic in relation to stresses. Objects having a nonuni form surface shape (such as an irregular cube) or heterogeneous composition will respond to the same stress differently depend ing upon the point of appl ication. These objects or materials are referred to as anisotropic. Most biologic structures fall i n to this category. As with s urface characteristics, the i n ternal structure or com position of an object will also determine i ts response character isrics to stresses. The object's composi tion and molecular i n fras trucrure determine how a force appl ied to a palTicular location is transmitted to the remainder of the object's mass. In objects that have an an isotropic i n ternal composition, such as biologic mate-

rials, localized i n ternal stresses are often the primary determinant of the toleration of the material for s tresses of a particular magn i rude and orientation of a stress. As discussed subsequently, bone, muscle, tendons, and ligaments have a linear cel l ular/molecular structure that causes the response to loads to differ dramatically depending upon the orientation of the applied stress. Strain Is Deformation Produced by Stress

As muscles contract, they apply primary localized tensile stresses to bone to accelerate the mobile segment(s) and to stabil ize the immobile segment(s) . Under this cond ition, the applied stresses produce a change in the shape of the bone or object (deformation) . The magn i rude of deformation produced by stress is referred to as strain. The actual deformation of an object will depend upon the same factors defi n i ng stress disrribution (i nternal composition and infrastructure) and is characterized as a sum of different srrain vectors. These vectors are usually named for the type of srress producing them (e.g., tensile strain, compressive strain, etc.). Many differen t strain vectors may be produced within an object by a particular type of stress. A simple example is a bendi ng stress that produces tensile strain on the side of the object opposite the neutral axis and compressive strain in the direction of bending ( Fig. 5 . 4 ) . A similar condition exists with strain on a spinal disc with bending between segments. The Elastic Modulus Shows the Relationship Between Stress and Strain

While it can generally be assumed that increases in stress on an object will produce an i ncrease in strain, the relationship is not di rect, particularly for biologic materials. The relationship between the amount of a particular stress applied ro an object and the re sulting deformation or strain is shown by a stress/strain curve (Fig. 5 . 5 ) . In this instance, a material is subjected to a defined stress such as tension. I n this model, the strain may be quantified as the change in length of the object (as with a tendon or l iga ment). A similar result could be obtai ned by the displacement of the center of a bend ing load (as with a bone). Stress/strain rela tionsh ips for most materials have a li near region (elastic behavior) in which increasi ng stress produces a corresponding amount of deformation (Fig. 5 . 5 ) . Reducing the stress or unloading of the

67

5. Biomechanics

Material failure

Elastic Stress Modulus - Strain _

•• 1========1••

\

.... tensile . stress

--

..

strain

•

•

rn rn Q)

..

....

en

Strain (deformation) FIGURE 5.5. A stress/strain curve (right) of an object undergoing increasing tensile stress (left). The change in length can be used as a measure of strain. The curve has an area of elastic behavior, in which a release of stress will allow the object to return to its original shape. In this area, the stress/strain relationship can be expressed as elastic modulus. With increasing stress, the material has permanent deformation or plastic behavior, followed by material failure.

object will allow it w re[Urn w i ts former shape withom a perma nem change in shape. In this elastic area of the stress/suai n curve, the slope of the line (suess/strain) is termed the elastic modulus. The elastic modulus is also a quamitative description of stiffness, a term commonly associated with the amount of force necessary w bend an object. When an applied stress is greater than that defined by the elastic area ( Fig. 5 . 5 ), a permanem deformation of the material or plasticiry will result. The plastic behavior area of the curve ends with the material failure or breaking of the object. Materials may also be described as brittle or ductile depending upon the amoum of deformation they can undergo before failure. Brittle objects such as glass will undergo l i ttle deformation before they break (fail) , and the pieces after breaking retain their shape such that pieces will fit wgether w produce a puzzlelike reproduction of the object with little deformation. Ductile materials s uch as a copper wire will have a permanently altered shape beyond their elastic region and after failure. Many facwrs other than basic suuc[Ure of a material may significantly affect the stress/strain relationship. The most common of these are temperature and the rate at which a stress is applied.

Viscoelasticity Is the Combination of Elastic and Viscous Properties of Materials in Response to Stress

The rate at which a stress is applied can be a particularly im portant determ inant in the response of materials that exhibit a combination of both elastic and viscous behavior in response w an applied stress. Viscous behavior can be described as resistance w flow, such as that observed with cold syrup. Viscosiry i n biologic materials arises largely, but not completely, from the resistance of their water content w flow i nw and out of the material with

appl ied suess. For example, spaces between molecules of collagen in ligamems comain a large amoum of water w i rh salts and other small relatively mobi le molecules. Tensile suess (suetchi ng) of the ligamem will decrease the available space between collagen molecules, forcing the fluid between them out of the l igament. This process is s imilar w stretching a wet sponge (Fig. 5 .6). If the suuc[Ure i s suetched rapidly, there is an i ncreasing resistance w fluid movement out of (and into ) these spaces, s ince this

reep

L2

b

.� CIJ

C Time

Stress/relaxation

Time FIGURE 5.6. left: Viscoelastic behavior occurs when a material con

taining a mobile fluid phase is stretched (or compressed) from a resting length (L 1) to force fluid out of an elastic matrix similar to a sponge to a greater length (L2). This can be modeled schematically (bottom) as a spring in parallel with a fluid containing resistance compartment with porous baffles. Right: Time-dependent viscoelastic behavior of a mate rial under tensile stress. Creep (top) is a measure of deformation (strain) over time with stress (stretch force) held constant. Stress/relaxation (bot tom) is a measure of stress over time with strain held constant. (Portions of this figure have been adapted from Carlstedt CA, Nordin M. Biome chanics of tendons and ligaments. In: Nordin M, Frankel VH, eds. Basic Biomechanics of the Musculoskeletal System, 2nd ed. Philadelphia, PA: lea & Febiger; 1989:59-74, with permission.)

68

II.


requires time. The time required for A u i ds to move out of i n termolecular spaces acts to slow the rate of deformation of an elastic material. This alters the elastic and plastic regions of the stress/strai n curve. In combi nation with the elastic properties of the material, this behavior i s described as viscoelasticity. This prop erty is usually modeled as a spring acti ng in parallel to a resistance provided by a Auid compartment (Fig. 5.6). Besides the Aow of small molecules from i ntermolecular spaces, frictional resistance due to molecular movement and ionic i nteractions between molecules also contributes to the viscosity in a material. These molecular i n teractions, along with the elastic properties of the material, are i mportant in the return of water and other small molecules back i nto the matrix, again m uch as a sponge reabsorbs A u i d after being squeezed. This recovery pro cess is i mportant if the biomaterial properties of the tissue are to be maintained under repeated loading. Additionally, s ince vis coelastic behavior involves the movement of small molecules and the i nteraction between molecules, temperature can significantly affect this property. Viscoelastic properties can produce significant alteration of material behavior when the rate of loading is too fast for the Auid exchange to occur. Under these conditions, a material may exh ibit a higher elastic modulus (that is, appear stiffer or more brittle) under h igh loading rates, as compared to the same load applied over a longer period of time. If a viscoelastic material is stretched rapidly and the load is sustained after the initial loading period, there will be a rapid i n itial deformation of the material followed by a slower deformation as the remain i ng Auid i n the matrix reaches a new equilibrium at a slower rate (Fig. 5.6). Two types of measurements are used to describe this property. First, if the material is subjected to an i n itial load, such as tensile stress (Fig. 5.6), which is then maintained, the material will stretch to an ini tial length and then more slowly increase in length as the more resistant Auid i n the matrix effuses. The slower phase after the ini tial stretch is called creep. Another measurement looks at the load necessary to maintain a constant deformation or, i n the case of Fig. 5.6, the length of the material. As the matrix reaches equilibrium, the load necessary to maintain the length will decrease. This property is referred to as stress/relaxation. Because of their high water and solute content, bone, muscle, ligament, tendon , and other biologic materials have viscoelastic properties that are i mportant for their function. Due to the dif ferences in the cellular structure and the matrix between cells in these materials, the actual viscoelastic properties of these tissues differ markedly.

adapt materials to repeated stress. For example, bone under re peated stress may u ndergo microfractures in its structure (see the following section). Depending upon the frequency of the stress and the ability of the bone to repair these microfractures, the bone may suffer a fatigue fracture or adapt to the stress by i ncreasi ng ItS mass.

PROPERTIES OF BIOLOGIC MATERIALS: BONE Bone Is an Anisotropic Material Comprised of Osteons

Mechanical models describing non biologic materials are difficult to apply to biologic systems directly, due in parr to their com plicated structure. The response of biologic materials to stresses is determined by structural properties layered down to the sub cellular level. Still, the material properties of bone structure as a whole are clearly traceable from tissue structure (I). Bone con sists of connective tissue cells organized and embedded in a highly m ineralized extracellular matrix. Although lower than other tis sues, this matrix also contains significant amounts of water and other small molecules, giving bone viscoelastic material proper ties. The basic unit of organization is the osteon or haversian system . These systems consist of concentric ri ngs of bone cells or osteocytes around a central cavity (the haversian canal) through which the blood vessels and nerves supplying the bone travel (Fig. 5 .7). The osteons are arranged in a dense, regular pattern around the shaft of long bones to form cortical or compact bone. The border between osteons is the cement line. The cement line is structurally weaker than the substance of the circularly oriented osteons and can often be identified m icroscopically as the site of failure of bone tissue under h igh stresses (2). Osteocyte lacunae may also be a site of structural weakness (3). Beneath the corti cal layer of compact bone is a cen tral core of more porous bone

Fatigue is the Failure of a Material as a Result of Repeated Stress

Fatigue is a mul tifaceted term that is used to describe material failure after repeated application of stresses that, if applied in dividually, would not produce failure. In non biologic materials such as metals, a significant part of fatigue failure can result from the accumulated breakdown of crystalline structure as the result of repeated stress, such as breaking a steel or copper wire by re peated bending. In biologic systems, the process of fatigue failure becomes more complicated, because of the ability to repair and

FIGURE 5.7. Histologic and structural properties of bone. A: Compact bone structure is organized into cylinder-shaped osteons with haver sian canals (H) that are separated by a cement line (outline). B: In long bones, osteons are oriented longitudinally along the axis of the bone and surrounded by circumferentially oriented lamellar bone (L). Both surround a marrow space that contains marrow and cancellous bone. C: The organization cancellous bone is not random in structures such as the femur, where the trabeculae (black) help to distribute stresses through the internal structure of the bone.

69

5. Biomechanics (termed cancellous, trabecular, or spongy bone), with lacunae comprisi ng the marrow space. While the structure of cancellous bone may i n itially appear as a random mesh of thin bone, it can be readily shown that areas of organization do exist and contribute to the structural stability of the bone as a whole by distributing stresses i n ternally i n the bone structure (4) (Fig. 5 .7). Bones Are Structured to Resist the Primary Functional Stresses Placed Upon Them

As might be expected, the h ighly o rganized cellular and gross structure of bone causes it to behave in an anisotropic manner to applied stresses. The ourward structure and i n frastructure of bones are organ ized to resist the major stresses to which they are subjected under normal physiologic conditions. For the structure of a long bone such the tibia, the compressive loading lengthwise will require much h igher stress before failure compared to a stress of similar magnitude applied perpendicularly to the long axis. In this manner, from the subcellular to gross structure, bone represents one of rhe most obvious examples of the structure to-function relationsh ip. This anisotropic behavior also defines the manner in which bones will undergo material failure when excessive stresses are placed upon them. Different Stress Vectors Produce Varying Types of Bone Failure {Fracture}

The material failure (fracture) of bone can be observed clinically for all major categories of stresses, wi th the mechanism of material failure varying with type of loading ( I). Also, the viscoelastic be havior of bone gives it sensitivity to load i ng rate. At rapid loadi ng rates, bone appears stiffer as the movement of Auid and molec ular friction increasingly resists deformation. This causes bone to store more energy before failure. When bone does fai l at h igh loading rates, its more brittle behavior makes it more l i kely to fragment, much like shattering glass (commi n u ted fracture) ( 5 ). Accordi ngly, fractures can also be categorized i nto different types accordi ng to the energy absorbed with the resulting failure, low energy, h igh energy, and very h igh energy. H igher energy fractures (automobile accidents, gunshot wounds) are typically accompa n ied by bone fragmentation and soft tissue damage, as the energy stored under rapid load i ng is dissipated with biomaterial failure. Under physiologic conditions, bones will experience a com bi nation of stress vectors at the same time and fail ures may result from the combination rather than a parricular stress type. How ever, fractures do begin in the stress component d i rection most prone to failure according to the material properties of the bone. This allows the description of some types of fracture resulting from particular stress categories. Muscles pulling on bone typi cally generate tensile stress fractures. The tensile fracture of the calcaneus adjacent to the Achilles tendon i nsertion is a frequent example ( Fig. 5 . 8 ). Compression fractures are most commonly found in the vertebral column, which is subject to h igh compres sive load and a weakening of the bones with age. S hear forces act parallel to bone surfaces, typically at articulations, where bones are in contact. Shear fractures can occur under conditions of com pression loading of a joint, coupled with a shear or lateral force across the articulation with a failure of the joint bony plateau.

A.

B.

c.

D.

t FIGURE 5.8. Examples of fracture types resulting from a material fail ure due to a primary stress component. A: Tensile fracture of the cal caneus. 8: Spiral fracture from torsional stress of the tibia. C: Bending stress fracture. D: Example of how muscle contraction forces can act to counter bending stress. Bending stress produces tensile forces on one side of the tibia and compressive stress on the other (see Fig. SA). Mus cle contraction can act to counter the tensile component by producing a compressive moment. (Portions of this figure have been adapted from Gollnick PO, Matoba H. The muscle fiber composition of skeletal mus cle as a predictor of athletic success. An overview. Am J Sports Med. 1984;12:212-217, with permission.)

Bending and torsional load i ng produce multiple types of material stresses on bone depending upon the d i rection of the loading. As described earlier, bending of an object produces tensile stress on one side of an object and compression on the other ( Fig. 5 . 4 ). Bone is weaker i n tension than compression, so bone material fai l u re begins upon the tensile stress side ( Fig. 5 . 8 ). Immature bone, which is less calcified and more ducti le, may be more sen sitive to compression and fractures may occur on the compressive side first. Torsional loading ( Fig. 5 . 8), or usually rwisting aroun d t h e l o n g a x i s of bones, produces shear stresses around t h e neutral axis while compression and tension loading are diagonal to the axis. The resulting failure (spiral fracture) is in i tially due to shear stress followed by tensile stress fai l u re along a diagonal axis. As should be expected, if there are weaknesses in the bone structure, such as duri ng rehabil itation after i n j u ry, failure will occur at the weakest poi n t or at the site of bony defect with bend i ng loads. The biomaterial fai l u re of bone u nder stresses is greatly in A uenced by the artachment and contraction of muscles. Muscle activity can decrease or counter stresses produced on bone by altering the d i rection of the resultant stress vectors to those to which bone may be more tolerant. Fig. 5 . 8 shows how m uscle activity may alter a bendi ng or tensile stress to produce compres sion stress. As bone is very resistant to compressive stress (such as weight on the l o ng axis of the tibia), this redistribution of stress can be important to avoiding stress fracture. Consequen tly, the physiologic tiring of muscle during strenuous exercise can con tribute significantly to fractures because the protective mech anism is lost. While sudden, large stresses are usually associated with bone fracture, failure of the material i tself can result from repetitive loading over a period of time. This fatigue-type fracture of bone i nvolves an accum ulation of smaller failures within the bone mi crostructure and is dependent upon the magn itude, frequency, and rate of loading. Even low-level repetitive loads may produce fatigue m icrofract ures in bone (6). In l iving bone, these m icrofrac tures will be repaired by cell ular reactions to the i n j ury. If the

70

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fatigue process outpaces the repair, failure will eventually occur as a repetitive stress fracture. A common example of this is the fatigue fracture of metatarsal bones in long distance runners (7).

A.

c.

Bone Remodels Its Structure in Response to Stress and Depends upon Stresses to Maintain Its Material Properties

In the presence of stresses, bone can alter size, shape, and struc ture to withstand stresses placed upon i t. The unusual corollary to this property is that bone must be subjected to stress in order to maintain i ts biomaterial properties. The underlying principle of this process i n bone has been expressed as Wolff law, which states that bone is increased where needed and resorbed where not needed (8). The resorption of bone under conditions of reduced usage or immobil ization (9) are of particular concern cli nically, since mechanical stress on bone is reduced during casting or i n more l i mited conditions, such as weightlessness i n space travel ( 1 0). Immobilization results in the resorption of periosteal and subperiosteal bone ( 1 1 ) and a decrease in bone strength and stiff ness ( 1 2). Conversely, the hypertrophy ( 1 3 , 1 4) and i n crease i n dens i ty o f bone ( J 5 ) may b e observed i n normal bones i n re sponse to strenuous exercise. Both hypertrophy and resorption of bone may be observed around implant screws and plates used to surgically stabil ize bone defects or to attach prosthetic j o ints ( 1 6). Bone properties also are altered with aging, with a progres sive loss of bone densi ty and size ( 1 7, 1 8). This is independent of the condition of osteoporosis. The result is a decrease i n bone strength and stiFFness a n d altered stress/strain properties, including an increase in brittleness and a reduction in energy storage capacity. These properties make bones more susceptible to material failure under h igh stress conditions with increas i ng age.

FIGURE 5.9. A: Schematic of the orientation (arrows) of collagen fib rils (drawn lines) in articular cartilage. The orientation varies from the articular surface to the bone interface. B: Representation of cartilage surface separated by a thin layer of lubricating fluid (L) that prevents direct surface contact. C: With a compressive force on the surface (ef) additional fluid is exuded and the matrix is compressed. Lateral move ment produces tensile (t) and shear (s) stress on the cartilage surface and matrix components.

The major collagen and proteoglycan structural element on the cartilage of articular surfaces is not randomly organized and can be divided i n to histologic zones that differ in cellular orga n ization from rhe surFace ro the underlying subchondral bone (20) (Fig. 5.9). The orientation of collagen fibril bundles within the matrix differs berween the layers (Fig. 5.9) with a tangential orientation at the surFace, random organ ization i n rhe middle zone, and radial oriemation near the subchondral bone surFace. This orientation provides the basic structural Framework for the cartilage and resistance to the loads placed upon it. Depending upon the particular joint function, the primary stresses may be compression, which, as the joint moves, contributes ro shear and tensile srresses on rhe cartilage surFaces (Fig. 5.9).

ARTICULAR CARTILAGE The Surfaces of Contact Between Bones in

Cartilage Has Significant Viscoelastic

Synovial Joints Is Hyaline Cartilage

Properties That Are Essential to Its Function

There are three identified primary types of cartilage in the h u man body: hyaline carti l age, fibrocartilage, and elastic cartilage. Hyal ine cartilage covers the surface of the articulations of almost all diarthrodial joints, and will be the focus of our description of basic biomateria.l properties of cartilage. Car t ilage has some simi larity to bone i n that i t consists of cells (chondrocytes) surrounded by an extensive extracellular matrix rhat rhey secrete. However, cartilage is avascular; lacking blood vessels, lymph channels, or nerves within its matrix and the matrix secreted is not calcified as in bone. The extracellular matrix of cartilage consists primarily of collagen (type I I ) , proteoglycans, and 60% to 87% water with in organic salts and orher m inor matrix proteins and lipids ( 1 9,20). The collagen and proteoglycans form the major structural ele ments of cartilage, and these i nteract extensively on a molecular level with the smaller molecules, i ncluding water. The i nterac tion of these e1emems with each other within cartilage and their interaction with the water in the matrix determine the primary biomaterial properties of cartilage.

The collagen and proreoglycan structural elemems of cartilage have spaces berween them fi lled with water, salts, and other small molecules, forming a matrix with viscoelastic properties as previously described. Further, the strucrural elements contain molecules such as hyaluronic acid and have ionically charged groups rhroughour their structure. This property allows them to strongly bind water and inorganic salt within the cartilagi nous matrix. The cartil age matrix has properties of flexibility from a pliable, porous collagen superstructure containing small molecules thar can be Forced our, but with some molecular and ionic i nteracrion based resistance to the efflux. The properties of this matrix allow a viscoelastic behavior in which the carti lage allows rapid, but declining deformation (cushioning) in re sponse to compressive loads followed by creep or stresslrelaxation ( 2 1 ) (Fig. 5.7). The slower deformation will continue until equilibrium is reached berween the load and the Forces resist i ng it within the matrix. The differi ng mechanical properties of the layers of articular cartilage i nteract dynamically to reach

5. Biomechanics equilibrium in response [Q a sustained compressive force (22). On a tissue level more closely related [Q normal funcrion, the viscoelastic response of carrilage can be explained by a compres sive stress that p[Qduces a rapid efflux of fluid forced out of the exrracellular man'ix direcdy beneath it and in areas immediately adjacenr [Q it ( Fig. 5.9). The resistance [Q this efflux of fluid is dependenr upon the effective porosiry or space available i n the carrilage marrix for Auid [Q move. Other resistance [Q marrix de formation i ncludes the i nrernal friction generated by movemenr berween long polymer molecules such as collagen and attached proteoglycans and the ionic binding of these chains [Q the wa ter and other small molecules. The time required for the fluid phase [Q reach a full equilibrium berween cartilage layers under the appl ied load may require hours (2 1 ). However, because of the elasticiry of the collagenous strucrural e1emenrs and ionic i nrerac tions with the small molecules of the matrix, this Auid exchange is reversible and supplies a pumping action of nutrienrs into and waste products out of cartilage in add ition to normal diffusion. This action is parricularly importan r because of the avascular nature of cartilage. Articular Cartilage Has Several Properties That Act to Prevent Wear Damage

Under physiologic conditions, cartilage surfaces of joinrs conracr each other under a variery of loading conditions while showing litde wear. This occurs in spite of the fact that j o i nr surfaces are not perfecdy smooth. The prevention of wear is due in part to a system of lubrication of synovial articular surfaces provided by synovial fluid and the properties of the carrilage itself. Fluids lubricate surfaces by prevenring their direct conract ( Fig. 5.9). The first level of lubrication of j oi nr surfaces is the absorption of lubricin, a glycoprotein in synovial Auid that is absorbed onro arricular surfaces. This provides a thin boundary of lubricanr o n the j o i n t surface. The synovial fluid itself also provides a thin film offluid berween the joint surfaces that can be redisrributed under loading conditions. Further, duri ng loading the Auid exrruded as a result of the compressive deformation of the cartilage will provide a Auid layer to separate the opposed surfaces (23). Under normal conditions, the fluid lubricating properties of the joint will prevenr the direct conracr of uneven sections or asperities of joint surfaces to contacr each other. If conract does occur, wear of the joinr surfaces or i nterfacial wear (mechanical removal of material from a solid surface) may occur. This may consist of abrasion of the joint surface because of contact of un even elements of the surface or small fragments of joinr surfaces may adhere to each other and be dislodged. The efficient lubricat ing properties of normal joinr usually preclude i nrerfacial wear, but it may occur in damaged or degenerated joints (22) . Cartilage Wear May Result from Several Different Mechanisms, Including Intrinsic Changes with Aging

While cartilage can be damaged as a result of rraumatic injury as in shearing stress applied to the meniscal cartilage of the knee, the mechanisms of abnormal wear are not as clear. Hypotheses of the

71

mechanism o f carrilage wear include the disruption o f the struc rural molecules of the cartilage matrix through repeated stress (24 , 2 5 ) and the alteration of the matrix contenr under the same conditions. As with bone, rapid loading of a viscoelastic mltrix i ncreases the stiffness of cartilage, and the loss of the fluid com ponenr of the matrix will also increase stiffness. This loss of fluid may include soluble proteoglycans from the carrilage surface that are importanr in the main tenance of its properties. Under con ditions of rapidly repeated high-impact loading, the fluid forced from the marrix that would normally provide a cushioning effect cannot be reabsorbed in time to cush ion subsequenr impacts. This may also produce plastic deformation of cartilage surfaces that does not sufficiendy recover for smooth surface conract upon subsequent loadi ng. The increased stiffness and deformation of the matrix increases the l i kelihood of mechanical wear in addi tion to rendering the subchondral bone surface more vulnerable to damage. Cartilage wear may also be complicated by the l imited capac i ry of cartilage to repair or regenerate. This properry gives it a limited capaciry to adapt to stress. In conjunction with repeated stresses and minor i njuries, a cycle of damage, wear, and i nsuffi cient recovery may occur, leading to joint degeneration and/or os teoarthritis. The inabil i ry of cartilage to recover during repeated h igh stress loads may be one source of macroscopic structural defects observed i n carrilage (26) and responsible for the high i ncidence of specific j oi nr degeneration and the development of osteoarthritis i n persons with certain occupations (football play ers and dancers). The i nrrinsic composi tion and properries of carti lage also change with age (27). The matrix composition changes and per meabiliry increases, decreasing carri lage stiffness and rendering it less resistant to rapid loadi ng. Along with the accumulation of injuries from which the tissue cannot recover, these age-related changes may conrribute to the i ncreased i ncidence of j o i nt de generation with age.

LIGAMENTS AND TENDONS Ligaments and Tendons Are Dense, Regular Connective Tissue with a High Resistance to Tensile Loading

Ligaments and tendons, along with j o i nr capsules, surround the arriculations of the skeletal system. Their functions are, i n the case of ligaments and joinr capsules, to structurally connect, sta bilize, and guide the bones formi ng the articulation ( 28). They may also act as a sensor for joint position and strain for the joint. Tendons connect muscle to bone and transmit forces from mus cle to bone to produce motion. Both tendons and I igamenrs are classified as dense, regular connective tissues. They have sparse cellular elements and abundant extracellular matrix in a highly organized array. The extracellular matrix is rich in collagen and water with a small amount of elastin, again produci ng a viscoelas tic behavior under stress. The collagen molecules are l i nked [Q gether in lengthwise overlapping arrays [Q microfibrils, that are in rurn combined i n similar overlapping arrays [Q form fibrils, then fibers, and bundles of fibers to form the macroscopic tendon (Fig. 5 . 1 0). This successive paral lel linkage down to the molecular

12

If.


Endotendon

Plastic Region

FIGURE 5.10. left: Schematic view of the structural organization of

tendon. Microfibrils are the smallest component consisting of collagen molecules. Microfibrils are organized into fibrils that are g rouped into fibers. Fibers are grouped into fascicles that comprise the tendon. Right: Idealized version of a stress/strain curve for tendon under tensile stress. The toe region is a nonlinear behavior attributed to the "slack" between collagen molecules. The elastic region has a linear relationship between stress and strain. In the plastic region, permanent deformation occurs, eventually resulting in failure.

level makes ligamems and tendons capable of handling high ten sile loads. The arrangemem of fibrils i n ligamem tissue i s less par allel than tendon and accoums for its higher resistance to tensile loadi ng in oriemations other than along the tissue axis. The colla gen molecules are also l inked to each other by cross-links. While there are some importam biomechanical differences between lig aments and tendons, most of their properties are basically similar and will be described together here.

The Primary Biomaterial Characteristics of Ligaments and Tendons Are Described by Elastic Modulus and Viscoelastic Properties

The primary stress response characteristics of ligamems and ten dons are described by their modulus of elasticity properties. Un der tensile loading (stretch), l igaments and tendons exhibit a modulus of elasticity that is variable with load (Fig. 5 . 1 0) . Un der low loading, there is a relatively large i ncrease i n length i n response t o t h e load applied (low elastic modulus). T h i s i s at tributed to lengthening as the result of macromolecular "slack" within the coll agen fiber structure that offers less resistance to an imposed load. As the slack is taken up, fibers slide relative to each other and A u id is extruded ftom the matrix. The elastic modulus then increases (stiffness increases) gradually with i ncreas i ng load and shows a l inear response up to the poi m where failure begins. The behavior of tendons and l igaments is similar except for l iga ment tissue such as the ligamemum flavum of the spinal column, where a high elastic content ptoduces a different pattern of the elastic modulus. The extracellular matrix of tendons and ligamems between the collagen fibrils has proteoglycans, a high water content, and other small ionically charged molecules that can imeract with structural elements. This matrix i s comparatively more porous than cartilage or bone, and is structured to resist tensile rather than compressive stresses. The viscoelastic properties become ev idem at high load i ng rates, where the tissue will demonstrate increased stiffness and offer i ncreased resistance to tensile stress (stretch). As with cartilage, repeated tensile loading i n cycles can result in a slow increase in elastic stiffness due to plastic de-

formation (29,30). This plastic deformation is presumably due to molecular deformation in the fibrous structural elemems of the tendon or l igament, and also to the inabili ty of fluid and small charged molecules to reequilibrate within the molecular structure. Ligamems and tendons also demonstrate the viscoelastic prop erties of stress or load relaxation and creep. To characterize these properties, the tissue is placed under a tensile load (stretch) within the l inear region of the elastic modulus and mai ntained at a con stam length (stress relaxation) or a constant load (creep). Liga meJ1[ and tendon tissue adjusts its molecular structure and A uid distribution to the load primarily within the first 6 to 8 hours, but will continue over a period of months. The creep phenomenon is used clinically as plaster casts or braces are employed to place a constam load to correct a soft-tissue deformity, such as some spinal curvatures (3 1 ) .

Material Failure of Ligaments and Tendons Is Preceded by Microfailure of the Molecular Structural Elements

Overall failure of the l igament or tendon is usually sudden and preceded by the m icrofailure of the attachments between colla gen fibers within the tissue and loss of the ability of the tendon or ligamem to recover i ts length. With tendon and ligament, it is also importam to distinguish eventual failure due to a sustai ned load (creep failure) from sustained cyclic loading and unload ing (fatigue failure). Both are important biomaterial properties for tendon and ligament. As with bone, a smaller degree of mi crofai lure may occur within the range of physiologic loading, suggesting that repeated stress may lead to decli ni ng strength or fatigue over time (32). There may be a range of damage depending upon the total deformation and extent of partial failure. I n flam mation resulting from such damage is associated with tendonitis (32). Failure of both tendons and l igaments may also occur at the bone i nterface. The site of failure may depend upon the loading rate (33). Tendons, with their attached muscles, typically have a h igher tensile strength than muscle, and rupture of muscle is more common than tendon. The instability of the joint that may result from tendon, or especially ligament, damage can contribute to and be complicated by damage to the joint capsule. This dam age and associated abnormal loading patterns may contribute to osteoarthri tis (3 1 ) .

Ligaments and Tendons Can Adapt to Stresses

Like other tissue, l igament and tendon structurally remodel i n response to t h e stresses placed upon them within the limits of damage (32). They become stronger and stiffer with increased stress and weaker and less stiff with a reduction in stress (34). Physical tra i n i ng can increase the strength of tendons and liga ments along with the l igament-bone i nterface (35 ,36). Immo bilization (such as from casting) can decrease the strength and stiffness of ligaments. While reconditioning can occur, it can re quire a considerable length of time (34,37).

5. Biomechanics

73

The Properties and Structure of Ligaments and Tendons Change with Age

During maturation, the number and quality of cross-l i n ks increases in the collagen of l igaments and tendons and fibril di ameter increases as well (38) , producing i ncreased tensile strength. The mechanical properties of collagen reach a m aximum with maturation and begin to decrease with age (39) . The coll agen content of l igaments and tendons decreases as well. This loss of collagen results in a decrease in strength, stiffness, and the amount of deformation requi red to produce to fai l u re (40). H owever, the overall biomechanical properties of tendon remain reasonably constant with age (4 1 ) . The amount of time requ ired for tissue re pai r and recondition ing (discussed previously) will also i ncrease. Other physiologic factors, such as pregnancy, can also affect the biomechanical properties of l igaments and tendons (3 1 ,40).

SKELETAL MUSCLE

erimesium Endomesium

Fascicle

Fiber

Myofibril

FIGURE 5.1 1 . Schematic of the structural organization of a muscle. The basic subcellular unit of the muscle is the myofibril. Collections of myofibrils are present in muscle cells (muscle fibers). Muscle fibers are organized into fascicles and groups of fascicles make up the muscle. The connective tissue coverings of the muscle include the endomysium that surrounds muscle fibers, the perimysium surrounding muscle fascicles, and the epimysium surrounding the entire muscle.

Skeletal Muscl e Provides the Forces for Body Movement

Since a more complete description of m uscle is given elsewhere i n this volume, only those elements essential t o understanding the biomechanical aspects of muscle tissue will be given here. Of the three types of muscle tissue, skeletal muscle is the most abundant tissue i n the body, accounti ng for 40% of body weight (42) . The forces necessary to provide movement to the body are provided by the contraction of skeletal muscles acting across joi nts. These contractions may produce dynamic work or participate in static maintenance of posture. While subcellular units known as sar comeres are the source of muscle contraction, the basic contractile unit of skeletal muscle as a tissue is the musclefiber. The fiber may range in size from 1 0 ro 1 00 fJ- m in diameter and between 1 and 30 cm in length (43). The metabolic and contractile properties of m uscle fibers may differ accordi ng to the physiologic demands placed upon them as described subsequently.

Both Contractile Elements and Connective Tissue Contribute to the Biomechanical Properties of Muscle

Muscle may be h istologically and mechanically described as bun dles of contractile elements in a series of connective tissue sheaths (Fig. 5 . 1 1 ) . The basic unit of the contractile/connective tissue relationship is an individual muscle fiber surrounded by a con nective tissue sheath, the endomysium. This basic unit of skeletal muscle is then organ ized into fascicles or groups of fibers by a thicker connective tissue sheath, the perimysium. Finally, groups of muscle fascicles are organ ized into the entire m uscle itself and covered by the epimysium, which surrounds the entire structure. The epimysium and loose connective tissue form the fascial planes between muscles. The connective tissue sheaths are continuous with each other and the m uscle tendon and/or attachments to bone. Both connective tissue and the contractile elements con tribute the biomechanical properties of m uscle. The contractile elements provide active energy expending forces with some elas tic and viscoelastic properties, while the connective tissue con-

tributes passive elastic and viscoelastic i n Auences on the pattern of force transduction to the skeleto n .

The Bas ic Relationship Between Nerve and Muscle Is Defined by the Motor Unit

Muscle fibers contract i n response to acetylchol ine released by motor nerves. An i ndividual motor neuro n , with the m uscle fibers contacted by i t , forms a motor unit. The size of motor units may vary dramatically between m uscles and within the m uscle itself. The motor neuron generates an action potential lasting 1 to 2 milliseconds that produces a contraction of all of the muscle fibers i n a motor unit i n an "on-off " fashion. The response of the motor u n i t to a s ingle action potential is termed a twitch, the basic u n i t of recordable m uscle activity. The time requ i red for a motor unit to fully contract and then return to resting length is variable (from 10 milliseconds to 1 00 milliseconds) according to fi ber type, but in all cases m uch longer than a nerve action potential. If addi tional nerve stimulation occurs before the contraction phase of the twitch has ended, contraction can be maintained and i ncreased in a process called summation. The limit of summation, such that contraction i s maintained and does not i ncrease with a greater frequency of stimulation, is called tetanic contraction or tetany. The force of contraction of the m uscle as a whole may be further regulated by increasing or decreasi ng the n umber of motor u n i ts used to produce the contraction, a process termed recruitment. In this way, the nervous system may control the force of muscle contraction by the size and number of motor units employed to produce the contraction and the frequency of activation of motor units.

Types of Muscl e Contraction Are Defined by the Movements Occurring During Contraction

Dynamic m uscle contractions in the processes of producing movement can be classified as concentricand eccentric. Concentric

74

If.


B.

A.

�

� i

Resting Length

Passive Tension Component

c.

the danger of injury. This energy storage also occurs as m uscles are stretched under load. The m uscle contractile elements may also have some elasticlike properties of energy storage (4 5 ,46). The sum of the interaction of the contractile elements and elas tic elements of muscle contraction can be demonstrated in the force-time curve of muscle contraction ( Fig. 5 . 1 2) . While the ten sion or force of contraction of the m uscle fibers may reach maxi m u m within a relatively short ti me, a m uch longer time is required for t h is tension to be transferred through the elastic components. Because of this time lag, the active contraction process must be long enough in t i me for the full transfer of tension to occur. Many Factors, Such as Length, Load, and

Time FIGURE 5.1 2. Left: Types of muscle contraction. A: Concentric. B: Ec

centric. C: Isometric. Right: (Top) Muscle tension relationship to muscle length. The greatest active tension is near the muscle-resting length. The passive tension component from stretch of connective tissue in creases beyond the resting length. Bottom: Force-time relationship of muscle contraction. The time lag in reaching maximum force is related to the elasticity of tissue components.

contractions produce movement in the d i rection of m uscle con traction ( Fig. 5 . 1 2) , while eccentric contractions act to decelerate or resist movement, as in slowly placing an object down rather than letting it fall. Muscles also produce contractions without substantial movement, as in static posture against gravity. This type of contraction is termed isometric, as no change in muscle length occurs d uring contraction. Another term, isotoniccontrac tion, refers to m uscle conn·aerion with a change in length under constant tension.

The Mechanical Properties of Contractile Elements and Their Connective Tissue in Muscle Is Described as a Musculotendinous Unit

The force production charaereristics of a m uscle as a whole are a combination of the material properties of i ts contractile compo nents, the connective tissue that surrounds them (and the whole m uscle), and the tendon of its insertion . From a mechanical view point this combination is a musculotendinous unit (44). The con tractile elements add a rapid tensile load on the connective tissue elements, which in turn respond according to their elastic and viscoelastic properties as described earlier. As with l igaments and tendons alone, this will mean that there is rapid component to stretch, produced in this case by contraction, followed by a slower change in length as the connective tissue elements reach equi lib rium with the contracting force ( Fig. 5 . 1 2) . The connective tissues surrounding the m uscle and its tendon have elastic properties that can store energy with stretch l i ke a rub ber band . In the process of m uscle contraction, the tendon and connective tissue are stretched. The energy is released by moving a body segmen t or by stretching the contractile elements as the m us cle relaxes. The elasticity also helps to keep the m uscle prepared for contraction by reducing slacken ing of contractile elements, preventing passive overstretch of m uscle fibers, thereby reducing

Temperature, May Affect the Force Produced by Muscle Contraction

The force of muscle contraction can be affected by various me chanical factors, including length-tension relationships, load velocity, and force-time properties (43). Other sign ificant factors may incl ude temperature, m uscle fatigue, and prestretching. The length-tension property of a m uscle as a whole ( Fig. 5 . 1 2) involves both the active contractile elements and the passive connective tissue elements (47). The maximum force or tension produced by contractile elements, such as the muscle fiber, is obtained at near its resting length. Contraction at lengths beyond or smaller than the resting length results in reduced tension production by the m uscle fiber. This is a result of intrinsic properties of muscle fiber sarcomeres. For the muscle as a whole, reducing or increas ing the m uscle length from its resting position will reduce the tension produced by contractile elements. However, increasing m uscle length will also produce a passive tension as a result of stretching the connective tissue elements, al though the contrac tile force is reduced. The passive component of stretch , which is readily detectable by passively stretching a relaxed li mb, will eventually become the dominant source of resistance or tension as m uscle length increases, effectively protecting the muscle from overstretch . ( Fig. 5 . 1 2) . Applied Loads Affect the Velocity of Muscl e Contraction

The relationship of the load applied to a m uscle and the veloc i ty with which it contracts defines the load-velocity property of muscle contraction. The shortening of muscles contracting con centrically is most rapid with no external load and progressively slows with increasing external loads (48). The shortening veloc i ty will reach zero as the load reaches the maximum contraction force of the muscle (isometric contraction) and then reverse to a lengthening velocity with eccentric contraction. As m ight be ex peered, eccentric contraction lengthening velocity increases with increasing external load. A Rise in Temperature Can Increase the Efficiency of Muscle Contraction

I n the process of contraction, muscle efficiency is usually no more than 20% to 25% in the translation of chemical energy into useful work, with the majority of the energy being dissi pated as heat (42). Even so, the heat dissipation can have positive

5. Biomechanics effects on muscle contraction properties by i ncreasing tempera ture. As would be attained through a warm-up procedure, tem perature i ncreases usually arise from i ncreased blood flow and the production of heat by the muscle itself from metabolic re actions and friction generated by the sliding of molecules past each other in the contractile and elastic elements. Withi n phys iologic ranges, i ncreases in temperature will increase the con duction velociry across the muscle fiber membrane (sarcolemma) (48), i ncreasi ng the rate of contraction and i ncreasi ng the rate at which the muscle can be stim ulated. This can mean an in crease i n the production of muscle force. A rise i n temperature can also increase enzymatic activi ry related [0 m uscle metabolism and i ncrease the efficiency of muscle contraction. The viscoelas tic properties of the musculotendinous u n i t are also affected by rises in temperature, generally increasing the elasticiry of the col lagen, decreasi ng stiffness, and enhancing the extensibil i ry of the unit. While these basic biomechanical properties of muscle tis sue change with temperature [0 enhance the contractile prop erties of the musculotendinous unit, the effects from stretching or "warming up" prior [0 activiry are m uch more complex and not completely unders[Ood (49,50) . The physiologic aspects of stretch (or release) i nvolve h ighly significant neural components and reflexes beyond the biomechan ical properties of the tissues alone. Muscle Fatigue Properties Are Affected by the Muscle Fiber Type(s) Comprising the Muscle

Fatigue of muscle with prolonged contraction activiry results from the depletion of the nutrients and oxygen required [0 produce adenosine triphosphate (ATP) as an energy supply from either aer obic or anaerobic glycolysis. The result is a decrease i n force pro duction by the muscle eventually [0 [Otal cessation (42). The rate at which a muscle will reach fatigue can vary according [0 the rypes of muscle fibers it contains. Muscle fiber rypes are distinguished by the rate at which ATP can be made avai lable [0 the sarcomeres for contraction and the metabolic pathways through which ATP is generated. The rate of availabiliry of ATP d i rectly affects the rate of contraction or rwitch time of a muscle fiber. Accordingly, muscle fiber rypes can be classified as slow or fast twitch. Two primary metabolic pathways involved [0 generate ATP (oxidative or glycolytic) further divides these two basic rypes of contractile behavior. Using these properties, three primary muscle fiber rypes are distinguished including rype I or slow-twitch oxidative (SO) fibers, rype l lA , fast-rwitch oxidative-glycolytic (FOG) fibers, and rype I I B, fast-twitch glycolytic (FG) fibers. These different fiber rypes have varying degrees of contraction time, resistance [0 fa tigue, and a dependence on aerobic or anaerobic metabolism. As their names suggest, rype I fibers have slower contraction rates, and, with a metabolism directed [Oward aerobic pathways, are resistant [0 fatigue. They are relatively small i n d iameter and produce a relatively low amou nt of tension per fiber. These prop erties make this fiber rype well suited for prolonged low-intensiry work ( 5 1 ) . Type l lA fibers are fast contracting and rich i n aerobic and anaerobic (glycolytic) enzymes with a moderate resistance [0 fatigue. They appear [0 be i ntermediate berween rype I and rype l i B in their capaciry for contractile force and resistance [0

75

fatigue. Type I I B fibers are fast contracting, rely primarily on gly colytic pathways, and may fatigue rapidly. H owever, they have a large fi ber diameter and can produce relatively large amounts of tensIOn . Muscles May Have Some Ability to Change Their Fiber Type According to Demand

Most m uscles are of mixed fi ber rypes with the proponion of fiber rypes determined by the nerve i n nervating the muscle ( 5 2 , 5 3) . T h e overall distribution of muscle fiber rypes i n the muscles of the body appears [0 have a strong genetic component (42,5 1 ,54). The fiber rype can be changed with nerve stim ulation ( 5 5 ) , suggesting that patterns of activiry may alter fi ber metabolism. Some changes i n fi ber rypes may also occur with physical tra i n i ng, but much of this change is a result of i ncreases i n the cross-sectional area of the fiber rype corresponding [0 the activiry rather than an actual change in fi ber rype ( 5 4 , 56). The extent [0 which actual alterations in the rype of muscle fi ber occur as a result of activiry demand therefore remains u nclear. Muscle Adapts to Physiologic Demands

Although the extent of fi ber rype change under physiologic con ditions is unclear, muscle will clearly remodel according [0 the stresses placed upon it. Muscle atrophies with disuse and hyper trophies with increased use. Studies of m uscle atrophy in both ani mal and cl in ical studies suggest that early dynamic Illotion after debilitating i n j ury may be important i n the m i n im ization of atrophy, particularly of rype I m uscle fibers (57,58). Electric stim ulation may also prevent some of this fi ber loss (56) . Hyper trophy of m uscle with physical training is generally the result of increases in the cross- sectional area of all m uscle fibers ( 5 8 ,5 9 ) .

MUSCULOSKELETAL BIOMECHANICS Primary Biomechanical Musculoskel etal Models Consist of Segments Moved by Muscles Across Joints

Biomechanical aspects of the skele[On i nvolve contributions from all of the biomechan ical aspects of the tissues described in the pro cess of produci ng movement. As a simplistic model, it is easiest [0 consider the body as a series of segments (bones) contai n i ng m uscles that are attached across the segments. Joint s form the j unctions between segments or bones and transfer the forces gen erated by m uscles or from external sources between the segments. In the fol lowing simple models of movement, joints will be re garded as simple p ivot points, moving in one plane (co-planar) . The more complex considerations of joint movement and shape of articulation will be addressed in subsequent sections. Force Moments Are Used to Describe Models of Musculoskeletal Movement

Using the simple model used for the descriptions of moments ear lier in the chapter, a j o i nt , such as the elbow ( Fig. 5 . 1 3) , becomes a rotation system with the flexor system and the extensors using the joint as a center of rotation [0 move the distal limb and any

76

II.


B.

A.

c.

m r

, t..I, � l'

lrf

_ _ _ _ _ _ _ _

d

FIGURE 5 , 1 3 , Schematic of basic joint moments and their variation with movement. Sections on top represent muscle contraction mo ments. Figures on the bottom show moments generated by the load. A: Right angle resistance to a load (I). Top: Moments about the joint cen ter (c) include the moment arm of the muscle (rna) that is moved by a re sisting component (r) of the muscle contraction force (m), this is resisted by the load (bottom) acting on a load moment arm (la). Joint reaction forces include the portion of the muscle force directed into the joint (jr) and a moment generated from the load into the joint with a cen ter of rotation about the muscle insertion (Irf, dotted lines displaced). B: At extension, the angle of muscle pull directs more of the muscle force into the joint (top) and a portion of the load force (I) moment pulls out on the joint as a distracting force (d). C: In a flexed position, the muscle moment (top) is divided into the resisting component (r) and a joint reaction distracting force away from the joint (jr). A portion of the load force (bottom) now is directed into the joint (lj).

load on the limb. I n mathematical model i ng of joint function, the descri ption of such movements is a system of balanced mo ments produced by rhe load on the limb and m uscle contraction forces. Characterizing movement in this way becomes particu larly impo rtant as other aspects of joint fu ncrion (non-co-planar movement, movement within the joint) and more mechanically compl icated j o i nt rypes are modeled. As a distal segment moves relative to a more proximal seg ment, the distal segment will rotate about the instant center of the joint or center of rotation (c, Fig. 5 . 1 3) . The effective distance from the center of the joi nt's rotation to where the force is acti ng (muscle i nsertion ) is the moment arm (rna) for the muscle. The product of the force appl ied from the m uscle and the moment arm (force x distance) is the moment (or torque) used to resist a load on the distal l i mb. For concentric con traction to occur, this moment of resistance m ust exceed the moment produced by the load (distance to the load from c x weigh t) . In a more complete model, the weight of the limb m ust also be considered. Note also that if the load moment is resisted by the pull of the llluscle, there is also a cenrer of rotation created at the point of m uscle i nser tion about which the load exerts a momenr i n to the j o i nt ( lrj Fig. 5 . 1 3) . Together with the portion of the m uscle contraction force directed into the j o i n t (discussed subsequently), this be comes part of the joint reaction force which applies a stress to the j o i nt duri ng movement. Muscle Moments Necessary to Resist a Load

(vector) that is applied to resist the load will vary as the limb is flexed. With the joint ful ly extended, most of the muscle contrac tion force vector is d irected i nto the joint. This muscle compo nent force also contributes to the j oint reaction force and may be particularly i mportant in the stabilization of load-bearing joints, such as the knee. The relative size of the j o i nt reaction and load resistive forces can be expressed by simple trigonometric functions in mathematical models, but it is sufficient here to be aware of how these forces change with joint position. In this model, the portion of the m uscle contraction vector used to resist the load in creases as the angle of tendon is closer to a right angle (Fig. 5 . 1 3, part A, orthogonal) to the forearm. Beyond this point, a portion of the load vector becomes directed i n to the j oi nt (Fig. 5 . 1 3, part C) reducing the effective load on the muscle, but placing stress on the j oi nt and more proximal segments. I n the flexed position, the angle of pull by the muscle directs a portion of the m uscle contraction force against this load i n to the j o i nt.

Muscle Moments Are Also Transferred Across Joints by Tendons

Muscle forces are also conveyed to distal segments across joints by tendons. I n j o i nt s associated with the knee, hands, and feet, tendons cross the joint(s) to produce a "pulley" effecr (Fig. 5 . 1 4) . I n this arrangement, as i n the knee, the distance between the center of rotation of the joint and the tendon defines the moment arm fo r rhe contracting m uscle. The wheel and axle mechanism (60) is an i nstructive related model used to ach ieve rotary movements ( Fig. 5 . 1 4) . [n this case, muscle contraction forces are applied to the opposite sides of a segment to produce rorarion about an axis. The length moment arm i n this case is the distance to the center of rotation. This mechanism is used widely throughout the body to achieve rota tion of limbs and the body, as in rotation of the head, torso, or shoulder. As with si mple flexors and extensors, muscles produc ing rotational components work in pairs and significant clinical problems may arise fro m imbalances in function of the pair.

A.

c.

D.

Vary with Joint Position

FIGURE 5.14. Strategies of muscles and tendons pulling across joints. A: A pulleylike mechanism in which the direction of pull is changed .

As can be seen from Fig. 5 . 1 3, although the length moment arm does not change, the proportion of m uscle contraction force

B: A similar mechanism i s used i n knee extension. C : A wheel and axle mechanism in which co-active forces act to rotate an axle, such as the shoulders (0) relative to the spine.

5. Biomechanics Muscle Moments General ly Have a Low Mechanical Advantage

As suggesred i n rhe examples rhar have been given, rhe lever ar rangemenr of muscle i nserrions and j o i nt s i n l imbs is such that a comparatively small disrance of muscle conrracrion can produce a large displacemenr of rhe load at the expense of needing large muscle contracrion forces. This is described as hav i ng a low me chanical advanrage. The relative mechanical advanrage is a func tion of the position of the m uscle origin and insertion on the rwo bony segmenrs relative to rhe joint. Because borh rhe momenr arm (distance, d) and contraction force (f) equally conrribuce to the momen t (f x d) producing the movement or resistance, small differences in the momenr arm can produce significanr changes in the amounr of muscle contraction requ i red. As ori gins and i nsertions of muscles and segmenr lengrhs vary markedly berween individuals, the abi l i ty to produce differenr types of movement using the same muscle conrraction force will also differ. While muscles must create large forces to produce movements at a low mechanical advanrage, d istally applied loads, such as to the hand acring rhrough rhe elbow, have a compararively large moment arm (Fig. 5 . 1 3) and require less force to produce large moments about the joint. This will be true of manipulative forces placed distally for purposes of applying passive strerch to m uscles and joi nts. Ir is a useful pri nciple, but must be approached with caution, since large, potentially damaging force moments can be generated. Joint Structure Defines How Movements Can Occur Between Body Segments

Beyond movement models that regard j o i nrs as simple pivot points for the transfer muscle forces berween body segmenrs, the next level of model ing must consider the srrucrure of rhese i nter segmental conracts. I n facr, the directions of movement that can occur berween body segmenrs are largely defined by the struc ture of the joints berween them. Joinr s are classi fi ed according to rhe type of tissue they conr a i n and their structure. On a tis sue level, joints are classified i n to three primary types: fibrous, carrilaginous, and synovial. Fibrous joint s are located in areas such as the arriculations of the skull, while carrilaginous j o i nts include rhe discs between vertebrae, and synovial joint s are 10cared in articulations of the li mbs. The vast majority of body motion occurs across synovial and cartilaginous j o i n ts. The pri mary cartilaginous articu lations will be described subsequen tly, with considerations of the spi nal column. The remain i ng synovial joi nts have been divided into several categories according to the primary types of movemenrs rhat occur across them . Anaromi cally, rhe major types are glidi ng, h inge, pivor, condyloid, saddle, and ball and socker (6 1 ) . Other rhan the j oi nr s described later i n this chapter, more detailed descriptions of these j o i n t structu res and rheir limirarions on range of motion can be found in general anatomic texts. Range of Motion Describes the Extent of Body Segment Movement Across Joints

Movements are usually described as occurring i n one of the pri mary body planes (frontal, sagirral, or transverse) . The extent of

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j o i n r motion i n a plane defines its range o/motion i n rhat plane, usually in degrees. Alrhough all synovial joinrs may have some minor range of motion i n all three planes, most j o i nt s in rhe ex rremities have a primary degree of freedom in one plane, such as in the knees, elbows, or fi ngers. Shoulder and h i p joints are an exception, as they have signi fi canr ranges of morion in all th ree planes. Join rs may also have a significant rorational component, usually expressed as range of morion of rhe distal rorated ele ment, as in pronarion and supi nation of rhe hand. In general, there is a trade-off berween i ntrinsic strucrural stabi l i ty of joint s and range of morion , depending u p o n t h e physiologic demands placed upon rhe joint.

Joint Surfaces Have Several Different Types of Relative Movement

As body segments are moved through their range of motion, surfaces wirhin rhe j o i n r will also move relative to each orher. This movement may con tribute to various aspects of rhe mo tion produced. The relative motion of j o i n r surfaces may include gliding, rolling, rorarion, comp ression, o r distracrion ( Fig. 5. 1 5 ) , or a combi nation of these movements. Gliding (also referred to as translation or slidi ng) represents a movement of one surface relative to anorher wirhout a rotational component. 1n rol l i ng, one s urface of the articularion rolls over the other, l i ke a ball rolling over a surface. Rotarion (sp i n n i ng) consists of o ne joint surface spinn i ng o n the surface of the other without a trans lational component. Compression represents force push ing the j oinr surfaces together, while d isrracrion rends to pull the su rfaces apart. Movements berween articular surfaces in a joint can occur in consistent comb i narions (coupled) such thar, one type of mo rion is always accompanied by another. This motion coupl ing can occur for movements wirhin the same articulation (see rhe upco m i ng example given u nder "The Knee") or in another joint rhat is part of an articulation complex (see rhe example given

Glide

Spin

Roll

Compress

Distract

FIGURE 5.1 5. Intraarticular movement of joint surfaces relative to each other. In gliding (also referred to as sliding or translation), surfaces move without rotation. In rolling, one surface rotates and translates over the other at a distance equal to the arc of the rotating surface. In spinning, one surface rotates on the other without translation. Compression and distraction are opposing ve rtical forces on the joint.

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/1.


with "The Elbow" later i n the chapter) (62). A disruption of one part of a coupled motion will affect the other and can produce dysfunction of the j o i nt or joint complex. An example of this is a coupling of the elbow complex where there i s a coupling of rhe i n traarticular motions of h umeroulnar and humeroradial joint s during flexion/extension movemenrs (see "The Elbow") . Cou pling of arricular su rface motions with i n the joint also depends upon which segment of rhe joint is mobile (62). A n example of this difference is the articular surface movement of the knee during weight bearing versus swing phase (see "The Knee" ) . Sig nificant alterations in the relative movements of joint surfaces can produce problems in joints, i nclud i ng abnormal wear and dislocation. The Instant Center Defines the Center of Rotation of a Body Segment at Any Given Time

In order to srudy movement within a joint d ur i ng functional movement, both the motion of the surfaces relative to each other and the shape of the art i culati ng surfaces must be considered. As one segment moves in a j o i nt such as the knee, the cenrer of rota tion located with i n the joint at any i nstant will have zero velocity. Because the femoral condyles and tibial plane are not spheric s ur faces and translational movement can occur withi n the j oi n t, the center of rotation of the leg will change as the leg is extended. To determ i ne properties such as the length of the moment arm u nder these circumstances, the center of rotation m ust be redefi ned as instant center of rotation joint at any given time (63 ) . The i nstan t center can be defi ned cl in ically from sequential roentgenograms or other picrures of movement usi ng the intersection oflines fro m defined poi nts from the joint segments. This techn ique can be im portant for identifying abnormal j oi nt movement. It should be noted, however, that displacement of the i nstant cen ter can occur in all three dimensions simultaneously. Roentgenograms or other planar depictions of joint motion can be m isleading. From a fu nctional point of view, changes in the location of the i nstant center will change the relative magni tude of the contraction-force vecrors of the muscle tendon acting across a j o i n t. This can result in weakness or abnormal stresses with i n the joint.

SOME PROPERTIES OF SPECIFIC JOINT ARTICULATIONS

The previous discussions in this chapter have focused on the biomechan ical properties of tissues and models of forces acting to create movements o r stresses on body segments. We will now consider how these properties apply to some of the primary ar ticulation systems in the body. The biomechan ical aspects to be considered are not i ntended to be comprehensive.

A FIGURE 5.16. A: The knee joint consists of the tibiofibular (t) and patellofibular joints (p). B: Moments produced by the load (L) of body weight require little muscle activity with the knee extended, but are maintained by a muscle contraction force through the patellar tendon (m), which produces moments through a moment arm (a) to the in stant center of rotation of the joint (e). The moment is divided by the angle of muscle pull into a joint reaction force (jr) and an extending component (e). C: With the knee flexed, the body weight produces a moment through the joint (e) that must be resisted by the extending component (e). In this instance, the patella increases the distance of the tendon from the femur to provide a more advantageous angle for the muscle contraction force on the tibia. This increases the proportion of the extension moment. Note that the position of the center of rotation (e) has changed slightly.

Because of i ts location and weight-bearing properties, the knee sustains relatively high load forces and is particularly suscepti ble ro i n j ury. Stability of the knee is obtained from the internal and external ligaments, joint capsule, and muscles acting across the joint. The cartil age menisci act to distribute the compressive stresses between the condyles of the femur and the tibial plateau.

The Knee Has One Primary Range of Motion in the Sagittal Plane

Although the knee joint i tself has some range of motion in all three planes of motion, i ts primary range of motion is in the sagittal plane where a range from full extension to full flexion is approximately 1 40 degrees (63). Motion in the transverse plane (i nternal and external rotation) and frontal planes (abduction and adduction) is dependent upon the posirio n i ng of the tibia relative to the femur. In the transverse and fron tal planes, ful l extension of the knee precludes almost all motion due to an i n terlocking of the femoral and tibial condyles, while range of motion i ncreases as the knee i s flexed. Maximal i n ternal and external rotation is possible with rhe knee flexed ar approximately 90 degrees ranging from a neutral posirion ro 45 degrees of external rotation and 30 degrees of i nternal rorarion. I n the frontal plane passive adducrion and abduction i s obtained at approximately 30 degrees of flexion, but ir is o nly a few degrees in eirher direction (63).

Primary Muscle Forces Through the Knee Are THE KNEE

The knee joins two of the body's longest moment arms (the th igh and leg) in a joint consisting of two primary articulations, the tibiofemoral joint and the patellofemoral j oi nt (Fig. 5 . 1 6) .

Conducted Through the Hamstrings and the Patellar Tendon

The primary m uscle forces through the joint occur rhrough the quadriceps tendon and hamstrings. The hamstrings use the knee joint as a pti mary lever in fl exi ng, while the quadriceps uses the

5. Biomechanics patellar tendon system as a pulley with the center of rotation within the femoral condyles ( Fig. 5 . 1 6) . As with other h inge-type joints, in a basic biomechanical model, muscle contraction forces are divided primarily i nto a joint reaction force d i rected i n to the joint and a force moment that acts to move the mobile segment. [ n extension of the knee, the moment that acts to straighten the knee pulls on the leg through the patella and tendon. This will act to rotate the tibial plateau relative to the condyles of the fem u r. Presuming a constan t muscle force, this component of moment decreases or mechanical advantage decreases in proportion to the joint reaction force as extension proceeds ( Fig. 5 . 1 6) . T h is decrease is to some extent compensated by the movement of the patella and the shape of the femoral condyles as described subsequently. With flexing a straightened knee, the opposi te is true; the proportion of the flexor moment i ncreases relative ro the joint reaction force as the movement proceeds. The Knee Must Withstand Very High Joint Reaction Stress Forces

[n a load or weight-bearing model of the knee, the leg is consid ered stable, and muscle contraction forces and j o i n t structure are used to resist gravity. The force exerted through the knee from the weight of the body is termed the ground reaction force (body mass X the acceleration of gravity) . Note that both the ground re action force and muscle contraction forces con tribute to produce the joint reaction force or total force directed into the j o i nt as de scribed previously. These combi ned forces, along with the i m pact ofland ing from activities such as jumping, can produce very h igh compressive and other stress forces on the knee j oi nt surfaces. If the knee is fully extended, most of the ground reaction force is d i rected through the bone structure of the fem ur and tibia (a moment arm through the joint of almost zero), and m i ni mal or no muscle contraction force is requi red to resist the ground re action force. This changes as the knee is bent, and at 90 degrees of flexion, extensor muscle react io n forces m ust resist the ground reaction force consisting of the body weight acting at a d istance of almost the entire length of the femur. At this angle, the extensor muscles have a relatively small moment arm. Accord i ngly, a very high m uscle contraction force in excess of body weight m ust be exerted to resist a moment of this magn itude. The knee joi n t has several mechanisms to help compensate for the rather low me chan ical advantage of muscle contraction forces in this situation. The Application of Muscle Contraction Forces to Movement Across the Knee Is Affected by the Structural Properties of the Joints

Beyond the basic segment model , there are basic structural prop erties of the knee that change the mechanical advantage m uscles across the joint. These primary structural properties include the patellofemoral joint and the shape and movement of the femoral condyles. The patella and tendon act to i ncrease the moment arm for the quadriceps by i ncreasing the effective distance of the tendon from the center of rotation of the joint, thereby i ncreas i ng the component of the muscle contraction force vector act i ng ro straighten the joint (Fig. 5 . 1 6) . This adds mechan ical advan rage to the exrensor muscle contraction forces in a partially flexed

79

knee. The gliding (slidi ng) motion of rhe parella between the medial and lateral femoral facers also alrers rhe moment arm over rhe range of morion of rhe knee. Addirionally, the parella acts ro disrribure rhis force over rhe surface of rhe femoral condyles. The primary properties of the femoral condyles rhat affect rhe mechanics of movement i nclude the noncircular shape of rhe condyles and rheir movement on rhe ribial plareau ( Fig. 5 . 1 6) . The shape o f the fem oral condyles i s such rhar rhe cen tel' o f ro rarion of the j o i nt changes rhrough rhe knee's range of morion, giving a grearer moment arm ro extensor forces as rhe knee is flexed. This can be i m portant i n resisting rhe high forces such as body weighr wirh a partially flexed knee. I n addirion to a non circular shape, rhe femoral condyles also have differences in their effective diamerers with rhe medial bei ng larger. This produces a coupli ng of flexion and exrension wirh a rorarional com ponent to rhe knee (called rhe screw-home mechanism), such thar flexion is accom panied by an i n ternal roration component and extension is accom panied by exrernal rotation of the femoral condyles relative to the tibial plateau (64 ) . This provides additional srability to rhe . . lOlllr In certain clrcumsrances. .

The Intraarticular Movements of the Knee Depend Upon Which Surface Is Moving and load Bearing

The femoral condyles also glide (slide, translate) on the ribial plateau as rhe knee is moved (described previously). These StruC tural properties of the femoral condyles can act to change the center of rotation as the joint progresses through its range of mo rion and alter the effective momen t arm length rhrough which the m uscle contracrion forces are acting. The relative movements of the joint surfaces in the knee give an example of how morion coupling can depend upon rhe load srarus of rhe joint and which joint surface is mobile (62). In walking, as rhe leg swings for ward (swing phase), the femoral condyles and ribial plareau are nor under the compressive load of the body. The movement is a gliding motion of the ribial plateau coupled wirh a roll ing of the tibia on the femoral condyles in rhe same direction. When the leg is p laced on the ground with the knee partially flexecl and then extended as the body is moved forward (see " Normal Locomotion (Gait) Employs the Entire Body for Efficiency of Movement" later in the chapter) , the tibial plareau is stable rel ative to the femoral condyles. The morion of rhe j o i nt surfaces now consists of a gliding and rolling of rhe femoral condyles on rhe tibia i n opposire direcrions. This is an example of how com pressive forces and segment stabil ization change articular s urface motion. This can have i m portanr impl icarions i n surface damage and dysfunction. Knee Joint Structure and the Movement of Joint Surfaces Promote Efficiency of Movement

Through their structure and i nt eraction during movement, rhe patellofemoral joint and femoral condyles contribute to the ef ficient use of muscle contraction forces for movement and joint stability by changing the moment arm ( mechan ical advantage) of the contracting muscles i n the process of extending or flexing rhe

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knee. This has i mporrant consequences for movement through the knee and load bearing. The effective use of these structural properries is dependent upon i nternal j o i n t movement and the joint stability provided by soft tissues. For this reason, soft-tissue inj ury or changes prod ucing either a lack of or excess of i n ternal "play" in the knee joint can contribute to serious problems with joint function.

THE HIP The Hip Is a Load-Bearing Ball-and-Socket Joint with Ranges of Motion in All Three Planes

The relatively rigid ball-and-socket arrangement of the h i p joint between the head of the femur and the acetabulum provides greater i n trinsic stabiliry compared to j o i n ts such as the knee. In addi tion to stability, the ball-and-socket structure of the h i p allows greater range o f motion in all three planes of body move ment. Motion in the sagittal plane is greatest with approximately 1 40 degrees of Hexion and 1 5 degrees of extension from a neutral position. The range of abduction is approximately 30 degrees and adduction 2 5 degrees. External rotation fro m a Hexed position is approximately 90 degrees and i n ternal rotation approximately 70 degrees. Rotation decreases with extension due to soft-tissue restrictions (65).

The Angular Alignment o f the Articular Components Is Important for Normal Hip Function

The angular structure of the j o i nt relative to the pelvis, femoral shaft, and knee j o i n t can vary significantly between i n d ividu als and have a great inHuence on the biomechanics of the lower l i mb. In the relationship of the j o i n t surface to the pelvis, the location of the acetabulum places the plane of i ts openi n g angled 40 degrees posterior to a sagittal plane and 60 degrees lateral to a transverse plane ( Fig. 5 . 1 7) . Both the femoral head and acetab ulum have roughly spheric surfaces of contact. The relationship of the femoral head through i ts neck with the femoral shaft is im portant i n the biomechanics of hip function and load-bearing

A.

stress on the neck. I t is an i mportant determ i nant of the effective moment arms of the muscles producing movement across the joint. The angle of i ncli nation of the neck to the shaft (Fig. 5 . 1 7) is approximately 1 25 degrees, but may vary between 90 to 1 35 degrees. Th is angle offsets the femoral shaft from the pelvis laterally. The angle in a transverse plane between l ines drawn through the femoral head and greater trochanter and between the medial and lateral condyles (angle of anteversion) determines the normal relationship of the primary plane of movement of the knee to the h i p . It is normally about 1 2 degrees but can vary widely (65) . An angle of greater than 1 2 degrees tends to pro d uce i n ternal compensatory rotation of the leg during gait, while an angle of less than 1 2 degrees produces an external rotation. These compensations are made to maintain the stabiliry of the hip. They are common in children and usually outgrown (65 ) .

Models of Hip Function Balance Ground Reaction, Joint, and Muscle Contraction Forces

Biomechanical models of the h i p can be used to illustrate some of the i mportant aspects of the structure-function relationshi p of t h e j o i n t . 5tabiliry of t h e h i p joint i s maintai ned through the alignment of the body over the joint (Fig. 5 . 1 8) , the joi nt capsule, and capsular ligaments and muscle contraction to cou nteract re maining ground force moments. The relative magnitude offorces applied i n to and across the h i p j o i n t can be considered through a model of a single leg stance wirh the body center of mass (or graviry) balanced (thar is, located on an axis of alignment) over one h i p j o i n t (Fig. 5 . 1 8 ) . I n this balanced condi tion, l ittle or no m uscle contracrion forces are necessary to maintain equilibrium,

A.

B.

B.

/ , , , ,

FIGURE 5.17. A: Angle of the opening of the acetabulum. The open ing is oriented 60 degrees lateral to a transverse plane and 40 degrees posterior to a sagittal plane. B: The angle between the femoral neck and shaft is approximately 125 degrees.

FIGURE 5. 1 8. A simple co-planar model of a single leg stance moment in balance. A: In the balanced state, the body weight (b) is balanced over the foot (not shown), which would be at the intersection of the dotted lines. In this balance, the body weight (b) acts as a force applied on a moment arm (d) through the center of rotation in the femoral head to produce a body moment (b x d). This is balanced by the rotational component (r) of the muscle contraction force (m) acting over a moment arm through the femur (h) to produce a muscle contraction moment (r x h). For balance to be maintained (b x d) = (r x h). B: The balanced condition can be disturbed by a shift of the body and a slight change of the angle of pull by the muscle (m). To restore balance, the moment (r) must be increased or altered so that the moments can be rebalanced.

5. Biomechanics as in the knee. The joinr reaction force or force directed i nto the joint will equal rhe ground reaction force produced by the

weight ofthe body above the hip. In al1 l1l1balal1ced state, (he body

center of mass is no longer d i rectly over the bony structure and produces an un balanced moment about the cenrer of rotation of the hip joint. To restore equilibrium, the force of the contracting abductor m uscles must generate an equal force momenr across the hip in me direction opposite of the momenr generated by me body weight. By measuring the length of the momenr arms for muscle conrraction in the body and knowing the body weight, the approximate resisting momenr of muscle contraction can be calculated along with the joint reaction component produced. Note that in this model, the angle of the femoral neck will affect the relative lengths of the moment arms (or the angle of pull) by muscles. Th is will di rectly inAuence the m uscle conrrac tion Forces requi red to resist the body weight moment and the proportion of the contraction Force directed into the joint. This is why an abnormal angle of the Femoral neck can adversely affect hip Function and the stresses on the joint. Hip Joint Function Requires High Muscle Contraction Forces and the Ability to Withstand High Joint Reaction Forces

As with the knee, it can be seen that h i p stability u nder load bearing conditions can requ i re high m uscle contraction forces because of a relatively short moment arm though which the m us cle forces are applied. As a combination of ground reaction force and the portion of the muscle contraction forces directed i nto the joint, the joint reaction Forces are also h igh relative to the body weight. Calculations suggest that under these conditions, the muscle contraction force is approximately twice the body weight and the joint reaction force almost th ree times the body weight (66,67) . Joint reaction forces are important in consider ation of stresses on the hip joint itself i n replacement or repair. Strategies to min imize the joint reaction force can also be impor tant in subjects with arthritic pain in the hip joint. As suggested by the model given earlier, a reduction in joint reaction forces may be achieved by altering the angle of the h i p by i ncreasing the muscle moment arms. This can also be accompl ished by using a support device, such as a cane on the opposite side, to reduce the opposing body weight moment.

THE ELBOW The Elbow Is a Compl ex of Three Joints with Two Primary Ranges of Motion

The upper limb analogue of the knee is the elbow, which has adapted for increased mobiliry of the upper limb and a reduced load-bearing requirement. In achieving this, the joint has become a complex of th ree articulations, i ncluding the h umeroulnar, the humeroradial, and the proximal radioulnar j oint s ( Fig. 5 . 1 9) . The joint complex allows two primary ranges o f motion: Aexion extension and pronation-supination. Flexion and extension occur across the humeroulnar and h u meroradial joints, which act as a hinged joint. The normal range of motion in Aexion-extension is approximately 1 40 degrees, with lim its established by the angular

A.

81

B.

ru FIGURE 5.1 9. A : The elbow joint complex consists o f the humeroulnar (hu), humeroradial (hr), and proximal radioulnar joints. B: The primary flexor (F) and extensor (E) moments across the joint.

characteristics of the bony components (68 ) . The axis of motion passes through the middle of the trochlea and is princi pally a glid ing motion (69) up to the last 5 to 1 0 degrees of Aexion, where rolling occurs. Pronation and supination occur at the humerora dial and proximal radioul nar joint. The reported normal range of motion varies between studies (68) with the American Academy of Orthopaedic Surgeons (70) reporting an average of 70 degrees of pronation and 8 5 degrees of supination. The range of motion required for typical daily activities of both Aexion-extension and pronation-supi nation can be performed between a m uch more l i mited range (7 1 ) . Much of the elbow joint's stability during normal use i s sup plied by the shape of the articulating surfaces. OF the th ree ar ticulations, the h umeroulnar articulation s uppl ies the primary anterior-posterior stabi l ity, although the radiohumoral artiCLI lation can contribute to stability from posterior dislocation at Aexion of 90 degrees or more. Beyond the bony stabiliry of the joint, the l igaments and joint capsules around the elbow pro vide remaining stability and the i n terosseous membrane bi nds the radial and ulnar shafts together. Basic Functions of the Elbow Can Be Described by Simple Joint Moments

The basic biomechanics of the elbow can be described largely as a system of simple levers or joint moments as suggested earl ier i n the section on basic mechanics of joint systems ( Figs. 1 3 and 1 9) . Muscle forces act at a low mechanical advantage to achieve a large movement. Due to disadvan tageous vector angles through some of their range, relatively h igh m uscle contraction forces are required. These muscle contraction forces typically generate large joint reaction force components that act through the bony elements to stabilize the elbow. These joint reaction forces may exceed body weight even during normal activities. The Elbow Complex Provides an Example of Dysfunctions from the Coupling of Intraarticular Motion

As a joint complex, the elbow provides a reasonably simple example of coupli ng relationships of in traarticular joint mo tions that, when disrupted, can produce dysfunction. During

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Aexion-extension movements, the h umeroul nar joint has a pri mary gl iding motion that is accom panied by a movement of the head of the radius on the capitulum of the h u merus. This produces a smaller proximal and distal gliding of the proximal rad i us in the radial notch of the ulna (62) . The extent of this latter movement is greatest when the joint is half-Aexed. Al though this motion is not a pri mary component of the segmental motion, its disruption can produce pain and dysfunction i n the joint during movement. It is therefore important ro understand the coupled movements of the complex as well as the i ndividual articulations. More compl icated examples can occur i n more extensive joint chai ns such as in the spi ne and feet.

THE SHOULDER The Shoulder Is a Complex of Four Joints with Different Properties

The shoulder consists of a complex of four articulations: the glenoh umeral, acromioclavicular, sternoclavicular, and scapulo thoracic articulations (Fig. 5 . 20 ) . Of these, the scapulothoracic articulation is not a true articu lation , but an indirect attachment of the scapula to the thoracic w�1I indirectly through muscles. The shoulder complex acts in concert with contributions from each joint to produce movement through greater than a hemisphere of range. The glenohu meral joint is a basic ball-and-socket joint, but has much less int ri nsic stability than i ts lower l i mb analogue at the h i p. The reduced stabi l i ty is reAected by the structure of

the articulating surfaces of the joint. The area of the glenoid fossa that contacts the h umerus is only one-third to one-fourth the size of the joint surface of the humeral head (72) . This allows a more circular range of motion relative to the scapula, but at the cost of i ntrinsic structural stability of the joint. Although some vertical structural support may be derived from the overlying acromion process and attached clavicle, the glenohumeral joint is rel iant, to a great degree, on soft-tissue structures (l igaments, tendons, joint capsules, and muscles) for stability (73) . During fu ncrion, the glenohumeral joint primarily rotates, bur rolling and translation may also take place. This translation may increase substantialry with soft-tissue i nj u ry or dislocation. The scapula attaches to the thoracic skeleton through a chain of two articulations, the acromioclavicular and sternoclavicular j o i n ts. The acromioclavicular joint between the clavicle and prox imal acromion of the scapula has a meniscus of cartilage, a th ick fibrous capsule, and supporting ligaments thaI' stabil ize the joint and allows the scapula motion i n th ree planes (74 ) . These planes i ncl ude a vertical axis (protraction and retraction) and transverse axes in the fron tal and sagittal planes. The prox imal end of the clavicle (sternoclavicular join t) is stabilized by a fibrocartilage, men iscus-con tai n i ng, articulation capsule and ligaments to the sternum and first rib. The joint allows protraction and retraction, elevation and depression, and rotation of the clavicle relative to the sternum. The concept of a scapulothoracic articulation involves a de scription of the movement of the scapula relative to the thorax as l i mited by its m uscular attachments and the clavicular chai n. This structural arrangement allows a wide range of motion of the scapula i ncluding protraction retraction, elevation, depression, and rotation. Movement of the scapula involves the transloca tion of the entire glenohumeral joint , contributing substantially to the range of motion of the arm. A si mple example is the con tribution of scapular motion to the elevation of the arm. In this circumstance the scapula rotates to elevate the shoulder and the glenohumeral joint as the arm is raised. Shoulder Range of Motion Is Usually Described for the Entire Joint Complex Rather than Individual Joints

Top: Front view of the shoulder complex consisting of the glenohumeral (gh) acromioclavicular (ae), and sternoclavicular (sc) articulations. The scapulothoracic junction is not a true articulation, but describes the relationship of the scapula and thorax as can be seen in the lower figure. Bottom: An example of the differences in the moment arms of shoulder muscles (m) and a load (L) in a lift with the shoulder abducted and arm extended. Co-contracting muscles (c, dotted arrows) are important to stabilize the shoulder complex during such tasks. FIGURE 5.20.

With the complex i n teraction of the individual articulations, the range of motion of the shoulder is usually described for the com plex as a whole. From a resting position at the side, the range of motion in the shoulder complex is typically described in the context of range of elevation of the shoulder or movement of the h umerus away from the thorax in any of the th ree primary planes. Forward Aexion and abduction are approximately 1 80 degrees, and in the plane of the scapula may exceed 1 80 degrees. Back ward elevation or extension is approximately 60 degrees. Other motions i ncluding bri nging the humerus in adduction beyond the midline l i m i t of the body in an upward direction is approxi mately 75 degrees (70). Horizontal Aexion in a transverse plane at 90 degrees of abduction is approximately 1 3 5 degrees, with horizontal extension of 45 degrees. Rotation about the long axis of the h umerus varies with the degree of arm elevation, but in general, both i nternal and external rotation can be approximately 90 degrees, with a total range of 1 80 degrees (74) .

5. Biomechanics The Gl enohumeral Joint Depends upon Muscl e Stabilizing Forces to Resist Distal Loads

Because of the relative lack of structural stability of the gleno h umeral joint, soft-tissue con nections through the j o i n t must play a greater role in its stability. In add ition to the j o i nt capsule and lig amentous connections, muscle contraction forces that essentially hold the joint together become more important in resisting the loads placed on the distal upper limb. The use of force-coupling arrangements in the muscles of the rotator cuff is particularly im portant in this process. [n force coupling, m uscles of the totator cuff act in concert to produce offsetting moments (a net j o i n t reaction force) t o stabilize t h e j o i nt (Fig. 5 . 2 0 ) a s elevation is pro duced. The actual calculations ofj o i n t reaction forces u nder these ci rcumstances is difficult due to the large numbers of muscles in volved i n arrangements that will vary according to the plane of motion. Esti mates of these forces suggest magnitudes near body weight (75 ) . ft is also important to note that the low mechanical advantage of muscles in the shoulder compared to the moment arm of a load i n the hand of an extended arm requ ires very h igh contraction forces ( Fig. 5 . 20). The low mechanical advantage of shoulder muscles under load ing and the dependency of the joint on soft tissues for stabil i ty make the shoulder particularly vulnerable to inj ury.

THE SPINE

The spine as a whole represents an extremely compl icated system of articulations and bony segments that act to protect the spinal cord while providing a basic support axis for the upper body. The structure and motion of spinal segments differs substantially over the spi nal column. Due to this complexity and variatio n, only some basic princi ples of spinal biomechanics can be covered here.

Spinal Motion Segments Consist of Two

segment is fu nctionally and physically divided i nto an terior and posterior segmen ts. The an terior portion consists of the verte bral body, the disc between them, and the longitud i nal l igaments (Fig. 5 . 2 1 ) . The posterior segment consists of the vertebral arches, the articulations between the facets, the transverse and spinous processes, and the l igaments b i n d i ng them together. Besides con tain i ng the spinal cord and associated structures, the arch itecture of the posterior segment acts to guide and l i m i t the motion that can occur between the vertebrae of the segment. The anterior segment of the u n i t is the primary load-bearing section, with the vertebral bodies and the i nt e rven ing disc increasing i n size i n the lower segments to sustain greater loading stress. Load beari ng in the posterior segment can be significant when the spine is hyper extended (76) and during forward bending coupled with rotation (77) . The Bony Structure of the Spine Is Supported by an Intricate Arrangement of Soft Tissues

The soft-tissue support for the spi nal column consists of the liga ments, j o i n t capsules, and muscles that con nect to the transverse and spi nous processes of the vertebrae as part of the posterior mo tion segments. The primary l igaments include the anterior and posterior l igaments, the l igamentum Aavum, the supraspi nous and i n terspinous l i gaments ( Fig. 5 . 2 1 ) , and the i n tertransverse ligaments, all of wh ich provide i ntrinsic support for the spi nal colu m n . The capsular ligaments for the facet articulations also contribute to stabil i ty and l i m i tation of motion . The l igaments have a high collagen content except for the ligamentum Aavu m, which has a high elastin content. The l igaments add stab ility and store energy during movement of the spinal column. For example, Aexion primarily strerches the interspinous ligaments, capsular ligaments, and the l igamentum Aavum. These store en ergy l i ke an elastic band and can be used fo r subsequent recovery to a neutral position. Other l igaments similarly partici pate in lateral bending and rotation.

Vertebrae and Associated Soft Tissues

Intervertebral Discs Are Structured to

The fu nctional unit of the spine or motion segment consists of twO vertebrae and their associated soft tissues ( Fig. 5 . 2 1 ) . The

between Vertebrae

p

A

1

vided into anterior (A) and posterior (P) portions. The anterior portion contains the vertebral bodies. the spinal disc. and the anterior longi tudinal (1) and posterior longitudinal (2) ligaments (right). The poste rior portion contains the vertebral canal. the bony segments associated with it. and assoc iated ligaments including the ligamentum flavum (3), the interspinous ligament (4). and the supraspinous ligament (5). Other soft-tissue structures (e.g.. capsular ligaments. etc.) are not shown. FIGURE 5.2 1 . Left: A basic motion segment of the lumbar spine di

83

Cushion and Distribute Stresses

The int ervertebral discs sustain and distribute pri marily com pressive loading of the vertebrae and restrict excessive motion. The disc consists of a tough outer covering of fibrocarTilage, the a n n ulus fibrosus, bounded above and below by a plate of hya line cartilage adjacent to the vertebrae. The collagen fibers of the a n n ulus fibrosus are arranged in concentric layers and differing orientations to the vertical axis of ±30 degrees in a cross-hatched arrangement. This covering encloses a gelatinous i n ner core, the nucleus pulposus, that acts to d istribute and redi rect stresses and store energy, similar to a partially i n Aated ball. The nucleus pul POSLlS contai ns a water-binding glycosaminoglycan gel (80% to 88% water) (78) that becomes progressively less hydrated with age (79) . This change can reduce the elastici ty, abi l i ty to store energy, and stress load ing distribution properries of the d isc and make it less capable of resisting loads. In the u nloaded condition, longitudinal ligaments and the l igamenta Aava exert pressure on the disc to create a pre-stress

84

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condi tion (80) . Compressive stress on the disc through the verte bral bodies creates a circumferen tial tensile stress that is resisted by the ann ular fibers of the ann ulus fi b rosus. During motions such as flexion bending, the vertebrae rotate forward, creating compression srress and some strain (bulging) on the anterior disc and tensile srress on the posterior portion of the disc ( Fig. 5 . 4 ) . Rotation produces rorsional stress on t h e disc, which is also redis tributed through i ts structure. These strain parrerns allow verre bral movement under load, and redistribution offorces across the vertebral-disc in terface, ro m i n i m ize localized extremes i n stress.

The Bony Structure of the Posterior Segment Is a Primary Determinant of Intervertebral Ranges of Motion

Aside from thei r con nection through the vertebral bodies and the i nterve n i ng disc, the verrebrae i n teract structurally through the facets of in tervertebral j o i n ts i n the posterior portion of the mo tion segment. Under most circumstances, vertebral movement is restricted by the orien tation of these facets relative ro the verrebral column and each other ( Fig. 5 .2 2 ) . Exceptions include particular regions of the spi nal column, where arriculations with structu res such as the skull, ribs, or sacrum may add add i tional constraints on vertebral movement. The orientation of i n terverrebral facets changes throughout the spinal column (8 1 ) and the actual angle of the facets may vary significantly between i ndividuals. The ori entation of in tervertebral facets also acts ro produce additional d i rectional components (motion coupli ng, as described in the next section) in vertebral motion during basic movement, such as flexion, extension, rotation, and lateral flexion. The pri mary variation in facet o rientation can be defined i n the transverse and frontal planes. A positive angle deviation from the transverse plane ind icates that the facets are orien ted above a hor-

A.

B.

c.

FIGURE 5.22. The orientation o f intervertebral joint facets i n the

frontal and transverse planes relative to the spinal column. In the cervi cal vertebrae (A, B), the surface of the facets on either side are pa rallel to each and to a frontal plane (A), but inclined at 45 degrees above a transverse plane through a vertebra as viewed from the side (B). In the lumbar spine (C, 0), the surfaces of the facets are oriented at 45 degrees to the frontal plane (C» and 90 degrees above a transverse plane as shown from the side (0). The facet orientations restrict the mobility of intervertebral movement and define the motion-coupling characteristics.

izontal (transverse) plane through the body (Fig. 5 . 22). Positive deviation in the fron tal plane effectively describes the orientation of the facet surfaces on each side of the vertebra relative ro each other, al though the angle is defined relative ro a frontal plane (Fig. 5 .2 2 ) . The atlas and axis have facets that are almost parallel ro the transverse plane, with the remai ning facets of the cervical vertebrae oriented at a 45-degree angle ro the transverse plane and parallel ro the frontal plane (Fig. 5 . 22 ) . The alignment of the C3-7 vertebrae allows flexion, extension, lateral flexion, and rotation (82). This can be compared ro the facets of thoracic verrebrae that are oriented 60 degrees from the transverse plane and 20 degrees from the frontal plane. This allows lateral bend i ng, rotation, and some flexion and extension. The lumbar ver tebrae have facets oriented 90 degrees to the transverse plane and 4 5 degrees ro the frontal plane. This allows almost no rota tion, but flexion, extension, and lateral bend ing. The lumbosacral j o i n ts do allow more rotation (83) , with facets oriented more obliquely ro the transverse plane. The Motion of the Spine Is a Composite of Small Movements in Individual Vertebrae and Coupling Between Vertebrae

The ki nematic and k inetic considerations of spinal movements are parricularly complicated, si nce overall movements are a com posite of comparatively small movements of each vertebral seg ment. Each vertebra has some degree of rotation or translation in each of i ts transverse, sagirral, and longitudi nal axes (or 6 de grees offreedom in movement) . This movement is largely limited by the i nterverrebral joint facet orientations. These orientations vary markedly over the spinal column (8 1 ) . Flexion-extension movements are greatest in the cervical, lower thoracic, and lum bar spine; rotation is greatest in the cervical and upper thoracic spine; and lateral bending is greatest in the cervical spine and more evenly distributed over remai ning vertebrae. It should be noted here that the convention in osteopathic medicine is ro describe rotation of a vertebra as the direction i n which t h e anterior part of the verrebral body or anterio r segment rotates. In some biomechan ical texts, rotation of the vertebra is described as the direction in which the posterior segment or spinous process rotates. Even though these conventions describe the same rotary motion, they are on opposite sides of the center of rotation and therefore the inverse of each other. This differ ence can become parricularly confusing in relation ro descriptions of motion coupling between vertebrae over the spine (discussed subsequently) . The osteopathic convention will be used here, unless specific reference is made ro the spi nous process. Another caveat of the descriptions of verrebral movements given is that active, muscle contraction-based movement characteristics may or may not be similar ro movements produced by external forces (e.g., manipulations) . This should be taken int o account in com parisons of these characteristics as described in the chapters on manipulation. Physiologically normal movements of the spinal column i n a n y of t h e primary directions (flexion-extension, lateral bend i ng, rotation) produce additional motion vecrors in the vertebrae as a consequence of the orientation of the i n tervertebral facets and other arriculations (Fig. 5 . 23 ) . This coupling may include

•

5. Biomechanics

B.

A.

c.

1

D.

FIGURE 5.23. Motion coupling as influenced by the orientation of in terve rtebral facets in cervical vertebrae. A: A lateral flexing force (F) on the side of the vertebrae acting to move the upper vertebrae relative to the bottom will be redirected by the facets in a new direction (Fl). The divided moment will have a remaining flexing component (f) and a rotational component (r) that will add (couple) rotation (R) of the vertebrae to the flexing movement (B). C: A rotational force (R) on one vertebra is redirected by the facets to glide in a new direction (R l). R 1 has both a vertical (v) and a remaining rotational component (r) (vec tors). The vertical component will cause the side of the vertebra to lift upward and produces lateral flexion on the opposite side (0). However, in isolated rotation movements, this flexing moment is restricted to pro duce vertical translation (telescoping) of the cervical spine, particularly at the ( 1 -(2 joint.

motions of lateral bending (Aexion), rotatio n , and translation i n several axes simultaneously, although only major coupling rela tionships are rypically noted as cl i n ically significanr. The coupling can differ markedly over the spine and only a l i m i ted description will be given here. I n the thoracic region, rotation is coupled with lateral Aexion. This is greatest in the upper thoracic region, with the vertebrae rotating toward the same side as the lateral Aexion (8 1 ) . In the lumbar spine, rotation is also coupled with lateral Aexion, but the vertebrae rotate in a direction opposite the lat eral Aexion. Additional motion coupling in the cervical spine is described subsequen tly.

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d ue to the orientation of the facets and the rib cage. Add itional Aexion is accomplished by the tilting of the pelvis. Restriction of movement in the l umbar spine can be replaced, to some extent, by greater and earlier tilting of the pelvis. The movement of the pelvis also contributes to lateral bending and rotation of the trunk, and may be used s i milarly to compensate for restrictions. As in other m ultiple-articulation chains, movements of the spine are accompl ished th rough complex i n teractions of agonist and antagonist muscle groups. Movement aspects are accom plished through the cooperative actions of antagonistic trunk and spinal muscles, some contracting to produce the movement, others co-contracting to provide stabil ization.

Some Kinetic Considerations of Spinal Loading

Loading characteristics of the spine are sim ilarly complex com pared to movement. The loading of the spine i ncludes body weight, muscle contraction, l igamentous pre-stressing, and ex ternally applied loads. The natural kyphosis and lordosis of the spine add to the elastic resistance to load of the discs, again by redistributi ng compressive stress i n to bending stresses that can be resisted by muscle contraction ( Fig. 5 . 24). The primary load bearing region of the spinal column is in the lu mbar spine. During normal standi ng, the center of gravity of the trunk passes ncar the center of the body of the fourth lumbar vertebra (86). This distribution and the static load o n the spine can be altered appre ciably by the angle of the pelvis. Tilting the pelvic angle (sacral angle) forward from i ts normal 30 degrees to the transverse plane accentuates the lumbar lordosis. Tilting backward from the nor mal angle fla[[ens the lumbar lordosis. Both movements affect the lever arm of the body weight on the spine and req u i re com pensatory muscle activity to resisr. This also creates greater loads

A.

B.

c.

Overall Range of Motion of the Spine Varies Widely Between Individuals

The composite nature of spinal movements along with i ndivid ual structural and soft-tissue differences help to explain a great variation in the range of motion in individuals. There are also significant variations in spinal range of motion with age and sex (.84). This makes the listing of normal values without specifica tion of these factors of litrle clin ical significance. Difficulties i n defining normal ranges o f motion also derive from a large capac iry of the spine to produce compensatory changes in movement to achieve a sim ilar net movement. In this strategy, a l i mitation of movement that exists in the structural aspects of one area of the spinal column can be alleviated by a compensatory greater mobiliry in other areas (85). For example, the movement of the spinal column is also accompan ied by motion i n the pelvis. I n body Aexion, the i nitial 50 t o 6 0 degrees o f motion occurs i n the lumbar spine with I i trle contribution from the thoracic vertebra

FIGURE 5.24. A : The normal curvatures o f the spine in situ and i n a model (right) will split vertical compression components into bending forces (b) that can be counteracted with muscle contraction. B: Force moments on the back are larger if an object is furtherfrom the vertebrae being compressed. The force moment is a product of the load (L) and the load arm (la). This compressive force alone is not dependent upon the bending of the knees (C), but bending of the knees can help to shorten the load arm.

86

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on the lumbar spine during sirri ng versus relaxed standing (87). Reorientation of the spine from its normal curvature also pro duces stresses on the discs by changing the alignment of the vertebrae. The Orientation of the Spine During Lifting Can Influence the Distribution of Stress on the Lumbar Spine

Lifting an object places added stress on the spine by creating an added load at a distance from the center of support in the spine ( Fig. 5 . 2 4 ) . The stress on the lu mbar vertebrae by the load is primarily a function of the distance of the load from the vertebrae (moment arm or lever arm) and the weight of the load. Bending the body forward adds distance from the body, whether or not the knees are bent (82) . Contraction of back muscles and to some degree, in traabdomi nal pressure must counterbalance the forward-bending forces. I n consideration of posture i n l ifti ng, the lumbar spine has less resistance to bending com pared ro direct com pressive forces (88) and lateral Aexion or Aexion combi ned with axial rotation (87) i ncreases pressure on lumbar discs. This further suggests that a vertical lift i ng position of the spine is preferred ro reduce pressu res on lumbar discs. The Cervical Spine Has Some Unique Structural Properties and Biomechanical Properties

The cervical spine and its articulation with the skull have some special biomechan ical and structural properties that require spe cial consideration. I t has five of seven verteb rae that are described as more or less typical, except for the presence of the transverse foramen for the vertebral artery in C3 to C6. The groovi ng of the transverse process for the exi t of the cervical nerves lends ro fu rther structural weakness. Both the presence of the vertebral artery and the com parative structural weakness of the transverse process suggest reason for cau tion with h igh-velocity mani pula tions of this region. This is particularly true for older adults in whom both soft tissue and bone biomechanical properties add weakness ro this region. Other structural differences in the C3-6 vertebrae include more pro m i nent uncinate processes and thin ner i n tervertebral discs. Because of this, uncinate processes may also play a role in guiding and l i m i ting cervical motion (89) . The Atlas and Axis Have Additional Structural Properties That Define Their Range of Movement

The atypical vertebrae (C I , C2) have unique bony structures that l i m i t their mobil ity. The arias (C I ) has no true vertebral body or disc, but an anterior arch with an articulating surface for the dens of the axis (C2 ) . The arias articulates with the skull i n two superior facets that have a semicircular shape. This limi ts the mo tion of the skull relative ro the arias to almost no rotation. The inferior facets of the arias articulate with C2 almost parallel to the transverse plane. The axis, with i ts superior protrusion, the dens, provides an axis of rotation for C 1 . Posterior translation of the dens with in the vertebral foramen is prevented by l igamen-

rous support from the cruciform l igament. It also contains two superior, convex-shaped facets for articulation, with two slightly convex-shaped articulations (62) of the atlas that affect motion coupling in rotation. These structural properties help to make the cervical region the most mobile region of the spine. The range of motion at the atlan ro-occip i tal articulation is approximately 1 0 to 1 5 degrees of Aexion extension and 8 degrees of lateral bend ing (8 J ,89) . Axial rotation is largely precluded by the structure of the articulation, and is transferted ro the C I -C2 articulation. The C I -C2 interface is the most mobile segment of the spine with about 47 degrees of axial rotation, or almost 50% of the axial rotation capability of the entire cervical spine (90). Flexion-extension is limited to 1 0 degrees, and l i ttle or no lateral bending occurs. Throughout the cervical spine, the combi ned range of motion is approxi mately 1 45 degrees of Aexion-extension, J 80 degrees of axial rotation, and 90 degrees of lateral Aexion (89) . Motion Coupling of the Cervical Spine Includes Transverse and Vertical Translation and Rotation

Motion coup l i ng of the cervical spine also has some im portant characteristics in addition ro those mentioned earlier due to its u nique anaromy. Flexion-extension is coupled with transverse translation, particularly at the C l -C2 interface (89,9 1 ) . As dis cussed previously, lateral Aexion (side bending) tends to rotate the spi nous process away (vertebral body toward) from the di rection of bending (Fig. 5 . 23) (8 1 ) . Isolated rotation produces a vertical translation , or telescoping, of the cervical spine due to the orientation of the facets and restriction of Aexor moments ( Fig. 5 . 23 ) . Increased Mobility o f the Cervical Spine Is Accompanied by Reduced Stability

The h igh range of motion in the cervical spi ne is accompanied by a lower i nt r i nsic stabili ty, but reduced load compared ro the lumbar spi ne. This makes the cervical spine and associated soft tissue support particularly vulnerable ro excessive dynamic load i ng, with Aexion-extension i n j uries the most common. As in other areas of the spi ne, restriction of movement in the cervical spine usually results i n an increased compensarory mobility of other areas ro achieve a functional range of motion. As a result re striction of motion at one level, due to inj ury or a brace, may produce increased motion (and increased suess) at other levels (83,92) . This consideration can be im portant in the determina tion of symptom-cause relationships in the diagnosis of spi nal dysfunction.

BIOMECHANICAL CONSIDERATIONS OF THE BODY AS A UNIT Normal Locomotion (Gait) Employs the Entire Body for Efficiency of Movement

Motions of the body incorporate the i ndividual biomechanical properties of soft and hard tissues and ki nematic aspects of the

5. Biomechanics

87

these compensatory adjustments may survive the heali ng of the original i n j u ry, particularly if the recuperative process has been lengthy. Th is emphasizes the i m�ortance of the subject's history and careful observation and knowledge of mechanical body fu nc tion in the diagnosis and treatment of somatic dysfunctions. ACKNOWLEDGMENTS

A.

B.

c.

D.

FIGURE 5.25. Basic gait patterns using computer-generated (Peak Per

formance Technologies. I nc.. Englewood. CO.) stick figures of an indi vidual in normal gait. The gait cycle arbitrarily begins with the contact of one heel with the floor (A). The force of the body weight and motion on the heel (arrow) is decelerated by the anterior muscle group of the leg (m, arrow) through the ankle. B: Body weight is transferred to the supporting leg. which supports the body with slight knee flexion. C: The moving leg is swung forward and the supporting leg is slightly extended (arrow) to raise the body center of mass to its high point (dotted line). 0: The body is propelled forward by plantar flexion of the supporting leg to be "caught" with the heel strike of the moving leg and the cycle begins for the opposite side.

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individual articulations i n to complicated movement processes. A parricularly good example of this i n tegration can be found in normal ambulation or gai t ( Fig. 5 . 2 5 ) . Gait may be described as a controlled fal ling with propulsion . In this process, the cen ter of mass of the body is subjected to relatively small vertical displacements. The actual energy expended is distributed over many muscle groups beyond the legs and by subtle, but sign i fi cant movements. I n normal gait, one leg is moved forward wh i le the weight of the body is supported by the opposing leg (swing phase) ( Fig. 5.25). In the swi ng phase of the leg, the foot goes from plantar Aexion to dorsal Aexion. The knee is Aexed and then extended, the hip moves from extension to Aexion, and the pelvis rotates and changes its tilt as muscles of the lower spine and trunk are used to generate power. Swi ngi ng the opposing arm will assist in com pensating balance and rotation moments through the trunk. The body is propelled forward and its center of mass moved slightly upward and then forward and down to be "caught" by the heel strike of the ex tended leg. As the heel hits a surface, the foot rocks down and is decelerated by the anterior muscle groups of the leg. The knee, which initially is almost completely extended, begins to Aex and becomes progressively loaded as the body weight is transferred from the opposing leg. The opposing h i p and pelvis are then rotated forward to begin the process for the opposite side. Small adjustments, such as increasing the tilt of the trunk and head in the direction of progression, bring the center of mass of the body forward and assist in increasi ng the rate of movement. This basic process, grossly si mplified here, can reAect one of the most frequently encountered examples of the ability of the body to adapt to injury or degenerative processes. Compensatory gait patterns can vary widely according to the underlying cause, but always have an underlying biomechan ical rationale, even though these adaptations may themselves produce problems. I n a typical example, an injur y to the knee or foot on one side may pro duce a compensatory shift of the body center of mass over the opposing limb. This will produce pain , stress i n j uries, or palpa ble dysfunctions i n the opposite knee, back, h ip, or even neck, if body posture has been significantly affected. Some aspects of

The writing of this chapter has been supported by the New York College of Osteopathic Medicine (NYCOM) of the New York I nsti tute of Tech nology, Old Westbury, N Y. The author wishes to acknowledge the hel pful comments of Dr. Stanley Sch iowitz, D.O., and other members of the N YCOM facu l ty and staff in the preparation of this chapter. REFERENCES I . Nordin M, Frankel V H . Biomechanics of bone. I n : Nordin M, Frankel

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AUTONOMIC NERVOUS SYSTEM FRANK H. WILLARD

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• •

•

The two components of the peripheral nervous system are: somatic and autonomic The somatic component provides innervation of the skeletal m uscle; while the i n fl uence of autonomic portion, representing the predominant component, is seen on almost all other tissues i n body Organ ization of the autonomic nervous system is similar to the somatic nervous system , i ncluding the fol lowing toles: receiv i ng afferent fibers, processing i n formation i n central circuits, and form i ng output t o connective tissue cells, smooth muscle cells, secretory cells, and i m mune cells The distinctive feature of the autonomic nervous system is the two-step output pathway involving centrally located preganglionic neurons and peripherally located ganglionic neurons There are two anatomically, biochemically, and functionally distinct divisions of the peripheral autonomic nervous system : sympathetic and parasympathetic, with dual effects o n many organ systems I n nervatio n of the visceral organs occurs through the great autonomic plexus that extends fro m the base of neck through the thorax, diaphragm, and abdomen and terminates i n the pelvis The great autonomic plexus is supplied with parasympathetic fibers fro m the vagus and pelvic splanch n ic nerves and sympathetic fibers fro m the thoracic, l u mbar, and sacral splanchnic nerves The central origin and i m portance of sympathetic and parasympathetic innervation for organ systems in the head, neck, thorax, abdomen, and pelvis The origin and importance of sympathetic i nnervation for the peri pheral vasculature The primary afferent i n nervation of organ systems is i nstrumental in controlling the output of the autonomic nervous system Neuropeptide markers in afferent nerve fibers and small-caliber, primary afferent fibers i nvolved with detection of nociceptive stimuli

Our daily existence depends on the coordinated activities of our internal organ systems. A major factor in orchestrating the diverse functions ofthese i nternal structures is the autonomic ner vous system . Through an extensive network of connections, the autonomic nervous system helps mai ntain the normal rhythm of activity in the visceral organs, adjusting their output to accommo date any external challenge. The limbic structures of the brain comrol the autonomic nervous system through the hypothala mus. The hypothalamus itself is closely imegrated into a com plex network involving the endocrine and immune systems. This conglomerate ofimerlocking systems, with its pervasive influence on our physiology and psychology, is called the neuroendocrine i m mune network. This neuroendocrine-imm une network is fur ther described in Chapter 8 . The terminology used t o describe the part o f the nervous system usually not under voluntary control varies widely. Since the 18th century, different terms have been used by researchers in different countries. None of these terms refers to the exact same gtoup of structures or functions. Examples include: Vegitive Nervensystem Grand symapathique Ganglionic nervous system Visceral nervous system The two most commonly used terms are vegetative and auto nomic nervous system . For a thorough discussion of the history of terminology concerning this system , see Clarke and Jacyna (I). The present chapter uses the term autonomic nervous system to refer to all components of the nervous system using pregangl ionic and ganglionic neurons as an efferent pathway. This defi nition excludes only the neuromuscular junctions between the ventral horn of the spinal cord (and a few cranial nuclei) and skeletal m uscle. The clinical i mportance of understanding the circuits of the autonomic nervous system cannot be overstated . Almost all com mun ication between neurons in these circuits occurs via synaptic transmission. This process depends on the production, d istribu tion, and recognition of specific neurochemicals. Most pharma ceutical agents, either as a desired first anion or as an undesired side effect, affect these metabolic and stereologic events. Knowl edge of nervous system structure, function, and chemistry is a necessity for the educated use of these substances and the i ntel li gent approach to the mai ntenance of health.

6. A u tonomic Nervous System

The autonomic nervous system is sensitive to evems occur ring in somatic tissue such as curaneous and musculoskeletal systems. The autonomic and somatic nervous systems are i n terlocked through numerous somatovisceral and viscerosomaric reAexes. Visceral symptoms may be the primary manifestations of somatic dysfunction and vice versa. This chapter examines the organ ization of the autonomic nervous system and its afferem componem and emphasizes the pattern of i nnervation reaching the major organs of the thoracoabdomi nopelvic viscera and the segmental represemation of these organs i n the spinal cord.

ORGANIZATION OF THE AUTONOMIC NERVOUS SYSTEM

The autonomic nervous system has components in both the cen tral and peripheral nervous systems ( Fig. 6. J). The maj o r auto nomic components of the central nervous system (CNS) i nclude: Limbic forebrain Hypothalamus Several brainstem nuclei [mermediolateral cell col u mn of the spinal cord The autonomic components of the peripheral nervous system (PNS) include numerous ganglia (collections of neuron cell bod ies located outside of the central nervous system) and a network of fibers distributed to all tissues of the body with the exception of the hyal ine cartilages, the cemers of the i mervertebral disks, and the parenchymal tissues of the cemral nervous system. This review focuses on the peripheral distribution of the autonomic nervous system.

1

91

Peripheral Nervous Systems

The axons from neurons located in the CNS enter the periphery through spinal and cranial nerves. The peripheral portion of the nervous system can be divided i nto two fundamental parts based on the target structures of efferem fibers. Axons derived from the somatic componem of the peripheral nervous system i n nervate skeletal muscle. Axons derived fro m the autonomic component of the peripheral nervous system emer the periphery and form complex i merwoven plexuses con taining clusters of cell bodies called ganglia. Neurons in these ganglia i nnervate all other targets, incl ud ing: Smooth m uscle Cardiac m uscle Glands Connective tissue Cells in the immune system This fundamemal d i vision in the peripheral nervous system also reflects differemial methods in cel lular communication. The mechanism of transmission in the neuromuscular j unction of the somatic system i n volves ionotrophic principles (2). This mech anism uses the ion-gated channels to quickly depolarize the cell membrane, a p rocess referred to as fast transmission. Conversely, chemical signali ng i n the autonomic peripheral nervous system uses metabotrophic principles and vol ume transmission (3), the diffusion of transmitter substance away from axonal vesicles, as well as fast synaptic transmission. The metabotrophic methods of signal ing usually involve a neuromodulator that binds to a mem brane receptor, activating second-messenger pathways with i n the target cell . These methods are also called slow transmission and often lead to altered gene expression. To further understand the distinction between somatic and visceral peripheral nervous sys tems, compare the typical neural circuitry p resent in reAex arcs.

Limbic Forebrain

SOMATIC REFLEX ARC

Hippocampus Amygdala Prefrontal Cortex Cingulate Cortex

CNS

/1 1

FIGURE 6.1. eNS,

Parasympathetic

•

, Hypothalamus

I� 1 •

Sympathetic

General organization of the autonomic nervous system. central nervous system; PNS, peripheral nervous system.

Input and output for the peripheral somatic nervous system oc cur through spinal and cranial nerves. Fig. 6.2 diagrams a typical spinal nerve, i l l ustrating the basic circuitry of the somatic reAex arc. I n its simplest form, the reflex arc comains a primary afferent neuron in a ganglion and a cemrally located motor neuron con nected by a synaptic j unction. Because only one synapse separates the input fro m the output, this circuit is called a monosynaptic reflex. The cell body of the primary sensory neuron i s located in the dorsal root ganglia or in the peripheral ganglia of a cranial nerve. The peripheral process of the sensory neuron is d i rected outward along a spinal or cranial nerve to reach i ts target in the peripheral tissue. This process e ither acts as a receptor end organ i tself or is attached to one located in skin , m uscle, or connec tive tissue. Each sensory neuron also has a central process (axon) that extends i nto the dorsal horn of the spinal cord or i n to the brainstem. Two fundamental types of primary afferem neurons are present in sensory gangli a . One class of sensory neuron features a large cell body with a myeli nated process; this kind of cell forms the A-afferem o r large-caliber fiber system and is i nvolved

II. Osteopathic Considerations in the Basic Sciences

92

Axon of interneuron

Central processes of primary sensory neurons

Primary sensory neuron

Muscle spindle

Dorsal horn

Skin Ventral root

Ventral horn

PreganglioniC fiber

Interneuron

Motor neuron

M uscle fiber & motor unit FIGURE 6.2.

Components of somatic reflex arc.

Postganglionic fiber

Afferent fiber Autonomic ganglia

in proprioception or discr i m inative mechanoreception (4). Con versely, other sensory neurons have small cell bodies, w i th lighrly myeli nated or un myel i n ated processes. These cells form the B afferenr or smal l-caliber fiber system and are i nvolved in crude rouch and nociception (4) (see Chapters 7 and 8 for additional discussion of this concept). The second component of the monosynaptic reflex arc, the moror neuron, has a cell body in the ventral horn of the spinal cord or a brainstem nucleus. Moror neuron axons leave the central nervous system in the ventral root of a spinal nerve or in a cranial nerve, eventually i nnervating i ts effecror organ, skeletal muscle, through a neuromuscular synaptic j unction. These monosynaptic reflex connections occur between the largest sensory neurons (the A-afferent system) and ventral horn moror neurons i nnervating skeletal muscle. All other somatic reflexes i nvolve the presence o f i n rerneurons situated between the central processes of the sensory neuron and the moroneurons; several synaptic connections m ust be traversed ro complete the arc. Such circuits are called disynaptic or polysy naptic reflex arcs. The polysynaptic reflexes i nvolve i nput from both A-afferenr and B-afferenr systems. Although the addi tion of i n terneurons i nro the circui t slows the conduction of i nforma tion through these reflex arcs, it greatly fac i l itates the construction of more complex circui ts and, consequently, more complicated behavior patterns in response to sensory i nformation.

AUTONOMIC REFLEX ARC

I n put and output for the peripheral auronomic nervous sys tem occurs via spinal, cranial , and splanchnic (visceral) nerves. Fig. 6.3 is a d iagram of a typical spinal nerve and its connections with a splanch nic nerve. The afferenr neuron has a peripheral

Intestinal wall FIGURE 6.3.

Com po n e nts of visceral reflex arc.

process ending i n a v isceral organ or a blood vessel, a cell body located in the dorsal root gangl ia, and a central process that ter m inates i n the dorsal horn of spinal cord. This central process ter m i nates on i n terneurons that, in turn, in nervate the effecror (moror or pseudomoror) neurons in the gray matter of the spinal cord or brainstem. The effecror or preganglionic neurons are found i n the lateral horn of the spinal cord or in specific brain stem nuclei; their myelinated pregangl ionic axons terminate on ganglionic neurons located outside of the central nervous sys tem. These per i pheral neurons are found either in encapsulated ganglia i n the fascia of the body wall or in ganglia embedded in the fascia surrounding a specific organ. Unmyelinated, postgan glionic axons travel from peripheral gangl ia ro cellular targets i n visceral organs. The presence o f two sequenrial neurons in the output pathway is a critical feature d istinguishing the auronomic fro m somatic peripheral nervous systems. The sensory neurons of these two systems are otherwise very s i m ilar in morphology and function. Gangl ionic neurons of the auronomic system are found pri marily in three locations (Fig. 6.4): 1. The paravertebral ganglia or sympathetic trunk lying along the side of the spinal cord.

6. A utonomic Nervous System

Preganglionic fibers --

Gray communicating rami to all spinal nerves

/

--

Distribution

Collateral ganglia and Prevertebral Plexuses

Trunk Ganglia

Central Origin

Postganglionic fibers -

Cardiac and pulmonary plexuses

-� ;�;�� __ medulla H yp -o "" " : " \ " gastric . ' plexus . \\ \ Small \\ \ intestine \ \ : \ \ : " ..

\'. '�,

/

.

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1,

' '

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ganglia

\

'o, . '"

:

I,

, '

'

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\ '\ it \ \./ \

I

:

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tol �� ,,;.- t.J

,''

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Kidn y ,:,

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'

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Sex organs FIGURE 6.4.

Sympathetic division of peri pheral autonomic system.

CG, celiac ganglion; SMG, superior mesenteric ganglion; IMG, i n ferior mesenteric ganglion. From Chusid JG . Correlative Neuroanatomy and Functional Neurology. Los Altos, CA: Lange Medical Publishers; 1985, with permission.

2. The prevertebral ganglia or collateral ganglia scattered in sev eral clusters associated with the large vessels of the abdominal cavley. 3. [n isolated ganglia or hypogastric ganglia embedded i n the adventitial tissue of specific visceral organs of the pelvis. These ganglia con tai n a varieey of chemically differentiated neurons producing numerous neuroregulators. The ratio between

93

pre- and postganglionic neurons has been reported to range from 1:2 to 1:196 for sympathetic ganglia and 1:1 to 1:6,000 for parasympathetic ganglia ( 5). This arrangement of a few central neurons i n A uencing effector organs through a large battery of chemically distinct, postganglionic neurons is divergent in na ture. As such, it allows for a l i m i ted number of input channels to ini tiate numerous, complex motor and secretomotor responses. M any of the peripheral ganglia, especially in the gastroin testinal system, also contain sensory neurons that do not com m u nicate with the central nervous system; instead, their axons terminate o n ganglionic efferent cells (6) . Local reAex arcs are established that do not communicate with the central nervous system . In this respect, the visceral autonomic ganglia act as small brains; in fact, these ganglia can maintain some visceral organ functions even when all com m un ication with the central nervous system is severed. In such cases, even though the organ responds to changing i nternal stimuli, it is not able to respond to changes in external stimuli. Autonomic ganglia are capable of managing thei r specific organ systems in isolation, but rely on input fro m the central nervous system for signals conce rn i ng the conditions in the external environment.

DIVISIONS OF THE AUTONOMIC NERVOUS SYSTEM

The peripheral autonomic nervous system can be separated into two major divisions based on structure, chemistry, and function: sympathetic and parasympathetic. In general, each organ receives innervation from both divisions, one acting to enhance or accel erate the activiey of the organ and the other division acting as an inhibitor or decelerator. The m aj o r exception to this rule is the innervation of the peripheral vasculature, hair foll icles, and sweat glands of the trunk and extremi ties. These latter structures are serviced solely by the sympathetic system. H owever, in this situation, cholinergic fibers arising in the sympathetic ganglia are i nvolved in at least hair follicle and sweat gland i nnervation , i f n o t t h e peripheral vasculature (7). These fibers have been termed the sympathetic cholinergic system. The distribution of the sym pathetic nervous system is illustrated in Fig. 6.4 and that of the parasympathetic nervous system in Fig. 6 . 5 . A morphologic distinction between sympathetic a n d parasym pathetic systems is seen in the arrangement of their ganglia. I n general, the ganglionic neurons of the sympathetic nervous sys tem are located i n the paravertebral and prevertebral ganglia with the exception of scattered ganglia found in the hypogastric plexus of the pelvis. Those of the parasympathetic nervous system are found in ganglia located on either cranial nerves or organ walls. The preganglionic axons of the sympathetic system tend to be short, reaching only to the paravertebral and prevertebral ganglid. , and the postganglionic axons, which reach to the visceral organs, are longer. The situation is reversed in the parasympathetic sys tem where the preganglionic axons tend to be long (extending all the way to the ganglia i n the organ wall) and the postgangl ionic axons tend.to be short (confined to a distribution along the organ wall) (Fig. 6.6). This distinction between the major divisions of the auto nomic nervous system is further reflected in their chem istry. The

94

If Osteopathic Considerations in the Basic Sciences +-88 cm (35").

(Modified from Grundy

SM, et al. Assessment of cardiovascul a r risk by use 1 999; 1 00: 1 48 1 -

of m u ltiple-risk-factor assessment equations. Circulation

1 492.)

2000-201 0 decade (92). Clearly, the vast majoriry of heart at tacks and manifestations of ischemic heart d isease are preventable, si nce the cause of coronary atherosclerosis is largely extrinsic to the person. Table 24. 1 l ists the standard risk factors for CAD. The major modifiable risk factors are cigarette smoking, diet, obesiry (and subsequent rype 2 diabetes), and a sedentary lifesryle. Only one, family history, might be considered to be an i ntrinsic risk factor. The most com mon conditions associated with heart failure i n the United States are CAD and hypertension. Since CAD is preventable, and hypertension is imminen tly treatable, most cases of heart fai l u re are potentially preventable. Figure 24.3 depicts the prevalence of certain conditions associated with heart fai l ure by gender, while Table 2 l ists the preci pitating causes of heart fai l ure. Molecular genetics offers the possibiliry of a new paradigm for cardiology and medicine. Despite our knowledge of diag nosis and treatment, we seldom know the etiology or the spe cific molecular defect responsible for disease. Over the next few years, when the H uman Genome Project is completed, there will be thousands of etiologies and specific molecular defects to be linked with their respective disease. Prevention will become the key to future success and represent the major initiative for the 2 1 st century. The field of pharmacogenomics will evolve rapidly in the next decade, and individualization of therapy (the antithe sis of health maintenance organizations and managed care) will be the norm (93,94). For example, ACE inhibitors may be more effective than angiotensin 1 (AT- I ) receptor blockade for the hy pertensive patient who has expressed a vulnerable polymorphism in the ACE, whereas the latter migh t be more appropriate for

24. A n Osteopathic Perspective on Cardiology Condition Hypertension

Coronary Heart Disease

endogenous neurohumoral mechanisms activated during heart faiJure played an advantageous, supportive role, and they were ad vised not to i nterfere with these compensatory mechanisms (96) . I t is now believed that systemic vasoconstriction will decrease left ven tricular systolic performance and accelerate the progression of heart fai lure. Consequently, neurohumoral blockade with ACE i n h ibitors and ,B-blockers represent the standard therapy in heart failure management. I n contrast, B-type natriuretic peptide is synthesized in the ventricular myocardium and released i n to the circulation i n response to ventricular dilation and pressure over load ( 97) . The serum level of brain natriuretic peptide ( B N P ) h a s n o w been shown t o have diagnostic a n d prognostic value. I ntravenous i n fusion of BNP i n pharmacologic amounts repre sents an effective form of vasodilator therapy for patients with decompensation of heart failure ( 98) .

•••

j{L..!�(LL,.CLL.l:tj

Cigarette Smoking

ECG-LVH

Valvular Heart Disease

iiii

Diabetes Mellitus

o

20

40

60

•

Men

121

Women

80

1 00

Prevalence (%) FIGURE 24.3. Prevalence of certa i n conditions among Fra m i ng h a m Heart Study subjects w i t h congestive heart fa i l u re, b y gender. ECG LVH, e lectroca rdiographic left ventricu l a r hypertrophy. (From Ho KK, Pinsky J, Kanne LWB, Levy D . The epidemio logy of heart fa i l u re; the Framingham Study. J Am Coli Cardiol. 1 993;22[Suppl AI:6A-1 3A, with permission.)

those with an expressed vul nerable polymorphism in the AT- I receptor. Familial hypertroph ic cardiomyopathy was the first primary cardiomyopathy to be defined in terms of a genetic linkage (95) . The early practitioners of osteopathic medicine believed that the body produced its own medicine for heali ng, especially i f there was normalization of structural abnormalities that affected circulation, the lymphatics, and nerve function. In cardiology, the challenge is to determine when the production of endoge nous substances is beneficial and needs to be supported, or when i t is deleterious. A few decades ago, physicians believed that the

TABLE 24. 2 . PRECI PITATING CAUSES OF HEART FAI LURE Acute myoca rdial ischemia or infarction Nonadherence to therapy ina ppropriate reduction i n medications noncompl iance with d ietary sod i u m restriction Systemic hypertension Arrhythm ias, espec i a l l y atrial fibril lation System i c i nfection Anem i a Thyrotoxicosis Infective endocarditis Myocard itis Physical, emotional, or environmental stress Burden of new u n related i l l ness renal fa i l u re volume overload following surgery Cardiac-depressant or salt-reta i n i n g drugs Cardiac toxins alcohol cocaine anti-cancer chemotherapy Pregnancy

349

Tenet IV: The Musculoskeletal System Significantl y Influences the Individual's Ability to Restore the Inherent Capacity to Maintain Health and Therefore to Resist Disease Process

A sedentary lifestyle was elevated to the status of a primary risk factor for CAD i n 1 994 ( 99). To a large degree, this risk may ac crue because of the rising importance of type 2 diabetes as a major risk for the development of CAD ( 1 00, 1 01 ) . The m usculoskele tal system plays a major role in the predisposi tion of patients to develop type 2 diabetes, because of the i n terrelationship between insulin resistance (which largely resides in the m usculoskeletal system), obesity, a sedentary lifestyle, and lack of physical fi tness. The National Heart, Lung and Blood Institute has identified smoking, obesity, and physical i nactivi ty to be the greatest threats to cardiovascular health i n this decade ( 92) . Fitness and exercise capacity represent an i m portant prognos tic marker for the general population ( 1 02) , patients with heart fail ure ( 1 03) , and patients with coronary heart disease ( 1 04). As described subsequently, the m uscle hypothesis is a new model of heart failure that proposes that the signs and symptoms of heart failure are often related to the abnormal activation of muscle er goreceptors, which causes an i ncrease in ven tilation and resultant sensation of breathlessness. For as many of one-fourth of patients with heart failure, functional l i m i tations are caused by the m us culoskeletal system, and not by diminished cardiac output. The i ntervemion of cardiac rehabil i tation exercise provides an increase in exercise capacity that is twice that achieved with ACE inhibitor therapy. The specific challenges to osteopathic medicine in the field of cardiology are many. The musculoskeletal system manifests subtle changes in response to chronic CAD ( 105) or acute MI ( 1 06) , which may be detected by a focused palpatory exam i nation. These basic observations give rise to additional questions. Can palpatory exami nation be used in a l o ngitudinal manner to learn more about the natural h istory of patients with CAD? Will an emphasis on the role of the musculoskeletal system in health and disease contribute to the effective treatment of patien ts with coronary heart disease or heart failure? Will the osteopathic physician's traditional role as primary caregiver lead to im proved therapy or more effective approaches to the prevemion of heart d isease?

350

VI. Osteopathic Considerations in the Clinical Specialties

Asymptomatic

Symptomatic L----.J

� �

Angina Myocardial infarction Sudden death

O Q Q) Q Decades

CORONARY ARTERY DISEASE Pathophysiology and Natural History

The pathophysiology of CAD has been investigated extensively on both sides of the Atlantic for the last century. The l i terature now clearly defines the pathophysiologic processes that underlie the development of the atherosclerotic lesion, from its beginni ngs as a fatty streak to the complex obstructive lesion that character izes ischemic heart disease ( J 07-1 1 0) . Similarly, cross-sectional and longitud inal epidemiologic surveys have clearly identified the role of risk factors in the development of coronary atheroscle rosis, which have been summarized in various reports ( 1 1 1 1 1 3) . O n e of the most i mportant clinical characteristics of ischemic heart disease is shown i n Fig. 24.4. Atherosclerotic lesions can progress slowly for decades before they become symptomatic. Then, in a matter of moments, the lesions become symptomatic, with three manifestations: angina pectoris, M I , and sudden car diac death. Angina is the only symptomatic presentation of is chemic heart disease in which there is neither permanent morbid i ty nor mortality, giving the physician the greatest opportun i ty to do the most good for the patient. Epidemiologic studies of ischemic heart disease have concen trated on risk factors for coronary atherosclerosis, the early de tection of asymptomatic disease, and the role of primary and secondary risk factor modification for the prevention or ame lioration of heart disease. Physicians are now calling for an in vestigation into the triggers that transform the atherosclerotic plaque from an asymptomatic lesion into a symptomatic lesion. The h istopathologic events associated with the transformation of stable atheroma i nto one of the acute coronary syndromes are now well defined from autopsy, cardiac catheterization, and in travascular ul trasound studies. The interrelationship offive vas cular mechan isms causing acute myocardial ischemia is shown i n Fig. 24.5. Recently, Braunwald proposed an etiologic approach to man agement of unstable angina ( 1 1 4) . He described five different, but not mutually exclusive, causes of angina: l.

FIGURE 24.4. Natural history of coronary heart disease.

Minutes

Nonocclusive thrombus on preexisting plaque

2. Dynamic obstruction (coronary vasoconstriction) 3. Progressive mechanical obstruction 4. InRammation and/or infection 5. Secondary angina pectoris ( unstable angina precipitated by conditions extrinsic to the coronary vascular bed, such as thy rotoxicosis, anemia, hypotension, etc.)

This chapter will focus only on those acute coronary syn dromes that share in common the pathophysiologic features of plaque fissure and/or rupture, and the subsequent development of thrombus on preexisting plaques. This type of u nstable angina represents approximately 75% of those patients described in the Braunwald classi fication ( 1 1 4) .

Vascular Biology of Acute Coronary Syndromes

The acute coronary syndromes represent a spectrum of conditions that hold in common the presence of plaque fissuring, which has been described as the cause of acute M I and unstable angina, as well as sudden ischemic death ( I 1 5) . The disruption of a formed plaque is a complex process that is the central feature of the i n i tiation of the acute coronary syndromes. The sudden total or near total occlusion of a coronary artery usually occurs at the site of stenosis that was previously not hemodynamically significant, or at least not critical ( 1 1 6) . The arterial lesion of unstable angina and MI is a complex eccentric plaque angiographically, which histologically represents a ruptured plaque with superi mposed thrombus.

Nonocclusive

P rogressive

thrombus

mechan ical

o n pre-existi n g

obstruction

p l aque

Secondary

Dynamic

u nstable

obstruction

angina

(Spasm) I nflammation/ I nfection

F I G U R E 24.5. A framework f o r express i ng t h e contribution of five pathophysiologic mechanisms that may cause unstable angina. Each component may contribute to the c l i n i ca l picture i n varying degrees. The most common occurs when atherosclerotic plaque causes moder ate obstruction a n d acute thrombus overlying the plaque causes very se vere narrow i n g . A common form of Prinzmetal angina occurs when the spasm is superimposed upon m i l d atherosclerotic obstruction. (Modified from Braunwald E. U nstable a n g i n a . An etiologic a pproach to manage ment. Circulation. 1 998;98:221 9-2222.)

24. A n Osteopathic Perspective on Cardiology There are cwo main componenrs ro the vulnerable atheroscle rotic plaque: the lipid-rich core, and the meshwork of extra cellular-matrix proteins that form the fibrous cap. The vulner able atherosclerotic lesion, although not necessarily stenotic at angiography ( 1 1 7) may be prone ro disruption because of i ts soft ness caused by a high .I ipid contenr and macrophage-dependent chemical properties. Chronic minimal inj ury ro the arterial endothelium is physi ologic and is often the result of a disturbance in the pattern of the blood Row at bending poinrs and near bifurcations in the arterial tree. In addition ro these local shear forces , endothelial dysfunc tion occurs because of hypertension, hypercholesterolemia, ad vanced glycation end products from diabetes, chemical irritants in robacco, circulating vasoactive amines, im mune complexes, and perhaps infections. Passive plaque disruption occurs most often where the fibro us cap is the most th i n , where it is most heavily infiltrated by foam cells and therefore weakest, and at sites of mechan ical stress. Active disruption of atherosclerotic plaques may be i n i tiated by proteinases that are secreted by macrophages which then enzy matically degrade the fibrous cap by phagocyrosis or secretion of proteolytic enzymes. These enzymes include plasmi nogen acti varors and matrix metalloproteinases. In addition ro degradation of the matrix of the fibrous cap, shedding of membrane mi croparticles leads ro a potent procoagulant activity. These shed particles account for almost all the tissue facror activity present in plaque, and may be a major contriburor in the initiation of the coagulation cascade after plaque disruption. Following plaque disruption, local thrombosis results from complex i n teractions becween the l ipid core, smooth muscle cells, macrophages, and collagen. Over the past 35 years the view has evolved that the acute coro nary syndromes are caused by plaque rupture and formation of a platelet thrombus. Greater platelet stability and transmural in farction have been attributed ro more severe or extensive plaque rupture. Unstable angina and non-Q wave infarction were be lieved ro be due ro less extensive, and less stable platelet thrombi that caused less severe, less extensive ischemia and/or infarction. However, more recent clin ical findi ngs have refined th is view point ( l 1 8) . The occlusive thrombi causing Q-wave M I contain more fibrin than the thrombi found in other acute coronary syn dromes that are characterized by more platelets and less fibrin. The higher fibrin content of thrombi causing Q-wave infarction explains their higher stability. Further, this higher fibrin content suggests that the coagulation cascade is activated ro a greater de gree during Q-wave infarction than during non-Q-wave infarc tion, in which platelets play a more dominant role. This patho physiologic feature defines the therapeutic role of thrombolytic agents for patients with ST-segment elevation M I , and the use of anti platelet agents (aspiri n , hepari n, platelet glycoprotein l Ib/IIIa recepror blocking agenrs) in non -Q-wave M I . I n about one-third of patients with acute coronary syndromes, and particularly in acute sudden coronary death, there is no dis ruption of a fairly small lipid-rich plaque, j ust a superficial erosion of a markedly stenotic and fibrotic plaque ( 1 1 9) . Thus, compli cated thrombi may well be dependent on a hypercoagulable state triggered by system ic facrors. Evidence conti nues ro evolve that circulating monocytes and white blood cel ls may be i nvolved i n

351

tissue facror expression a n d thrombogenicity. Further, t h e pre dictive value for coronary evenrs of h igh ti ters of C-reactive pro tein may be a mani festation of such systemic phenomena ( 1 201 22) . Hypercholesterolemia, a high catecholami ne drive, and perhaps infection may also be triggers of such hypercoagulable phenomena. Up until recently, the embol ization of plaque content and of platelet-thrombus i nro the distal m icrovasculature was thought ro be uncommon. However, recent studies indicate that m icrovascu lar embol ization is not only common, but carries an adverse prog nosis ( 1 23) . H isrologic studies have confirmed platelet thrombus as part of occlusive material in the downstream m icrovasculature, and atherosclerotic particulate material has been identi fied as well. I n addition, endotheli al cells have been found ro be present in the circulation with a h igher frequency in patients with acute coro nary syndrome compared with control patients, or those with stable effort angina. The benefits of short-term platelet glycopro tein I IblI l la-recepror blocking agents appears ro be related ro a decrease in m icrovascular obstruction from embol ization with a subsequent decrease i n myocardial necrosis and decrease in risk for mal ignanr arrhythmias. These agents do not decrease the em bolization of atherosclerotic lipid and matrix constituents. The embolic evenrs may also reRect significant inRam mation in the diseased artery. In summary, for patients with chron ic, stable CAD , angina or si lent ischemia commonly results from increases in myocard ial oxygen demand that o utstrips the abi l i ty of stenosed coronary arteries ro supply the needed blood Row. I n contrast, in acute coronary syndromes, there is an abrupt reduction in coronary Row. In unstable angina, a relatively small erosion or fissuring of an atherosclerotic plaque may lead ro an acute change in plaque structure and a reduction in coronary blood Row, resulting in exacerbation of angina. Transient episodes of thrombotic ves sel occlusion at the site of plaque injury may occur, leadi ng ro angina at rest. This thrombus is usually labile and results in tem porary vascular occlusion, perhaps lasting only 10 ro 20 minutes. In non-Q-wave M I , more severe plaque damage would result in more persistent thrombotic occl usion, perhaps lasting up ro 1 hour. Resol ution of vasoconstriction may also be patholog ically important in non-Q-wave M l . Therefore, spontaneous thrombolysis, vasoconstriction resolution, and the presence of collateral circulation are important in preventing the develop menr of Q-wave infarction by l i m i ting the duration of myocar dial ischemia. In Q-wave M I , larger plaque fissures may result in the formation of a fixed and persistent thrombus, which is rich in fibrin.

DIAGNOSIS

The process of screen i ng patients for heart disease involves the use of the h isrory, physical exam ination, ECG , and chest roentgenogram. The diagnosis of ischemic heart disease is most easily accomplished with patients who are sympromatic. When more attention was given ro annual health screening evaluations, treadmill stress tests were often employed as part of executive physical examinations. Testing for asympromatic CAD is not generally considered ro be a fruitful endeavor however, except in

352


TABLE 24. 3 . LIKELIHOO D OF D E F I N I N G CORONARY ARTERY D I SEASE AFTER STANDARD TREADMILL EXERCISE TESTING ACCOR D I N G TO AGE, SEX, AND SYMPTOMS I N A GROUP OF PATIE NTS WITH 1-1 . 5 M m ST SEGMENT DEPRESSION Asymptomatic

Age

Typical Angina

Atypical Angina

Nonanginal Chest Pain

Years

Men

Women

Men

Women

Men

Women

Men

Women

30-39 40-49 50-59 60-69

3.9 1 1 .0 1 8. 5 22.9

0.6 2.1 6.5 1 4.7

1 0.4 2 5.8 36.7 45 . 3

1 .7 5.8 1 6. 3 32.6

37.7 64.4 75.2 8 1 .2

8.5 24.5 50.4 7 1 .6

83.0 93.6 96.1 97.2

42.4 72.3 89. 1 95.3

(From Diamond GA. Analysis of probability as an aid in the clin ical diagnosis of coronary artery disease.

selected circumstances such as before noncardiac vascular surgery or in patienrs with multiple cardiovascular risk facrors. Diagnostic studies for patienrs w i th suspected or proven CAD fal l i n ro rwo general categories. The first consideration i nvolves establishing the diagnosis of CAD. The h isrory is the cenrral el ement in this diagnosis. N umerous studies over the past three decades have validated Bayes theorem, clarifying that virtually every cardiovascular study performed has l itde meani ng by itself bur is properly undersrood i n the conrext of the patienr's clini cal presentation ( 124) (Table 24. 3) . I n patienrs with established heart disease, the second diagnostic consideration is ro stage the severity of the disease process, and ro define the patienr's position on the continuum of stable or unstable coronary atherosclerotic syndromes described previously. A h igh correlation exists berween the clinical impression of stable angina, accelerated angi n a, resting angina, and acute M I with the findings demonstrated o n angiography ( 125) and an gioscopy ( 1 26) . The ini tial evaluation should distinguish berween those patienrs at low risk for M I who can be further evaluated on an outpatienr basis and those patienrs for whom immediate hospitalization is required (127). The evaluation of patients presenring with chest pain contin ues ro be challenging. This is in spite of new advances in our understanding of the pathophysiology of acute coronary syn dromes, new biochemical markers for cardiac injury, and i nsights from large, randomized conrrolled trials that provide i mportanr data on risk stratification and appropriate algorithms for patienr managemen t. The assessmenr ofchest pain represenrs the starti ng poin r for evaluating the possibility that a person m ight have an acute coronary syndrome. The pertinenr features of this evalua tion are equally i mportant for the primary care physician, emer gency room physician, cardiologist, or house officer. The critical componenrs of the evaluation i nclude the hisrory, physical ex amination , and ECC. There are several impl ications that arise from this apparendy sim ple precept. Evaluation of the patienr for chest pain cannot be conducted by telephone. An individ ual who telephones their primary care physician w i th a descrip tion of chest pain m ust be referred to a clinical setting where an ECC can be performed. Some of these patienrs will be shown ro have acute M I , when it is appropriate for i mmediate resrora tion of Aow through thrombolytic agents or direct angioplasty. Si nce the only h i nr that would reveal the urgency for this action is the description of chest pai n , quality assurance programs for the evaluation of patients with acute coronary syndrome should not j ust look at door-ro-needle time for thrombolysis. Rather, an

N

Engl ) Med. 1 979;300 : 1 3 50-1 3 58, with permission.)

assessmenr needs ro include door-ro-ECC i nterpretation time, door-to-cardiac marker result time, and door-ro-initiation ofgen eral treatmenr time (Fig. 24.6) . The general category of diagnostic studies for cardiovascular disease i ncl udes imagi ng techniques, tests of myocardial function, and physiologic assessments of cardiac performance. The new imaging techniques (magnetic resonance imaging, conventional or rapid sequence computed romography, and ECC studies) are expensive compared with plain chest x-ray fi lms and cardiac Au oroscopy. Many tests (such as treadmill exercise stress testing) provide functional data; they may be supplemented by imaging techniques such as postexercise myocardial perfusion imaging or postexercise ECC. Pharmacologic stress testing with dobutamine or dipyridamole is i ncreasingly being substituted for exercise stress testing. Some studies provide physiologic information alone, such as radionuclide ejection fraction. The developmenr of such a wide array of tests forces decision making. Using all noni nvasive studies is cost-prohibitive. If only a small n umber are ro be used, they have ro be carefully tailored ro the patient's cli nical state. These simple questions should be answered: Is this study being performed ro establish the diagnosis

Admission

Eyaluation forChest Pain Yes

Yes

Yes

Yes

Acute infarction Restore blood flow immediately

Evolving infarction or unstable angina

Evolving infarction

Evolving infarction

Discharge

FIGURE 24.6. Stepwise evaluation of patients presenting with chest pain.

24. An Osteopathic Perspective on CardioLogy of heart disease or ro stage known heart disease? Will the study provide useful information concerning the patient's prognosis? I s the study necessary r o determi ne the best form of therapy for a patient, to assess the benefits of previously performed procedures, or to risk-stratify for noncardiac surgery? Which test is the safest and the most feasible to perform and yields the most information, with the least possibility of confounding information? Each of these issues is widely discussed in the medical literature ( 1 281 3 1 ) . Clinical experience and thoughtful j udgment are the most important features of decision making in this area.

DISTINCTIVE CONSIDERATIONS IN THE APPROACH TO THE PATIENT WITH CORONARY HEART DISEASE

The history is a critical feature of the evaluation of patients sus pected of having CAD. From the start, as J. Willis Hurst points out, the physician interview with the patient has a dual pur pose: to obtain important medical information and ro establish a bond berween the patient and the physician ( 1 32). Since the management of CAD involves lifestyle changes recommended by the physician, the initial h istory may also be considered as the first step in establishing the foundation for later risk facror modification programs. Physicians should recall that the history of chest pain typical for angina pectoris may be present in a minority of patients with ischemic heart disease. Unusual somatic representation of chest pain to a site of previously experienced somatic pain may occur because of facilitation, convergence, or other mechanisms at the spinal level ( 1 33, 1 3 4) . Unti l recen rly, episodes of angina were thought to be synonymous with myocardial ischemia, and chest pain was considered to be a reliable indicator of ischemia. Several reports have since demonstrated that episodes of asymptomatic myocardial ischemia are common in patients with known CAD ( 1 35- 1 37) . Similarly, the Framingham Study has shown that unrecognized M Is are common, responsible for at least one out of every four infarctions. Half of the unrecognized infarctions are silent; the remainder are so atypical that neither the patient nor the physician entertains their possibility ( 1 3 8) . Clinical studies o n the manifestations o f pain have been per formed in a variety of cardiac condi tions. At the opposite end of the spectrum from silent ischemia are patients with a sensitive heart ( 1 39) or syndrome X ( 1 40), in whom an abnormal car diac pain perception is a fundamental component of the clinical presentation. The relationsh ip berween the myocardial locus of ischem ia or infarction and the distribution of angina has been studied in several clinical circumstances. The distribution of cardiac pain during different locations of intracoronary stimulation by local injection of adenosine was experienced in the same body area by a majority of patients ( l 41 ) . For all patients with Q-wave M I , pain location, radiation, duration, and severity were similar, although gastrointestinal symptoms were more common with inferior wall MI ( 1 42) . For the same group of patients, a second M I with a different location of pain was highly predictive of ischemia i n a different cardiac region. I n a study of palpatory fi nd ings o f musculoskeletal changes with M I , abnormalities of paraspinal

353

soft-tissue texture were more often associated with anterior than with inferior M I ( 1 43). Clinical observations since the time of Sir William H arvey are consistent with the idea that myocardial nociceptors are suffi cienrly sparse that a certain mass of myocardium m ust be affected for pain to be perceived ( 1 44-1 47) . A prospective radiographic study that showed a higher incidence of cervical osteochondro sis in patients with painful ischemia compared with painless is chemia proposed summation of pain input from a m usculoskele tal reflexogenic zone as a possible mechanism to explain pain perception in these patients ( 1 48) . (Osteophytic l ipping of the lower thoracic spine has been shown to be more common in pa tients with coronary disease than in control patients ( 1 49) , but this study did not distinguish patients with painful and silent ischemia.) Because cardiac pain is transmitted to the spinal cord by sym pathetic afferent nerves, osteopathic physicians have exami ned the paraspi nal musculature and soft tissue for a segmental so matic expression of this visceral disturbance. Beal ( 1 50) reviewed the osteopathi c l i terature, noting a preponderance of changes in the areas of T I -5. It should be noted that an exami nation of the entire axial skeleton was performed only in rwo studies in which the status of the coronary arteries was defined by angiography ( 1 05, 1 06) . In the study of patients with acute MI ( 1 07) , the pal patory examination was restricted to the 1 2 thoracic segments. In approximately one-third of patients who present with chest discomfort, no cardiac cause is found, and these patients are la beled as having noncardiac chest pain. In most of these patients, the pain is attributed to the esophagus on clin ical grounds ( 1 5 1 ), but typical investigations do not identify the cause of the pai n. One research group ( 1 52) has hypothesized that central sensiti zation, an activity-dependent amplification of sensory transfer in the central nervous system , is underlying visceral pain hypersen sitivity and noncardiac chest pai n . On the other hand, "li nked angina" is a clin ical situation in which esophageal acid stimu lation causes anginal attacks and significanrly reduces coronary blood flow in patients with CAD by a viscero-visceral reflex. The lack of any significant effect in heart transplant recipients with heart denervation suggests a neural reflex ( 1 53) . This re flex mechanism only becomes important in the presence of an impaired coronary flow reserve, endothelial dysfu nction, or sig n ificant coronary stenoses. To date, clinical protocols for the assessment of patients with chest pain have not yet i ncluded palpatory findi ngs as a prospec tive aid for the diagnosis of coronary disease. The reproduction of chest discomfort by palpation is part of an algorithm for the evaluation of chest pain in the emergency room ( 1 54) . Because somatic factors can coexist with cardiac d isease, and spinal seg mental faci l i tation may augment the severity of chest wall pain ( 1 55) , the osteopathic profession could make a contribution to clinical medicine by a study of palpatory musculoskeletal findings in patients wirh chest pain.

THERAPY

The ideal approach to patients with potential ischemic heart disease is primary prevention, so symptomatic or significant

354


coronary arherosclerosis never develops. A holisric approach ro rhe parienr wirh coronary hean diseases recognizes rhar a mul rifacrorial disease process requ i res a comprehensive therapeutic plan. Ar least 25% of coronary patients have sudden death or nonfa ral M l without any prior symproms ( 1 56) . Therefore, rhe search for rhe coronary patient with subclinical disease who could po rentially benefir from i ntensive primary prevention efforts is crir ically im portant. A recent American Heart Association (AHA) conference ( 1 57) addressed ways ro identify more patients who are asympromatic and cli nically free of coronary disease, but are at sufficiently h igh risk for future events ro j ustify a more in tensive risk reduction effort. Key findings from that report have been incorporated inro an office-based approach ro screen all pa tients, ro better define their coronary event risk ( 1 58) ( F ig. 24.7) . Asympromatic adulrs are strarified as low risk (about 35% of parients). They are reassured of rhis sratus by rheir physician and rhen retested in about 5 years. A second caregory is high risk (abour 25% of pariems) . They are candidates for intensive risk facror i ntervention. Noni nvasive testing is not needed ro de rerm ine treatment goals. Intermediate-risk patients may benefit from noninvasive resring for further risk assessment. Tests would include rhe ankle-brachial blood pressure index ( 1 59) , electron beam computed romography ( E BCT) ( 1 60) , and exercise mess resring ( 1 61 ) . While each parient deserves the benefir of a m ul rifacrorial risk facror modification program, rhe intensity of rhat program and the goals ser for ideal cholesterol levels, and so forth, vary according ro the patient's risk for subsequent cardiac evems. The components of a multifacrorial program include regular pro gressive aerobic exercise, weight loss where appropriate, control of hypertension and diabetes, cessation of cigarette smoking, educa rion about cardiovascular disease, reduction of serum cholesrerol, dierary modificarion of cholesrerol and fats, and comrol of stress and hosril i ty. Emotional and psychological support are key fea rures in successful risk facror modificarion programs. Parients with diaberes develop accelerated CAD and are 1 0 ro 20 times overrepresented among rhose suffering from acure M I .

Mortality in rhe year following infarction i s u p r o twice that of nondiaberics, and CAD remains the mosr common single cause of death in diaberic patients. Accordingly, rhe American Diabetes Association has set goals for the treatment of cardiovascular risk facrors in diabetic parients rhat are so stringent they presume the existence of significam coronary heart disease. Trearment guide l i nes for diabetic dysl ipidemia call for lowering the low-density l i poprotein (LDL) cholesrerol to less than 1 00 mg per dL, raising h igh-density l i poprotein ( H D L) ro more than 45 mg/dL, and lowering rriglycerides to less than 200 mg per dL ( 1 62). Most experts recommend a target blood pressure of 1 30/85 mm Hg. The target glycosylated hemoglobin value is 6.0. Exercise is a particularly important component of a risk fac tor modification program. Exercise is recommended for healthy people, patients identified at risk for CAD, patients with defined ischemic heart d isease, and parients following MI or revascu larization ( 1 63) . The type of program a patient enters depends on rheir physiologic srare and cardiovascular status at rhe rime of enrollment. Many patienrs enter rehabilitation while hospi ral ized and continue in a phase I l posthospital program that is monirored and supervised. Others begin wirh a phase I I I main tenance program that is supervised bur not monirored. Strength development through circuit weight training is both safe and fea sible in selecred patients with CAD ( 1 64) . The primary goals of cardiac rehabilitarion include a rerum ro ful l functional sta tus, resumption of previous occupation, and improved quality of life. Exercise i tself has important additional benefirs in terms of promoting the reduction of other cardiovascular risk factors such as obesiry, hypertension, diabetes, and dyslipidemias ( 1 63) . A meta-analysis of cardiac rehabilitation programs demonstrares a decrease in mortality for participants ( 1 65) . It is important ro recall the mechanism whereby cardiac rehabilitation works is not rhrough improvement of coronary collaterals or myocardial blood flow but rather through enhancement of musculoskeletal efficiency. Because striated m uscle represents the largest potential demand for cardiac ourput, improved function ing of this pri mary machi nery oflife has a significant effect on cardiovascular srarus.

C o r o n a ry H e a rt D i s e a s e R i s k A s s e s s m e n t in A s y m pto m a tic Patie n ts : Se lective Use of N o n i n v a s ive T e s t i n g fo l l o w i n g Offi c e Based Risk Assessment

STEP 1

�

STEP 2

Low-Risk

(-35%

of Patients)

Low-risk patients have a low-risk Framingham Risk Score and no major CHD risk factors (see text)

STEP 3

I

I n it i a l Office- B a s ed A s s e s s m e n t in a l l Asym pto m a tic a d u lts u s i n g M u ltiple C o ro n a ry D i s e a s e R i s k F a ctors / G l o b a l R i s k Ass e s s m e n t

Based on low risk status. provide reassurance and retest i n about 5 years.

+

H i g h R isk

Intermed iate R i s k

(-40%

(-25%

of Patients)

Intermediate risk patients have a t least one major risk factor outside the desirable ran e o r a positive family history of H D (see text). Global risk estimate is 0.6 - 2.0 percent per year.

8

Intermediate risk patients may benefit from noninvasive testing for further risk assessment (see text for test choices).

of Patients)

��?� l:� �fci' � �1f �\��?5."m� �

e i b ; f atherosclerotic disease including peripheral arterial disease, abdominal aortic aneurysm, carotid TIA or stroke; and middlearte a g e o r older patients w i t h t e diabetes o r multiple other C 0 ac hard CHD risk > 20 % s � v

;£,

r

� J ��;i

{'fl

High risk patients are candidate for intenSIve risk factor intervention. Non-Invasive testing of asymptomatic patients is not required to determine treatment goals.

FIGURE 24.7. A selective use of noni nvasive test i n g for the detection of coronary a rtery d i sease in asymptomatic i ndividua ls, fol lowing office-based risk assessment. (From Greenland P, Smith SC, Grundy SM. I m proving coronary heart disease risk assess ment in asymptomatic people. Role of traditional risk factors in non-i nvasive cardiovascular tests. Cir culation. 2001 ; 1 04:1 863-1867, with permission.)

24. An Osteopathic Perspective on CardioLogy All patients with ischemic heart disease should also have their spouse and family involved in this risk facror modification pro gram. Fam ily can be a significanr source ofsupporr for the patienr. Often , other family members have the same needs in terms ofedu cation, exercise, smoking behavior, and other risk behaviors. Last, ischemic hean disease is a frightening proposition. Even with an exercise program, many patienrs remain unable ro break through the barrier of fear and rerum ro ful ly functional l ives. They repre sent clear examples of i ndividuals who need psychological, social, and spiritual support as they cope with their i l lness.

ANGINA PECTORIS

UNSTABLE ANGINA

Unstable angina has three possible presentations: (a) symproms of angina at rest (usually prolonged for more than 20 m i nutes); (b) new onset (less than 2 monrhs), exerrional angina of at least Canadian Cardiovascular Society Classification (CCSC) I I I i n severity; o r (c) recent (less than 2 monrhs) acceleration o f angina reflected by an increase in severity of at least one CCSC class ro at least CCSC I I I ( 1 27) (Table 24.4).

Aspirin and an ti

TABLE 24.4. GRADING OF A N G I N A PECTORIS B Y THE CA NADIAN CARDIOVASCULAR SOCIETY CLASS IFICA TION SYSTEM Class Class I

Class II

Cl ass I I I

Patienrs with chron ic, stable angi na pecroris are fortunate that a large number of effective pharmacologic agenrs are now avail able ro them ( 1 66, 1 67). Unless this benefit is rumed ro the curse of polypharmacy, cerrain guiding principles should be fol lowed. First, a therapeutic agenr should be selected based on the patho physiology of the disease state, especially related ro coexisting disease processes, and on other cardiovascular characteristics. Al though ,B-blocking agenrs, n itrates, and calcium enrry blockers all represent effecrive first-line agenrs for rreating angina, some drugs may be superior ro others in cenain siruations. Because the pathophysiology of ischemic hean disease involves healing of the i nri mal disruption in unstable angina, patienrs started on an tianginal therapy during the acute phase of their illness may not require that medication indefinitely. A time should be selected ro withdraw these drugs unless their conrinued use can be shown ro be associated with a decreased risk of cardiovascular mortality, as is true with a ,B-blocking agent ( Fig. 24.8). The pathophysiology of acute coronary syndromes indicates that aspirin is appropriate for all patients with defined ischemic heart disease. Many physicians also advocate aspirin use for cur rently healthy individuals at risk, even without any evidence of CAD.

-

angi nals

Beta-blocker and blood pressure

355

Class IV

Description of Stage O rd i n a ry physical activity does not cause a ng i na, such as wa l k i ng, c l i m b i n g stairs. Angina [occurs] with strenuous, rapid, or prolonged exertion at work or recreation. S l i g ht l i m itation of ord i n a ry activity. A n g i n a occurs on w a l k i n g or c l i m bing stairs rapid ly, w a l k i n g u p h i l l , w a l k i n g or sta i r c l i m b i n g after meals, or i n c o l d , or i n w i n d , or u n d e r emotional stress, or only during t h e few hours after awakening. Wa l k i n g more than two blocks on the level and c l i m b i n g more than one fl i g ht of ord i n a ry stairs at a normal pace and in normal cond ition. Marked l i m itations o f ord i n a ry physical activity. Angina occurs o n w a l k i n g one to two blocks on the level a n d c l i m bing o n e f l i g ht of stairs i n n o r m a l conditions a n d a t a normal pace. I n a b i l ity to carry o n a ny physical activity without d iscomfort-a n g i n a l symptoms may be present at rest.

(Reprinted with permission from Campeau l. Grading of angina pectoris by the Canadian cardiovascular society classification system.

54:522-523, with

Circulation. 1 976;

permission.)

The major treatment goals for patienrs with u nstable angina are ro control chest discomfort, relieve ischemia, and prevenr the developmenr of acute M I . G uidelines for the diagnosis and treat ment of angina have been developed by an expert panel, based on scien rific and clinical evidence ( 1 27) and recent review ( 1 68). MYOCARDIAL INFARCTION

The rreatment of M I roday represenrs a combination of public health efforrs, medical technology, and the application of molecu lar and cel l ular biology ro patient care issues. Standard therapeutic interventions, i ncluding ,B -blockers, thrombolytic agents, ACE inhibitors, balloon angioplasty, and the coronary care unit itself, have all been developed o n ly in the last few decades. Although controversy continues over specific issues related to optimal treat menr, inremational m u lticenrer rrials and metaanalysis have es tablished strong scientific evidence ro suppon recommendations for therapy for M I ( 1 69- 1 75). In the last decade, the strategy to treat M I has shifted from an approach to prevenr or manage malignanr arrhythmias to efforts to reduce the extenr of i n farc tion, prevent reinfarction, and protect against deleterious effects of ventricular remodeling. Fig. 24. 9 summarizes the managemenr of patienrs with M I . The role o f early ambulation and cardiac rehabilitation i s im porranr ro avoid complications of MI and to mai nrain cardio vascular fi tness before it is lost because of bed resr. Cardiac reha bilitation takes advantage of the patient being receptive ro this intervenrion at this time, and it can be a part of a risk facror modification program that is begun in the hospital.

Cholesterol and c igarettes Diet and diabetes Education and ex erc i se

FIGURE 24.8. The ABCs of g u i d e l ines for the management of stable angina, as recommended by the American Heart Association. Ten areas of i ntervention for each patient.

CHALLENGES

The foremost challenge i n the managemenr of patients in regard ro CAD involves a change in m indser. Because CAD is the

356

Vl. Osteopathic Considerations in the CLinical Specialties

Pharmacologic therapy Discharge

Hours

Medication

Fi rst

Aspirin

Chewed in ED

Reperfusion for ST elevation M I

Thrombolytics or Primary PTCA

Heparin ( U FH)

I V 60 U/kg bolus, infusion 1 2U/kglhr

Low molecular weight heparin

Alternative to UFH

Beta-blocker

IV metoprolol (up to 1 5 mg i n 3 divided doses) or atenolol IV ( 1 0 mg in 2 divided doses)

Oral daily indefinitely

ACE inhibitor

Captopril, or lisinopril

Oral daily indefinitely

G P l i b/I l i a

Eptifibitide o r tirofiban

Nitroglycerin

IV for 24-48 hours � no contraind.

24

8 1 mg indefinitely

Coumadin for 3-6 mo if LV thrombus; chronically for AF

Oral for residual ischem ia I ndefinitely if LDL

Statins

>

1 00 mg/dl

Non-Pharmacolog ic Therapy Recommend low-fat diet

Dietary Advice Smoking

Reinforce cessation

Refer to smoking cessation class

Exercise

Education

Recommend regular aerobic exercise

Pre-discharge Stress Test

Plan for day 4-5 if uncomplicated M I

Cath patients with sign�icant ischemia

Measure LVEF Cardiac Rehabilitation

Refer to rehab program near their home

FIGURE 24.9. Management of acute myoca rd i a l infarction ( M I ) . This figure summarizes the pha rmaco logic and nonpharmacologic therapy for the ma nagement of the patient with acute MI, emphasizing treatment i n the fi rst 24 hours, and recommendations at the time of hospital discharge. (Modified from Ryan TJ . ACCIAHA g u i d e l i nes for the management of patients with acute myocard i a l infarction: 1 999 update. Circulation . 1 999; 1 00: 1 0 1 6-1 030.)

most common cause of death in the United States, most people presume it to be i nevi table, and medical schools, hospitals, and physicians devote m uch of their energy to the diagnosis and treatment of the various man ifestations of this disease. We need to adopt the attitude that most, if not all heart attacks are preventable. While this has been promoted in the popular press ( 1 76), there is considerable scientific support for this paradigm shift. As one example, the N urses' Health Study ( 177) followed 84, 1 29 women who were free from diagnosed cardiovascular disease, cancer, and diabetes in 1980. Low-risk subjects were de fined as those who were currently not smoking, had a body-mass index under 25 , consumed at least one half a drink of an alcoholic beverage dai ly, engaged in moderate-to-vigorous physical activity for at least 30 minutes daily, and consumed a heart healthy diet.

At 1 4 years' follow-up, this low-risk cohort had a relative risk of cardiac death and nonfatal heart attack of 0. 1 7 ( 95% confidence i n tervals 0.07 to 0. 41) compared with all the other women. Eigh teen percent of the coronary events that occurred in the study cohort could be attributed to lack of adherence to this low-risk pattern. A similar analysis of 84,941 women in the same Nurses' Health Study showed that 91 % of the subjects who developed type 2 diabetes over a 1 6-year follow-up had habits and behaviors that did not conform to this same low-risk pattern ( J 78) . A second challenge is to recognize that coronary arrery bypass graft (CABG) surgery and percutaneous rransluminal coronary angioplasty (PTCA) do not prevent M I ( 1 79). Because of the prominent position given to these interventions, and the im portance of these services to building a high-visibility cardiology

24. An Osteopathic Perspective on Cardiology p rogram, most p at i ents and many physi ci ans assume th at revas cul ar i zat i on will p rotect aga i nst subseq uent M I . I n fact, t h e ves sel s t h at undergo revascul ar i zat i on h ave h igh -g rade stenosi s, b ut generally rep resent stabl e ath eromatous pl aq ue. Th e "vul nerabl e" pl aq ue rypi ca lly i s o f borderl i ne h emody nami c sig nifi cance and would not b e a target for CABG or PTCA. Wh at d oes p re vent M I ? Pl aq ue stabili zat i on and r i sk factor mo difi cat i on wi t h di et, exerc i se, ch o l esterol -l oweri ng th erapy, and control of co ex i st i ng condi t i ons such as hyp ertens i on, di ab etes, and ob esi ry. As one exampl e, th e Atorvastat i n vs. Revascul ari zat i on Treatment (AVERT) tr i al ( 1 S0) enrol l ed p ati ents wi t h ch ron i c stabl e angi na and 70% to 90% stenosi s o f one or two coronary vessel s. Th e p at i ents were randomi zed to recei ve PTCA or t h e lipid -l oweri ng agent arorvastat i n. Th e study was h a l ted p rematurely b ecause o f t h e sup er i or i ry o f lipid -l ower i ng t h erapy. Fi na l ly, t h e magn i tud e of survi va l benefi t o f CABG surgery i s a smal l fract i on o f t h e benefi t o f l ipid- l ower i ng t h erapy, ACE i nhibi tors, and asp i r i n use.

J ust as PTCA and CABG ga i n attent i on as i nterventi ons over " " ordi nary medi ca l management, t h e i mmedi ate treatment of MI recei ves much more attent i on th an th e h ospi tal di s post h ospi tal management. Th e gap between accep ted gu id el i nes and treatment compli ance i s so great th at th e Ameri can Co ll ege o f Cardi o l ogy (ACC) establi sh ed an i ni t i at i ve i n 2000 to enh ance q ua li ty care t h rough a mul t idi sc ipli nary p ro gram. Th e G uid el i nes Appli ed i n Practi ce (GAP) p ro j ect ( 1 S 1 ) i s d esigned to p rovid e too l s t hat h ospi tal -b ased caregi vers can ut i l i ze to i m p rove adh erence to guide li nes ( 1 66). E ven so, wi t h a h ospi tal l engt h o f stay For MI at 3 to 5 d ays, and unsta bl e angi na at 1 to 2 d ay s, i t sh ould b e cl ear t h at t h e resp ons ibili ry For i mpl ement i ng t h ese r i sk Factor modifi cat i on p rograms fal l s to t h e out p at i ent cardi ol ogi st and p ri mar y care physi c i an. A thi rd p aradigm shift i s ro recogni ze th at consensus state ments and guid e li nes not only refl ect sc i ent ifi c ev idence, b ut al so t h e personal o pi n i ons of t h e i nd i v id ual s wh o craft t h ese d ocu ments, and a sub t l e or overt i nfl uence from maj or med i cal centers and t h e ph armaceut i cal i nd ustry. For exampl e, i n t h e ACC/AHA guid el i nes For unstabl e angi na and non-ST-segment el evat i on M I , th e weigh t o f ev id ence i s ranked as: acute

ch arge and

H igh est (A), iF t h e d ata are d eri ved from mul tipl e, rand omi zed cl i n i cal tr i a l s i nvo l v i ng l arge numbers o f p at i ents. I ntermedi ate ( B ) , iF th e d ata are deri ved from a li mi ted num b er of rand om i zed tri al s i nvol v i ng small numb ers of p ati ents or from careful analys i s o f nonrand omi zed studi es or observati onal reg lsrnes. Low (C), if ex p ert consensus i s t h e p ri mary b asi s For t h e rec ommend at i on. I n th ose guid eli nes ( 1 6S) th e l arge maj o ri ty o f recommend ati ons C. A s anoth er examp le, b ecause of b road ad vert i si ng , i ncl udi ng di rect-to-consumer ad s, i t i s now wide ly known t h at ch ol esrerol -I ower i ng d rugs i n t h e stati n cl ass red uce t h e ri sk of card i ac events. H owever, consump t i on of nuts ( 1 S 2-1 S6) will red uce cardi ac events by a si mi l ar ord er of magn i tude. Consum pti on of nuts i s a maj or p art o f t h e M edi terranean di et, t he only di et p roven to red uce th e ri sk o F M l ( l S7). lr i s cl ear wh o p romotes stat i ns for cardi ac p at i ents. B ut wh o i s p romoti ng

were a l eve l o f ev id ence of B or

357

th e

M edi terranean di et and consump t i on o f nuts? Thi s auth or b eli eves th at th e osteo p athi c tenets and p ri nc ipl es For p at i ent care (1) rep resent a cl ear mand ate for thi s to Fal l i n th e domai n o f os teop at h i c medi ci ne. O steop ath i c mani p ul ati ve th erapy (OMT) h as b een ad vocated on t h e b asi s t h at i t red uces somat i c dysfunct i on, i nterrup ts t h e v i scerosomat i c refl ex arcs, i n fl uences t h e v i scus t h rough st i mu l a t i on o f somatov i sceral e FFerents, and red uces t h e p otent i al p recon di t i on i ng effect of somati c dysfunct i on to bo dy stressors ( 1 50). o MT h as b een recommend ed for t h e treatment of coronar y h eart di sease b ased on a p resumed mech ani sm to Favorably al ter auto nomi c nervous sy stem funct i on ( 1 SS). Th ere i s a signifi cant need for skill ed p ract i t i oners o f osteo p at hi c p alp atory di agnosi s and man i p ul at i ve t h erapy i n h ospi tal s. Spec i al i sts i n osteop ath i c mani p ul at i ve medi ci ne oFten aid i n th e di agnosi s o f p at i ents w i th ch est p ai n arypi cal For angi na. I n t h ose p at i ents Fot wh om M I i s rul ed out, OMT i s esp ec i al ly useful For t h ose w i t h ch est wal l p a i n. I n p at i ents w i t h p roven M I , OMT h as b een saFely emp l oy ed i n t h e coronary care un i t and th e step d own uni t, wi th favorab le cl i n i cal resp onses. Th ose p ati ents wh o rece i ve t h e b enefi t of rout i ne OMT Fo l l ow i ng o p en-h eart surgery o ften h ave d ramat i c responses to treatment. U n Fortunate ly, t h ese cli n i cal ob servat i ons h ave not b een srudi ed i n control l ed tr i a l s. Even a systemati c recordi ng of ob servat i ons on a l ongi tudi nal or case-contro l b asi s woul d b e o f sign ifi cant i nterest. Th e fo ll ow i ng q uartet o f cl i ni cal vignettes p rov id es a gli mp se o f h ow an osteo p at hi c p ersp ecti ve i nfl uences th e management o f p at i ents wi t h h eart di sease.

A QUARTET OF CLINICAL VIGNETTES

I . A 72 -y ear-old man ( Pat i ent N o. I ) wi th h eart Fai l ure com pl ai ns of excessi ve fatigue and dysp nea wi th exert i on. H e i s al ready on a ful l p rog ram of max i mal medi cal t h erapy, wh i ch meets all consensus gui del i nes. Wh en h e sees t h e osteo p at hi c physi c i an, an i nvenrory of h i s act i v i t i es o f d a i ly l i vi ng and exerc i se h abi ts i ndi cate a very sed entary lifesryl e wi th signi fi cant l i mi tat ion i n performi ng routi ne acti v i t i es. You enroll him in a program ofcar

diac rehabilitation exercise while he continues on the same pharma ceutical therapy. Six weeks later, hisfonctional aerobic capacity has increased 25%, and he is pleased with the significant improvement in his symptoms during activities ofdaily living. 2. A n SO -y ear-old woman ( Pat i ent No. 2) wi th known th ree CAD and hyp ertensi on p resents to th e emergency d ep art ment wi t h p a i n i n t h e l ower anter i or ch est. Th e ECG sh ows l eft ventr i cul ar hyp ertrophy wi t h rep o l ar i zat i on ch anges. Sh e i s ad mi tted to t h e cardi o l ogy serv i ce to rul e out M I and i s started on h ep ari n and i ntravenous pl atel et i nhibi tors. The next d ay t h ere i s no obj ect i ve evid ence of M I, b ut t h e h emogl obi n h as d ropp ed 3 g and t h e stool occul t bl ood test i s p osi ti ve. Th e gastroenterol ogy serv i ce i s rel uctant to p erform end osco py i n t h e sett i ng o f p ossi bl e unstabl e angi na. The p ati ent conti nues to ex peri ence anter i or c h est di scomfort. The patient is seen by the consultant in osteopathic vessel

manipulative medicine (OMM), who obtains a history not recorded by the house staffor specialist. The patient has had low back pain for 3 weeks and took over-the-counter nonsteroidal antiinflammatory agents for pain relief The OMM consultant identifies and treats

358


musculoskeletal abnormalities that account for the chest pain and the patient obtains reliefofher symptoms. 3. A 62-year-old man (Patient No. 3) has end-stage ischemic heart disease. He has had open-heart surgery twice, and four coro nary angioplasty procedures. He now has severe ischemic dilated cardiomyopathy and is not a candidate for revascularization. I n spite o f the severity o f h is heart disease, what h e complains about most is pain in his neck and shoulders. An empiric trial of niuo glycerin is not beneficial. Somatic dysfu nction is noted on phys ical exami nation. He is sent for further osteopathic evaluation and manipulative treatment. The OMM consultant finds somatic

dysfonction in multiple regions. The most symptomatic is the left trapezius counterstrain tenderpoint. He also has clear abnormalities in the left shoulder, left costosternal area, sacrum, and innominate. However, after three encounters, he experienced little improvement. The OMM specialist attributed this to the effects ofstress related to an ongoing custody battle with his ex-wife over their mentally im paired daughter. He was further managed through counseling and stress management education. 4. A 58-year-old woman (Patient No. 4) with type 2 diabetes presents with unstable angina pectoris. Cardiac catheterization demonstrates 90% stenosis of the left anterior descending coro nary artery. The patient undergoes coronary angioplasty with placement of a stent. She is discharged home on aspirin, clo pridogrel, a ,B-blocker, and an oral agent for diabetes mel l i (Us. She sees you, the osteopathic physician i n follow-up. Neither the cholesterol nor glycosylated hemoglobin had been evaluated at the cardiac intervention center. When the patient presents to your office, she is pleased to be completely symptom-free and anxious to return to her work as a secretary. Her weight is 50 lbs above ideal, she has not been instructed in a diabetic diet, and she has stage J systemic arterial hypertension. You enroll her in a super

vised, but un monitored program of cardiac rehabilitation exercise. She meets with the dietitian to learn about a low-fat weight loss diet patternedfor a diabetic. Baseline cholesterol profile and hemoglobin (Hgb) A 1 C levels are obtained. Six weeks later she returns and reports an improvement in her exercise tolerance and weight loss of 8 lbs. She indicates that she is enjoying her new diet. However, her LDL cholesterol levels are above target values. You add a statin agent to lower cholesterol. You arrange for follow-up evaluation to include a repeat cholesterol profile, liver enzyme studies in 6 weeks. A repeat HgbA 1 C is evaluated in 3 months. Besides involving a component of cardiovascular disease what key features are incorporated in each of these clinical vignettes? First of all, it should be clear that the osteopathic physician utilizes the best clinical research and evidence-based treatment protocols in patient care management. One distinctive feature of each of these cases is an emphasis on the role of the musculoskele tal system. In Patient No. 2, abnormali ties of the m usculoskeletal system in fact represented the primary cause of the patient's presenting symptoms, but were several steps removed from the presenting complaint. It may be that an orientation toward the role of the m usculoskeletal system led the O M M consultant to inquire more specifically about m usculoskeletal symptoms. Certainly, the expertise of the special ist in manipulative medicine was critical in identifying m usculoskeletal abnormalities that

explained the patient's symptoms that were subsequently relieved by manipulative treatment. Another focus of the intervention in each case was an empha sis on l i festyle, behavior, and diet in addition to the usual phar macologic support. In Patient No. 4, modifications of diet and l i festyle were major components of the treatment plan. In Patient No. 3, the patient's behavioral response to significant stress in his life elucidated the difficulty in obtai ning a satisfactory treatment response to pharmacologic therapy and OMT. In Patient No. 1 and Patient No. 4 the intervention directed to the m usculoskeletal system was cardiac rehabilitation exercise. I n heart fai lure patients, the improvement in functional capac i ty gained by exercise is twice the improvement demonstrated with pharmacologic suppOrt in the form of agents such as ACE inhibitors. Finally, the solution to problems may take more than one per spective. Treatment for patients is often multifaceted and needs to be specifically tailored to each individual. Patient No. 4 did nor achieve target LDL cholesterol levels with a program of diet, ex ercise, and weight loss and therefore a cholesterol-lowering med ication was added.

HEART FAILURE Pathophysiology and Natural History

Heart fai lure is a clinical syndrome or condition characterized by (a) signs and symptoms of i ntravascular and i n terstitial volume overload including shortness of breath, rales, and edema, or (b) manifestations of i n adequate tissue perfusion such as fatigue or poor exercise tolerance ( 189). Patients may have one or both of these features. The term "heart failure" has been recom mended i nstead of the term "congestive heart failure" because many pa tients with heart fai lure do not manifest pulmonary or systemic congestion ( 189). I t is estimated that more that more than 5 million U.S. cit izens have heart fai lure and approximately 500,000 new cases are diagnosed annually. It accounts for 12 to 1 5 million office visits and l . 5 m i l l ion hospital days each year ( 190). In the last 10 years, the number of patients hospital ized annually has in creased from 550,000 to 900,000 when heart failure is a primary diagnosis and from 1.7 to 2. 6 million when heart failure is a primary or secondary diagnosis (191). Nearly 300, 000 patients die from heart fai l u re being a primary or contributory cause each year. The n umber of deaths has increased stead ily, even though there has been a reduction in mortality due to coronary heart disease and systemic arterial hypertension (192), which represent the two most common causes of heart failure. Heart fai lure is primarily a d isease of older adults (193). Ap proximately 6% to 10% of people older than 65 years of age have heart failure and approximately 80% of patients hospitalized with heart fai l u re are more than 65 years old ( I 91). Heart failure is the most common Medicare diagnosis-related group, and more Medicare dollars are spent for the diagnosis and treatment of heart fai lure than for any other diagnosis ( 1 94). A recent practice guideline from the ACC/AHA (195) sug gests a new approach to the classification of heart fail ure thar

24. An Osteopathic Perspective on Cardiology emphasizes borh rhe evolurion and progression of rhe d isease. This describes four srages of heart failure. Srage A idenrifies rhe parienr who is ar high risk for developing hearr failure, bur has no srrucrural disorder of rhe hearr. • Srage B refers ro a parienr wirh a strucrural disorder of the heart, bur who has never developed symproms of heart failure. • Stage C denotes the patienr with past or currenr symproms of heart failure associated with underlying strucrural heart dis ease. • Stage D designares rhe patienr with end-stage disease who requires special ized rreatmenr strategies such as mechanical circularory supporr, continuous inotropic infusions, cardiac transplantarion, or hospice care. •

Only the latter two stages qualify for the traditional clinical di agnosis of heart failure for diagnostic or coding purposes. This classification system is inrended ro complement but not ro replace the New York Heart Association (NYHA) functional classifica tion. Fig. 24. 1 0 shows how rhese stages of hearr failure are used ro defi ne rrearmenr approaches ro parienrs. The clinical syndrome of hearr fai lure may resulr from dis orders of rhe pericardium, myocardium, endocardium, or grear vessels, but rhe majority of parients with heart failure have symp roms due ro an im pairmenr of left venrricular function. In the

Stage A

Stage B

At high risk for

Structural heart

heart failure but

disease but without

without structural

symptoms of HF

heart disease or

United Stares, the mosr common cause of hearr failure due ro muscle damage is cO'r onary heart disease; the most common eti ology of heart failure due ro pressure overload of the heart is systemic arterial hypertension ( 196) . I n Sourh America, Chagas disease is the most common cause of hearr failure because of left venrricular damage; in Third World counrries, volume over load because of rheumatic heart disease remains an importan t cause of heart fai lure. Often rhe disease entity is mulrifacrorial, i ncluding features of hypertension, ischemic hearr disease, and volume overload. Typically, hearr failure involves sysrolic dys funcrion with depression of contracrile performance leading ro depressed ejection fracrion and cardiac output, and, frequenrly, venrricular chamber dilation. Diasrolic dysfu nction is increas i ngly recogn ized as a significant feature in a mi nority of patienrs wirh hearr failure ( 197) . This term implies i m paired left ventricu lar fi l ling and normal left atrial pressures, resulting in pulmonary and system i c venous congestion with l itrle or no systolic dys function. D iastolic dysfunction is especially common in patienrs with system ic arterial hypertension, ventricular hypertrophy, or infiltrative disease. Ir should be emphasized that heart fai l ure is not equivalent ro cardiomyoparhy or ro left ventricular dysfu ncrion. These latter terms describe possible strucrural reasons for rhe development of heart failure. I nstead, heart failure is a cli nical syndrome rhat

Stage C

Stage D

Structural beart

Refractory HF

disease with prior or

requiring

current symptoms of

specialized

HF

interventions

symptoms of HF e.g .• Patients who have e. g., fitli�D� with: - hypertension

e. g.. Patients with: - previous Ml

- coronary artery

- LV systolic dysfunction

disease

- asymptomatic

- diabetes mellitus or

valvular disease

e. g.• Patients with: - known structural heart disease - shortness of breath

marked symptoms at rest despite maximal medical therapy (e.g.• those wbo are recurrently bospital

and fatigue. reduced

ized or cannot be safely

exercise tolerance

discharged from tbe

Patients

bospital without

. using cardiotoxins

specialized inteIVentions)

- with FHx CM

r

' tween or through the greater and lesser trochanters. When pos sible, intracapsular fractures are treated with reduction and pin fixation. When this is not possible, prosthetic replacement is nec essary. Intertrochanteric fractu res are usually held in a reduced position with the use of a sliding compression screw.

483

Intracapsular fracture

Screw fixation

Prosthetic replacement

Intertrochanteric fracture

Sliding compression screw

OSTEOARTHRITIS OF THE KNEE

To examine and treat the arthritic knee requires that one under stand how arthritis affects the whole body. The term arthritis is used with little specificity and can refer to different types and causes of joint pain. Arthritis is joint inAammation. An arthritic problem can be the result of a systemic disorder that may be immunologically based, the effect of infection, or a metabolic disorder such as rickets. It can be a late effect of trauma such as a fall, a vehicular accident, or a sports-related ligamentous injury. Before evaluating the joint for which a patient presents to the office because of pain or swelling, the physician must first ascertain if there is a systemic cause for arthritis. Often the types and presentations of the common arthritides are recogniz able with a thorough histOry and physical examination. A careful history allows the physician to recognize that a young woman who presents with morning stiffness and symmetric polyarticular disease might have rheumatoid arthritis. It allows for the assump tion that a middle-aged man with a history of recurrent great toe pain associated with dietary indiscretions, who presents with a hot, inflamed knee joint, probably has gout. Examination of the

FIGURE 33.6. Fractures of proximal femur.

gowned patient forces even the most casual examiner to recog nize advanced psoriatic skin changes in an arthritic patient. To paraphrase one of the tenets of osteopathic medicine, a patient's disease affects their entire body system. It is appropriate and nec essary that the osteopathic physician understand the relationship of an arthritic joint to the whole patient. The most common kind of knee arthritis that presents to the orthopedist is that of a wearing out or erosion of the articular sur face of the medial compartment of the knee, called osteoarthritis. This is usually the result of repeated major and minor trauma or

484


B FIGURE 33.7. G e n u va rum. A: A lower extremity with extreme g e n u v a r u m i n which t h e weightbea ring l i n e f r o m the hip t o the foot passes m e d i a l to the knee joint. B: A l i m b after a high t i b i a l osteotomy in which the wei ghtbea ring l i n e passes through a point lateral to the center of the knee jo int.

wear. Oftentimes, this is coupled with a normal varus or mild bowlegged body habitus. As shown in Fig. 33.7A, in this presen tation, a line of weightbearing from the center of the axis of the femur passing to the center of rhe ankle joint passes inside of or medial to the center of the knee. In rhis case, rhe vasr amount of forces and stresses that pass through rhe knee pass entirely through the medial compartment or through the medial femoral condyle and tibial plateau. If rhere has been an injury to the ligaments or cartilage of the knee, with time and rhe increase of stresses, there is increasing wear and debris in rhe joint. To optimize treat ment requires some understanding of how articular cartilage is nourished, what steps can be taken to decrease the wear debris or particulare gravel in the knee, and how to diminish stresses in rhe medial joint. The articular surface, or the cartilaginous weightbearing ele ment of a joinr, is made up of a matrix of water-heavy proteins with few living chondrocytes present. This anatomic area has no direct blood Aow. The metabolites necessary for the nutrition and repair of the cartilage pass into the structure through the spongelike cartilage. With pressure from weightbearing or mus cle contracrure, the cartilage surfaces collapse, pushing rhe Auid into the joint. As the pressure is relieved, the joint Auid seeps back into rhe cartilaginous matrix, bringing the necessary metabolires and oxygen required for cell life. Therefore, it is important to

maintain the motion and normal stresses to rhe knee. As part of the trearment of the arthriric patient, rhe osteopathic physi cian needs to encourage morion and acrivity. Some of rhe kinds of activities that are helpful in the maintenance of joint struc ture include low-impact aerobics, water exercises, and repetirive low-stress activities such as treadmills, cross-country skiing, and bicycling. Eccentrically loaded high-stress activiries such as jump ing are not recommended because rhe stresses across rhe joint are too great. Twisting or torquing motions, especially in a joint with weak ligaments, increase the forces and shear thar occur across the cartilaginous area. If, as a result of previous trauma or the ravages of aging, rhe cartilage of the joint is damaged, then rhe irregularly shaped edges of this normally smooth articular carti lage may be easily ripped or torn with compression and shear. Judicious exercise is important to maintain the metabolic nutri tion of the cartilaginous matrix, but overuse may cause serious problems. Assisting the patient to obtain and maintain a body weight within normal limits also helps to diminish the stresses in the join t. Disabling unilateral medial knee arthritis has other effects as well. The patient wirh a painful joint has an antalgic gait: he or she limps. Limping causes a twisting motion to the joints above and below the painful joint. A common problem with limping is an imbalance in the sacroiliac articularion with a resultant so matic dysfunction in this joint. Often, as the knee bows medially, an effective leg length difference occurs that may need to be ad dressed with a lift. Patients with pronated feet increase the stresses over the medial knee joint. The use of a custom orthosis in the shoe, often changes the dynamics, relieves pain, and allows the patella to track more normally in the patella-femoral trochlear groove. Wirh pain, the patient fails to exercise and becomes de conditioned; their entire cardiopulmonary status may deteriorate if left unattended. Many patients with pain cannot work as hard at their jobs and their hobbies as they would like and become depressed. Counseling and the use of antidepressant medications may be helpful. At the present time in the development of orthopedic im plants, laboratory designed and manufactured biomaterials do not have the same degree of biologic function as do normal tis sues. They are not self-reparative. They have different moduli of elasticity than the human tissues; they do not bend the same amount with forces as do human bones. The result of this is increased stress ar rhe interface between the implant and the bio logic tissue. Recently, researchers and clinicians have discovered that particles of wear debris that occur normally with time, par ticularly rhose of rhe high-density polyerhylene that serves as the bearing surface in mosr prostheses, are read by the host cells as foreign. This causes an intense foreign body reaction in some patients. A side effect of this foreign body reaction is a release of biologically active mediators from the tissue macrophages and other immunologically competent cells of osteoclasr-srimulating factors. These in turn cause the body, somerimes quickly, to resorb rhe bone surrounding the implanr, weakening the junction be tween the prosthesis and the bone and allowing loosening, pain, and fracture to occur. The options for the physician trearing osreoarthritis are lim ited because no surgical implant can guarantee a. relief of pain. As in the case of the younger parient with a hip fracture, replacement

33. Orthopedics

arrhroplasry should be avoided for as long as possible. The fol lowing paragraphs and the accompanying diagrams describe the various braces used and surgical procedures done to alleviate dis comfort. A physician recommends one modaJiry for a particular patient with knee arthritis based on the understanding of that patient's physiology, age, life requirements, and goals, as well as on their knowledge of the rypes of treatment available. One of the simplest treatments is the application of a knee brace that applies pressure to the tibia below and the femur above, thereby increasing the forces applied over the lateral joint line. This brace is similar to those worn by athletes with torn ligaments; in fact, it was developed for use in arthritic patients through an offshoot of the sports medicine designs. For many the btace is successful for pain relief, although it may be cumbersome to apply and bulky under clothes. For those who have an angular defOl'miry that is severe and painful, osteotomy may realign the mechanical problems associ ated with genu varum. As depicted in Fig. 33.78, a simple form of osteotomy removes a wedge of bone ftom the lateral proximal tibia. If this wedge is properly calculated, when the osteotomy heals, the center of graviry or the forces acting through the knee pass through the lateral joint, thus diminishing the forces through the arthritic medial joint. For many, as an adjunct to or substitute for osteotomy or bracing, arthroscopy may afford relief. If there is a degree of effusion and torn tissues with multiple loose panicles floating inside the knee joint, a debridement or vacuuming of the knee can wash out the offending particles. While this is not curative, for many it affords a long period of pain relief. . For those whose knee joint is not a candidate for osteotomy and whose lifesryle and physiologic age are appropriate, joint replacement arthroplasry is indicated. Joint replacement arthro plasry requires adherence to a host of mechanical constraints. The joint must be in a normal and mechanically sound position, and the components need to be securely fixated to the bones of the knee joint. There are many options, ranging from the unicom partmental hemiarthroplasties that simply replace the damaged medial compartment to constrained systems in which the design attempts to substitute for damaged ligaments. The osteopathic physician needs to understand some of the features of the implants and the physiologic changes that oc cur with implant arthroplasry. The risks of thrombophlebitis are high. Precautions are necessary, ranging from early activiry and external compression devices to therapeutic anticoagulation with warfarin, heparin, or dextran derivatives. The risk of infection, both early and late, although not great is disastrous when it oc curs. The risks are diminished through good surgical technique, by decreasing the number of bacteria that can come into con tact with the wound, and with the use of appropriate antibiotics. Finally, the physician must recognize that a joint implant is a for eign body. With any systemic infection, circulating bacteria may adhere to the implant and cause a late infection. The judicious use of antibiotics in the face of systemic infections or bacteremia may decrease the incidence of infection. Many physicians recommend the prophylactic use of antibiotics with oral surgical procedures or at other times of predictable risk for bacteremia. The osteopathic physician who evaluates the patient for a total joint arthroplasry must address the variery of problems that are

485

involved in knee arthritis. Weight control, physical conditioning, exercise, and proper nutrition are helpful to encourage healing and to maximize the gains from the procedure. Ongoing research into the efficacy of osteopathic manipulative procedures in the preoperative period should encourage the physician to maintain a normalized spine. A study of the adjunctive use of OMT in the early postoperative period following joint arthroplasry showed that those who underwent OMT reported less pain, used fewer analgesic medications, and walked farther than those patients who were not manipulated ( 1 3). LOW BACK PAIN

The most frequently seen problem for general orthopedists to day is low back pain. Back pain is ubiquitous in the population. The costs of treatment, the expenses of failed work, and the problems frequently associated with blame and the legal system make these the treatment of low back pain one of urgency. The patient and family need to have a return-to-work schedule and sense of normalcy restored; sociery needs some surcease from the huge costs necessitated by the disabiliry structure. Every physi cian sees the patient with acute disabling back pain who is un able to walk and unrelieved of discomfort. From the orthopedist's point of view, the urgency to relieve pain and disabiliry quickly makes a dispassionate evaluation and treatment plan impossible. The new technological advances in imaging and in surgical tech nique have led many patients to believe that a rapid, easy, risk-free anodyne is available by surgery. Everyone has known someone who, following a back surgery, did not get better but may have gotten worse. The litigants would have us believe it is because of faulry technique or poor technology or inadequate screws. Spine surgeons are still evolving techniques, materials, and methods to find out which patients with low back pain can benefit from which procedure. Other surgeons often do not want to exam ine, evaluate, or treat the patient with acute or chronic back pain because such patients are often difficult and demanding. The osteopathic orthopedic surgeon approaches the patient with low back pain with a systematic protocol. The primary ob jective for all physicians and surgeons is to define a distinct diag nosis: a diagnosis that has an accurate anatomic and pathologic basis. The great problem for surgeons in general and for ortho pedists in particular is to identify appropriate surgical pathologic conditions. Most back pain does not need to be treated surgi cally. In a great percentage of patients with low back pain, the final diagnosis is idiopathic. This means essentially that nobody knows what is the cause of the disease. Some estimates indicate that more than 50% of all patients with low back pain do not have a firm, accurate, anatomically defined reason for their pain. To operate is problematic if the diagnosis is uncertain. Just because a surgeon may be predisposed to seek a surgical solution to a problem does not mean that the spine surgeon looks to operate first. Spine surgeons realize that for people with the same pathologic diagnosis, the long-term result of surgical and nonsurgical treatment may be the same. The outcome in equiva lent groups of patients with low back pain and myelographically proven herniated discs is the same as for those who have un dergone surgery and those treated nonsurgically. This does not

486

VI. Osteopathic Considerations in the ClinicaL SpeciaLties

mean that the patient with a frank neurologic deficit, weakness, numbness, and intractable pain over the ipsilateral dermatome should not be operated on. The immediate results of pain relief usually outweigh the fact that later, after the settling down of the disc space and the degenerative changes that occur in the sur rounding structures, the postsurgical patient may subsequently have episodes of severe back and buttock pain. The spine sur geon approaches each patient who has been referred as having problematic back pain, pain that the referring physician thinks is severe enough to warrant consideration for operative treatment. The orthopedic spinal surgeon who evaluates the patient re ferred by the family practitioner, emergency room physician, in ternist, or family members first has to understand the reasons for referral. Back pain that is severe enough to make the bearer nauseous, that has defied the palliative or curative modalities that often prove successful, and that is untelieved by narcotic med ications, rest, and antiinflammatory shots, pills, and emollients must be a surgical disease. If pain is the anathema of life or, as Herkowitz has stated, "Life is the avoidance of pain" (Annual Spine Session, 1993), then those who suffer and complain have an urgent imperative to seek the services of the surgeon. Patients and physicians are eager believers in the curative possibilities of the newer technologies. IfMRI shows a bulging disc and a person has back pain, it follows that the excision of the disc will relieve the pain. This does not always prove true. The fact that the pa tient may not improve following a surgical experience does not necessarily mean that the surgeon was inept. The imaging diag nostics may not have been as precise or as helpful as we would want, or the acute episode is but one point in time of an ongoing process. Asymptomatic herniations in the lumbar spine are common (14). It is impossible for the person suffering severe intractable back pain to think rationally about the nature of their pain. As compassionate as the physician-surgeon may be, it is their job to review the possible causes of back pain (Table 33. 1 ) to be able TABLE 33 . 1 . CAUSES OF BACK PAI N Mechanical Spinal arthritis

Tumor P r i m a ry

Degenerative d isk d isease

myeloma

Facet arthritis

sarcoma

Fracture Spondylolysis

neural tumor Secon d a ry (metastatic)

Spondylolisthesis

prostate

Congenital

lung

genetic malformations

breast

achondroplasia

k i d ney

Nonmechanical Viscerogenic ren a l col i c inflam matory bowel d isease endometriosis Vasculogenic

Rheu matologic Seronegative spondyloar-

psoriatic arthritis Reiter syndrome Beh�et syndrome

ischemic s p i n a l c l a u d ication

f i bromya l g i a

I nfection Discitis

Age of 50 years or older Previous history of cancer Unexplained weight loss Failure to improve with 1 month of therapy No relief with bed rest For a patient suffering from a known trauma or with a his tory of corticosteroid use, fracture is suspected. Intravenous drug abuse, urinary tract infection (UTI), or skin infection in a patient with back pain suggests osteomyelitis or disci tis. Sciatica suggests disc herniation and pseudoclaudication; the symptom ofincreas ing leg pain or weakness that is eased with forward flexion or rest suggests spinal stenosis ( I S) .

thropathy a n kylosing spondylitis

aortic a n e u rysm e p i d u r a l venous anoma l i es

to outline the appropriate steps to best understand and treat the acute episode. Low back pain is so ubiquitous that its definition is elusive. In the context of this chapter, low back pain is that symptom com plex in which the person experiencing pain describes it as encom passing the area of the lumbar spine and the associated muscula ture of the lumbar spine, as well as the sacrum and buttocks. Pain in the lumbar spine may be oflocal origin or may be referred. Dis orders causing low back pain may, in turn, cause radiculopathy, which is a pain radiating through the peripheral nervous system, usually into a defined dermatome or somatome. There are large lists of entities that can be associated with back pain. Lists in medicine are useful if only to refresh our memories of possibil ities in diagnosis not readily at hand. Too often, however, they serve as diagnostic maps in which the observer-physician finds an easy way to choose tests for diagnostic possibilities. For instance, most people with back pain do not have myeloma. To run a gamut of blood and urine tests on an otherwise healthy 30-year-old to rule out myeloma is not reasonable until the more common and statistically significant clinical entities have been differentiated. Tests should be chosen with a degree of scientific aplomb, using the test to help firm up a diagnosis only after a careful his tory has been elicited and a physical examination has explored abdominal, pelvic, and spinal structures. In Acute Low Back Prob Lems in AduLts (15), a clinical practice guideline published by the U.S. Department of Health and Human Services, the authors have included a series of red flags that help alert the examiner to responses or findings that merit detailed evaluation. Their algo rithm (Fig. 33.8) outlines an approach to assessing low back pain symptoms. Throughout the patient evaluation, as the physician is considering the diagnostic tests and therapeutic regimens, they should be continually asking if there is some reason for this pain outside of or beyond the spinal area. The red flags that can sug gest to the examiner that a serious underlying condition, such as cancer, is present include:

polymya l g i a rheumatica Rheumatoid arthritis Metabolic

H erpes zoster

Osteoporosis

Osteomyel itis

Paget d isease

H i story and Physical Exa m i nation

As in most areas of medical care, the history is of primary impor tance. A quiet listening attitude on the part of the physician may encourage the patient to be more open and frank. The algorithm for the evaluation of back pain is so large that one item or another from the history given by the patient leads the physician inter viewer to follow one pathway in his or her continued guestioning and in test ordering. Examples of questions {hat can help guide

33. Orthopedics

Perform focused medical history and physical examination.

Adults with

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Pressure (em H20) FIGURE 34.1. Representative volume-pressure curves from adult sub jects of same age, sex, and body size showing changes caused by em physema and pulmonary fibrosis compared with normal lu ngs.

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pressure difference causing the airflow. Ai rflow is easy to measure, but measuring the pressure di fferences that cause the air to flow requi res specialized equipment. The flow-resistance properties of i ndividual components of the respiratory system can be analyzed separately (e.g., the airways and the tissues of the lungs and chest wall ) . Figure 34.2 i l lustrates three types of work that are associated with the i nspiratory effort: Compliance Tissue resistance Airway resistance During normal quiet breathing, most of the work performed by the respiratory m uscles is used si mply to expand the l ungs. Conversely, during heavy b reathing when air movement must flow through the respiratory passages at very high velocity, the greater proportion of work is then used to overcome airway and tissue resistance. In pulmonary disease, all three of the different work components can be vastly i ncreased. Compliance work and tissue resistance work are especially increased by diseases that dif fusely i nvolve the l ung parenchyma and/or involve the chest wall. Ai rway resistance work is especially increased in d iseases that ob struct the airways, such as asthma and other forms of chronic obstructive pulmonary disease ( COPD) . However, even diseases that do not involve the ai rways, often with i ncreasing severity, affect tissue resistance work. [n advanced obstructive airway dis eases, the presence of malnutrition, respi ratory muscle decondi tioni ng, and somatic dysfunction can enhance tissue resistance work. During normal quiet breathing, no muscle work is performed during exhalation, which results from passive elastic recoil of the l ungs and chest. In heavy breathing or when ai rway and tissue

34. Pulrnonology resistances are increased, expiratory work does occur and at times can be greater than inspiratory work. Normally, the lungs sit within the chest wall and diaphragm. The pressures and forces acting on these structures are i nterre lated. At the end of normal exhalation, during quiet breathing, the lungs are partially inflated. This is measured as the functional residual capacity (FRC) . The elastic recoil of the l ungs exerts a force that tends to empty the lungs. At the same time, chest wall volume is such that its elastic recoi l promotes outward expansio n . FRC occurs at t h e l u n g volume a t which t h e tendency o ft h e lungs to cgllapse is opposed by the equal and opposite tendency of the chest wall to expand. For the lungs to achieve a volume other than the F RC, or resting volume, the respiratory m uscles must actively oppose the tendency of the lungs and the chest wall to return ro FRC Dur ing inhalation to volumes above F RC, the i nspiratory muscles must actively overcome the tendency of the respiratory system to decrease volume back to FRC During active exhalation below F RC, expiratory muscle activity m ust overcome the tendency of the respi ratory system to increase volume back to F RC At peak inhalation (rotal l ung capacity, or TLC) , the force applied by the inspiratory muscles to expand the lungs is balanced by the inward recoil of the lungs. The major determ i nants of TLC are compliance and inspiratory muscle strength. If the l ungs become stiffer or less com pliant, such as in patients with lung fi brosis, the TLC decreases; if the lungs become more compl iant, such as in patients with emphysema, the TLC increases. If the inspira tory muscles are significantly weakened or i mpaired, such as is seen with somatic dysfunction, they are less able to overcome the inward elastic recoil of the lungs and the TLC is reduced . At the end of a maximal exhalation (residual volume, or RV) , the force exerted by the expiratory muscles to decrease lung vol ume further is balanced by the outward recoi l of the chest wall. The wall becomes extremely stiff at low lung volumes. The vol ume of gas found within the lungs at RV is influenced by two factors. The first factor is the ability of the subject to exert a pro longed expiratory effort. This is often related to thoracic skeletal muscle strength and performance and the abili ty of the patient to override certain sensory sti muli from the chest wal l . These stimuli create a sensation that tends to stop the expiratory effort. The second factor is the ability of the lungs to empty to a smaller volume. In lungs with diseased airways, flow limitation or dy namic airway closure can limit the amount of gas that is exhaled. Thoracic cage dysfunction, including muscle weakness or airflow obstructive disease can result in an elevated RV or air trapping which disturbs ventilation. From this discussion it is easy to appreciate how the respira tory system is an ideal example of structure-function interdepen dence involving a musculoskeletal-visceral relationship. Somatic dysfunction at any spinal segmental level can adversely affect any of the previously described relationships through several poten tial mechanisms involving somatovisceral, somatosomatic, and nociceptive reflexes. Pulmonary Circulation

The principal function of pulmonary circulation is to deliver blood in a thin film to terminal respiratory units so that the ex-

503

change of CO2 for oxygen can occur. Other functions occur be sides gas exchange. This circulation acts as a fi l ter of the venous drainage from virtually the en tire body. Pulmonary circulation provides nutritional substrates to the l ung parenchyma that are important for the synthesis of l ung su rfactant, which is essen tial for maintain i ng alveolar integri ty. The blood present in the lungs serves as a reservoir or sump for the left ventricle. Finally, pul monary circulation modifies a variety of circulating hormones by biochemical transformation. The pulmonary vasculature must normally accommodate the entire output of the right ventricle. The thin-walled pulmonary vasculature has minimal resistance to blood flow and is capable of handling large volumes of blood at low perfusion pressures compared with that of the systemic circulation . The distribution of blood flow throughout the lungs principally depends on hy drostatic forces. W ith an increase in blood flow during exercise, the pulmonary vasculature is capable of recruiti ng and distend ing underperfused vessels. Therefore, the pulmonary vasculature is capable of handling large i ncrements in blood flow with a min imal change in vascular resistance and pressure. Certain neurogenic, h umoral, and chemical sti muli cause ac tive pulmonary vasomoto r reactions. Pu lmonary arteries and veins are i n nervated wi th nerve fi bers from the sym pathetic trunks and the vagus nerves. The degree of infl uence that the autonomic nervous system exerts over the pul monary ci rculation in the nor mal human adult is u ncertain. Hu moral influences, on the other hand, are likely more i mportant. Several naturally occurring h umoral agents can cause either vasoconstrictor or vasodilator responses of the pulmonary vas cular bed. Vasoconstrictors have been shown to i n fluence the human pulmonary vascular bed. These include catecholami nes, angiotensin, and prostaglandins. Certain vasodilators, such as prostacyclin and acetylcholine, also influence the pulmonary vas cular bed. The role of these substances in the control of the pulmonary circulation in health and disease remains speculative. Alveolar hypoxia, at a local level, i nduces pul monary vasocon striction. Therefore, a close relationship between ven tilation and perfusion is evident. A synergistic relationshi p exists between the effects of alveolar hypoxia and acidosis on pul monary vascular resistance (Fig. 34.3). In the presence of blood or tissue acidosis, as hypoxia becomes more significant, the increase in pulmonary vascular resistance accelerates. Regardless of the etiology, thoracic somatic dysfunction adversely affects the lung's circulation, gas exchange, and immunology via substantial negative autonomic and humoral influences. Pulmonary vascular resistance also increases if thrombi or vascular p roliferation diminishes the intraluminal cross-sectional area of the pulmonary circulation. Pulmonary vascular resistance can also i ncrease in any disease state in which the small pul monary vessels are obliterated. Over time, the pulmonary arterial pressure rises, and cardiac output eventually decreases as the right ventricle fai ls. Pulmonary hypertension may be the result of res piratory or cardiovascular disease and may compl icate the cou rse and managemen t of the primary disorder responsible for its devel opment. It may also result fro m certain hematologic, infectious, and inflammatory conditions not solely involving the cardiores piratory system, or it may occur in the absence of an identifiable precipitating disorder. Regardless of the cause of the pulmonary

504

VI. Osteopathic Considerations in the CLinical Specialties

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600

3. Adequate gas movement across the membranes that make up the alveoli and pulmonary capillaries.

500

4. Appropriate matching of l ung ventilation and perfusion. Hypoxemia is associated with a variety of diseases that affect the lungs or other components of the respiratory system. The four basic mechanisms of hypoxemia are:

400

300 200

pH

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7.1

2. Hypoventilation

7.2

4 . Ventilation-perfusion inequali ty

3 . Shunt 100

7.3 7.4

0 25

50

75

100

FIGURE 34.3. Effect of changes in inspired P02 on pulmonary vascu lar resistance (PVR) under con d itions of d i fferent arterial blood pH. As inspi red P02 is decreased, pulmonary vascular resistance i ncreases; this effect becomes exaggerated and occurs at p rogressively higher P02 val ues as pH is decreased.

hypertension, this pathophysiologic alteration usually remains clinically silent until the process is advanced. Patients then of ten present with signs of right heart fai lure. Extrapulmonary diseases, such as severe kyphoscoliosis and fibrothorax, produce distortion o f the chest cavity, mechanical compression o f l u ng parenchyma, and alveolar hypoventilation. These changes often lead to substantial degrees of pulmonary hypertension. Obvi ously, these structural maladies may be amenable to OMT and other structural corrective i nterventions, so the potential for pos itive inAuences on the pulmonary circulation by improving l ung gas exchange relationships exists. Furthermore, OMT may af fect certain autonomic and hormonal inAuences and reduce pul monary vascular resistance i n a more d i rect way. Bronchial, intercostal, internal thoracic, superior epigastric, subclavian, and m usculophrenic vessels supply the lungs, chest wal l , and diaphragm. The venous and lymphatic drainage systems are complex, numerous, and closely associated with the m uscu loskeletal system of the thorax. Pulmonary Gas Exchange

The primary function of the respiratory system is to remove the appropriate amount o f CO2 fro m blood entering the pulmonary circulation and to provide adequate oxygen to the blood leaving the pulmonary vascular bed. Therefore, an adequate supply of fresh air to the alveoli and an appropriate degree of ventilation to remove CO2 fro m the l ungs and, hence, fro m the circulation, must be available. For these functions to occur there m ust be: 1 . Adequate ventilation or delivery of oxygen to the alveoli and removal of CO2 fro m the alveoli. 2 . Adequate circulation in terms o f both perfusi o n and distribu tion of blood Aow through the lung vascular bed.

D i ffusion i mpairment contributes to hypoxemia in only select clinical circumstances, which are generally extreme in character and uncommon in occurrence. The most common cause of hy poxemia is ventilation-perfusion inequality. Lung regions with low ventilation-perfusion ratios are most important for the de velopment of arterial hypoxemia. The essential mechanism underlying hypercapnia is inade quate alveolar ventilation for the amount of CO2 that is being produced. The causes of arterial hypercapnia i nclude: •

Increased CO2 production Decreased ventilatory drive • Disease of the respiratory pump • Increased airway resistance making it difficult to sustain ade quate ventilation • I nefficiency of gas exchange resulting from an increase i n dead space andlor excessive ventilation-perfusion i nequality •

For many patients with disease, more than one mechanism is responsible for the hypercapnia. Different clinical situations a;e generally associated with a certain mechanism that is responsible for hypoxemia. Hypoventilation as a cause of hypoxemia is always associated with an elevated arterial Peo2 . A loss of respiratory drive and a variety of neuromuscular diseases are associated with this mechanism of hypoxemia. Shunt as a cause of hy.poxemia can result from the movemenr of blood from the right to the left side of the heart without entering the pulmonary circulation, as occurs with i ntracardiac shunts . Shunting of blood through the pulmonary parenchyma can also occur and is most often the result of disease in which there is an absence of ventilation in areas of lung that remain perfused. Atelectasis and alveolar fi l ling diseases, such as pneumonia, respiratory distress syndrome, and pulmonary edema, often i ncrease the shunr fraction ofblood that goes through l ung parenchyma. As mentioned, ventilation-perfusion i nequality is the most common clinical cause of hypoxemia. Lung airway and parenchy mal diseases, including asthma, emphysema, chronic bronchi tis, and i n terstitial l ung diseases, including all of the infiltra tive diseases, demonstrate hypoxemia by this mechanism. All of these diseases are associated with thoracic somatic dysfunction, which could i nfluence lung function and further complicate gas exchange. Finally, a low mixed venous saturation can also in Auence the arterial blood in patients with an increased shunt fraction andlor ventilation-perfusion inequality made worse by hypoxemia.

34. PuLmonoLogy Ventilatory Control

The many inAuences that affect breathing and gas exchange are mediated by a control system that incorporates peripheral and central receptors in a complex network of nerve pathways and integrating centers in the brain and spinal cord. The neurologic respiratory control system contains three principal interconnect ing components: •

A controller located within the central nervous system that ini . tiates signals of its own, in addition to integrating information from sensing units • A group of effectors in the lungs, airways, and m uscles of respiration that carry out commands from the controller • Different central and peripheral sensors that monitor the ad equacy of breathing Control of respiration by the central nervous system is functionally and anatomically partitioned. The brainstem reg ulates au romatic respiration, whereas the cerebral cortex affects voluntary breathing. The cerebral cortex is involved in breath holding complex behaviors, such as talking, crying, and laugh ing, and the respiratory responses to pain, apprehension, ex citement, and exercise. I ntegrating neurons in the spinal cord possess efferen t information from both upper and lower respira tory centers in the brain as well as afferent information from peripheral proprioceptors. The neurons send the fi nal signals to the muscles of respiration. Efferent autonomic impulses also travel in the vagus nerves fro m the central nervous system to the airways and lung parenchyma. Branches from the vagus nerves make up the parasympathetic innervation of the airways and with stimulation produce secrerory and bronchoconstrictive inA uences. The medulla is the center for spontaneous respiration . Inspi ratory neurons are found in the dorsal medulla, whereas, expira tory neurons are in the ventral medulla. The respiratory activity found in the pons serves to smooth the transition from inhalation to exhalation. The pons also contains two important regulatory centers: the apneustic center and the pneumotaxic center. These centers also play a role in modulating respiratory activity. The apneustic center appears to contain the normal inspiratory in hibitory mechanism. The pneumotaxic center is believed to act as a fine tuner of the pattern of breathing by influencing the response to afferent stimuli generated during hypoxia, hypercap nia, and lung inAation. Stimulation of respiratory components of the cortex inhibits respiratory movements and, in other areas, increases respiratory frequency. Whether the signal to breathe originates from the cortex or medulla, the phrenic nerves m ust eventually be stimulated. The phrenic nerves, which arise from the ventral rami of C3 th rough C5 and pass over the anterior scaleni and under the sternocleidomastoid muscles p rovide the sole motor supply to the diaphragm and carry afferent sensory fibers from the peritoneum. Behavior-related activities involv ing breathing, such as talking, swallowing, crying, and laughing, cause marked changes in ventilation that may completely over ride the autonomic control, which responds chiefly to chemical stimuli and to changes in lung inAation.

505

The descending neurologic tracts that originate in the cortical breathing centers and control vol u ntary breathing are separate fro m those that originate in the brainstem that involve invol untary breathing. The neurologic inAuence in these descending tracts is integrated with local reAex information at the level of the spinal cord from which the segmental motoneurons that in nervate respiratory muscles emerge. These interrelated processes at the segmental level are complex and might differ in various respiratory muscles. The main effectors of breathing are the m uscles of respi ration. Other central neuromechanisms regulate both the par ticipation in breathing by skeletal muscle in the upper airway and the response of smooth m uscle and mucous glands of the tracheobronchial tree. Inspiratory neurons and the medulla re ceive input fro m chemoreceptors, peripheral receptors, cerebral cortex, temperature, and facilitory cenrral neural feedback cir cuits involving the hypothalamus, pons, and reticular-activating system. The respiratory system must be responsive to a wide variety of needs for ventilation. Therefore, it is desirable to have suitable sensors to initiate changes and to monitor whether any correction that occurs in ventilation is appropriate. Four sets of well-defined sensors have been described. The carotid bodies at the bifurcation of the com mo n carotid arteries and the aortic bodies along the aortic arch function as chemoreceptors, monitoring the chemical composition of the arterial blood. I m mediate hyperventilation is one of the principal compensatory responses to sudden hypox emia. A decrease in arterial Po2, an increase in arterial PC02, or a decrease i n arterial p H increases chemoreceptor activity from the carotid bodies. The aortic body chemoreceptors act in a similar fashion. Stimulation of the carotid body with signal transmission via the glossopharyngeal nerve to the m edulla causes bradycardia and hypotension, whereas, stimulation of the aortic body with vagus nerve stimulation to the m edulla induces tachycardia and hypertension. Certain central receptors work to maintain acid-base balance in the central nervous system. Chemoreceptors near the medulla respond to changes in bicarbonate and hydrogen ion concen trations in the blood and the PC02 in the synovial Auid. The l ungs and upper airways are equipped with a multitude of recep tors that, when stimulated, have profound effects on breathing as well as on the circulation of other visceral and somatic systems. Receptors in the skeletal muscles of respiration help regulate mus cle behavior at the spinal segmental level. Afferent impulses that originate fro m these sensors and go to the brain in the ascending spinal tract likely have some inAuence on the control of breath ing. Muscle sensors have been linked to the sensation of dyspnea. Nociceptor inAuence at a spinal segmental level could easily in Auence not only respiratory muscle function and the sensation of dyspnea but also lung function including gas exchange and hemo dynamics. This nociceptor reflex could have visceral or somatic disease origins. Located in the walls of the airways throughout the l ungs are stretch receptors that transmit signals through the vagal system into the central nervous system when the l ungs become over stretched. These signals affect inhalation in a similar way as sig nals from the pneumotaxic center (i.e., they limit the duration of

506


inhalation). This breathing control process is called the Heri ng Breuer inAation reAex. This reAex helps protect the l ungs from overinAation and from the development of barotrauma. o

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THE OSTEOPATHIC APPROACH

We have reviewed various components of the respiratory system and discussed certain disturbances commonly encountered in patients with respiratory disease. As mentioned previously, breath ing is a dynamic p rocess involving moment-to-moment active gas exchange at the level of the l ungs. The thoracic cage acts as a pump coordinated by a complex central controller mech anism and inAuenced by coordinated neural reAex activity. When the thorax acts as a pump, i t involves complex muscular relaxation and contraction, motion of fascial planes, and the movement of nearly 1 50 join ts of the body. It is clear that the thoracic viscera affect i ts musculoskeletal pump. Likewise, the thoracic pump, when dysfunctional, nega tively affects the thoracic viscera. Maintaining normal respiratory motion during i n halation and exhalation inherently tends to cre ate a healthy environ ment for the thoracic viscera. Dysfunction of the thoracic cage, therefore, must have a negative inAuence. Unimpeded physiologic motion of the thoracic cage is important to maintain: Sufficient arterial supply Adequate venous drainage Efficient lymphatic drai n age Sensitive and responsive neural regulatory i n A uences on the respiratory system Branches from the vagus nerves, containing both afferent and efferent com ponents, make up the parasympathetic innervation of pulmonary structLIres, particularly the airways. The principal vagal effects are mainly secretory and bronchoconstrictive in char acter. The sympathetic supply to the lungs originates in the first to the fourth or fifth thoracic spi nal cord segments (Fig. 34.4) . The postganglionic fibers are derived fro m the stellate ganglion and the upper thoracic paravertebral ganglions. At times, the middle and superior cervical ganglia also contribute to the sym pathetic innervation of the pulmonary system. The sympathetic innervation supplies vasomotor fibers to the trachea, bronchi , a n d pulmonary blood vessels. Visceromoto r reAexes from the lungs express themselves in the somatic area of the upper thoracic regio n and at times the cervical area. Viscerosensory reA exes can be found in the same region . T h e most com mon clinical response t o enhanced reAex activity is muscle rigidity in the upper thoracic area, involving mainly the paravertebral m usculature. This response is also experienced in the cervical area, involving the sternocleidomastoid, scaleni, and diaph ragm muscles. The neuroregulation of the diaphragm is the function of the phrenic nerves. The autonomic nerves found in the diaphragm are probably vasomotor afferents. Again, the sympathetic nerves arise from the first four thoracic segments of the spinal cord, the parasympathetic supply is derived from the vagus nerves, and the neurons pass through both the thoracic and abdominal plexuses before innervating the m uscle ( Fig. 34.4) .

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The excursion of the diaphragm is important for proper pul monary function. Additionally, its rhythmic pumping action with respiration is likely to favorably affect abdominal organ func tion. The rhythmic motion of the diaphragm may have a posi tive inAuence on gastrointestinal function and perhaps even en hances venous drai nage of other visceral organs such as the liver and spleen. Certainly, proper diaphragmatic motion is necessary for optimized lung function. With inhibition of diaphragmatic motion, there is marked disruption in pulmonary gas exchange secondary to l ung parenchymal atelectasis. Likewise, visceroso matic reAexes, emanating from ei ther the lungs or pleura, wi ll affect movement of the thoracic cage. This restrictive movement process could induce a splinting effect, asymmetric movement of the chest, and intercostal hyperalgesia. It could also induce pain on palpation and, in severe cases, on voluntary motion. This reduced thoracic cage motion can also inA uence gas ex change by the induction of l ung parenchymal atelectasis or by altering l ung volumes, such as FRC and TLC, and distribu tive airAow. Finally, respiratory motion and fu nction are inAu enced by the activity of somatic structures in the upper and

34. Pulmonology lower extremities, head and neck regions, and the abdominopelvic regions. Reduction or impai rment of thoracic cage mobil ity influences lymphatic drai nage. A reduction in lymphatic drainage from the thoracic viscera may help contribute to the development o f pul monary congestion and a higher l i kelihood of lung i nflamma tion and infection. I t is clear that thoracic somatic dysfunction through negative influences on lym ph flow, circulation, and vis ceral fu nction substantially weakens lung defenses against disease. We have noticed in our patients that a reduction or elimination ofsomatic dysfunction by OMT enhances healing; improves pul monary function and general well being; and helps prevent dis eases or exacerbation of diseases from occurring. The Viscerosomatic Reflex and Lung Disease

Studies have confi rmed the existence of somatOvisceral and vis cerosomatic reflexes ( 1 , 2) . The viscerosomatic reflex is the result of afferent stimuli arising from a visceral disorder affecting so matic tissue. Afferent impulses from visceral receptOrs are trans mitted to the dorsal horn of the spinal cord, where they synapse with interconnecting neurons. These neurons convey the stim ulus to sympathetic and peripheral motOr efferents, resulting in sensory and motOr changes i n skeletal muscle and the overlying tissue, including ski n . Skeletal muscle spasms resulting ftO m no ciceptive visceral stimuli have been observed clinically i n patients. These spasms can be detected as a muscle contraction or as local ized tenderness and paravertebral muscle spli nting. It is possible that presymptOmatic signs of visceral disease may be evident i n the somatic system. The intensity and the extent o f the tissue response di ffer among individuals and disease states. Preliminary studies suggest that the i n tensity of the somatic dysfunction is greater in patients with cardiac disease who ptesent with symp tOms of severe pain than in patients with pulmonary disease who are more apt to present with symptOms of dyspnea (2,3) . Spinal segmental sites for somatic dysfunction associated with visceral disease are related to the autOnomic nervous system sup ply for various organs. Viscerosomatic reference sites for the l ungs are generally C3 and C4, and T2 to T9 (4-6) (Fig. 34.5). Areas of somatic dysfunction associated with visceral disease have been identified by palpatOry examination by a n umber of investigatOrs (6) . Osteopathic physicians have shown a particular i nterest in the identification of somatic dysfunction related to or ganic disease (7) . Generally, these findings ofsomatic dysfunction are located at the level of the segmental sympathetic autOnomic nerve supply of the dysfunctional viscera. In a 5-year, double-blind study of 5 ,000 hospi talized patients who were examined for evidence of somatic dysfunction and its relationship to diagnosis, most visceral diseases appeared to have more than one region with an increased frequency of segmental findings (8) . Unpaired viscera were also found to have an in creased frequency of fi ndings on the side of the dysfunctional viscera, and the number of spinal segments involved appeared to be related to the duration and severity of the disease. In a sub sequent report, Kelso and colleagues (9) observed an increased incidence of palpatOry fi ndings in the cervical spine in patients with upper ai rway diseases. Upper thoracic involvement was seen in patients with lower respi ratOry disease.

507

In a study by Beal and Morlock (3) , 40 patients with a di agnosis o f pulmonary disease mainly COPD were examined for evidence of somatic dysfunction . A prevalence of spinal findings was found in the T2-7 paraspinal area. The somatic dysfunction that was found generally i nvolved two or more adjacent spi nal segments, deep-muscle splinting, and resistance to a compression motion test (Fig. 34.6) . Other investigatOrs have reported simi lar fi ndings in patients with respiratOry disease ( l 0- l 3) . Nicholas evaluated ten patients with respi ratOry disease and found an in creased incidence of paravertebral m uscle tension at C4-7 and T2-9 bilaterally ( 1 2) . In patients with COPD, a palpatOry exam ination tested skin drag, red reaction, side-bending, and hyper mobility. The greatest n umber of findi ngs were seen in the spinal segments T l -9 ( 1 3) . With l ung disease, especially i f inflammation is present, vis ceral afferent nerve activity l i kely increases based on the nocicep tive reflex model. This i ncrease results in a change in the par avertebral muscular anatOmy from the T I -7 cord levels and can be extended as low as T9 or T I 0. When the l u ngs are irritated, visceral afferents usually travel to the seven upper thoracic cord segments and these have been found to have low reflex thresholds that discharge easily. Viscerosomatic reflexes l i kely occur even with subthreshold stimuli. This low threshold phenomenon is termed facilitation. Viscerosomatic reflexes from the lungs may be responsible for initiating the facilitated cord segments in this example. These reflexes will also i nteract with somatic nerves in the spinal cord to i n i tiate reflexes, al lowing the physician to palpate the paravertebral musculature and discern changes that indicate l ung dysfunction. Even though there are two lungs in each thorax, the palpable musculoskeletal fi ndi ngs of lung disease in the upper thoracic area are more frequently found on the left side than on the right side (3). During states that produce an i ncrease i n sympathetic tOne in the lung, certain hypersympathetic effects are speculated to occur. I ncreased sympathetic tone results in lung vasoconstriction with regional hypoperfusion and airway epithelial hyperplasia. With ai rway epithelial hyperplasia, an i ncrease in goblet cells occurs and luminal secretions increase. The musculoskeletal effects described often restrict chest cage excursion and further i n terfere with the mechanical portion of res piration. The cervical paravertebral area is another high-incidence area of somatic dysfunction in respiratory disease. This area of spinal faci litation could i n terfere with appropriate diaphragmatic function. Diaphragmatic function is al ready stressed by the rela tive immobility of the ribs and spine as influenced by the viscero somatic reflex in the thoracic area. The i ncreased workload on the diaphragm could result in enhanced fatigability. In patients who have recruited use of the secondary muscles of respiration (often patients with advanced respiratory disease), fatigue of the scaleni and sternocleidomastoid muscle may result in dysfunction of the upper thoracic rib cage, including the fi rst rib. This mechanical disruption l i kely further impairs breathing efficiency. Thoracic Lymphatic Drainage

Osteopathic physicians have long been concerned with optimal lymphatic drainage from tissues ( 1 4, 1 5) . The maintenance of proper lymphatic drainage is thought to encourage proper tissue


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activity and metabolism and have a particular i mportance in pro viding for a proper i m munologic environment. Normally, comraction of the diaphragm and thoracic cage movement during respiration produces substantial pressure gra dients between the thoracic and abdom i nal cavities, resulting in effective lymphatic drainage and venous return to the heart. Proper movement and lymphatic drai nage throughout the l ungs are considered important for the maintenance of normal function and a disease-free existence. Additionally, proper movement is essemial for I1gh ting infection and for reducing healing time. Tis sue congestion is thought to decrease the effectiveness of medical therapy si nce both leukocytes and medication have more diffi culty getting to the target tissues and there is also the risk ofinef ficiem toxin and waste removal. Therefore, osteopathic medicine

uses manipulative treatments, rib raising, diaphragm relaxation, and thoracic inlet release, to name a few techniques, to enhance movement and lymphatic drainage, with both preventive and curative influences on disease. Osteopathic Manipulative Treatment

Many musculoskeletal patterns may arise as a reflex or mechani- ' cal consequence of pulmonary disease; they may serve to exacer bate or complicate the disease. Therefore, the treatmem options of the osteopathic physician include pharmacological, surgical, and osteopathic manipulation. I f OMT can reduce the pain and immobility associated with somatic dysfunction as it relates to pulmonary disease, then this treatment modality should enhance

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thoracic excursion. OMT should not only improve breathing and respiration but also enhance the heali ng process for patients with inAammatory and infectious d iseases involving the lung. Addi tionally, if manipulative treatment can enhance thoracic lym phatic d rainage, then this process can also be associated with ac celerated healing. Prophylactic rib elevation and thoracic pump techniques are likely useful in the prevention of venous stasis. They should play a role in prophylaxis of deep venous throm botic disease and pulmonary embolism for patients at bed rest. OMT may do more than improve motion and enhance blood and lymphatic Aow related to the thoracic cage. Improving tho racic motion may have a positive inAuence i n maintaining proper lung function and enhancing heali ng. Manipulation potentially has direct effects on the lung parenchyma itself. OMT l i kely af fects the neurohumoral system in a way that benefits the l ungs. Osteopathic research can make a major contribution to the health care of patients suffering from respiratory disease. Through the use of manipulative treatment, patients with respi ratory disease could have improved functional performance during the daytime.

FIGURE 34.6. Location of somatic dysfunction i n 40 patients with p u l monary d isease.

They could also enjoy enhanced sleep at night, with or without the concom itant use o f standard medical therapy.

PULMON ARY FUNCTION

Attempts have been made to determi ne how OMT alters physi ologic function. Eggleston ( 1 6) and Detwiler ( 1 7) have observed the i m mediate favorable effects ofOMT on vital signs, including respiratory rate. The design of these studies lacked proper con trols, however, making it d i fficult to draw conclusions from their data. A more carefu l ly controlled study by Ortley and associates ( 1 8) designed experiments to determine, in healthy subjects, if mea surable physiologic changes resulted from manipulation. Healthy male medical students were selected and participated in five in terventional sessions, which included two control periods. There was an emphasis on observing the effects of OMT on respira tio n . H igh-velocity, short-amplitude man ipulation was used as

510

VI. Osteopathic Considerations i n the ClinicaL Specialties

osteopath ic i ntervention. A decrease in heart rate in a n umber o f subjects a n d a decrease i n s k i n resistance and respiratory rate i n four of six subjects was found. I n the fou r subjects who showed a drop in respi ratory rate, three had a compensatory i ncrease i n tidal volume (VT). The i ncrease i n VT appeared t o b e the result of a greater abdominal d iaphragmatic movement component. Mani pulation had no effect on expiratory or inspiratory reserve volumes, Vc, forced expiratory volumes, and maximal m idex piratory flow rate as determi ned by pulmonary function testing. Obvious problems with the study were that the subjects were healthy and only a few were studied. A series of experiments observing the effects of OMT o n pul monary function was conducted by Murphy ( 1 9-2 1 ) . Restricted breathing, including a loss in l u ng compliance, has been associ ated with altered lung gas exchange and the eventual development of hypoxemia. I mproving restricted breathi ng improves gas ex change. Murphy attempted to exam ine the influence of thoracic mobi lization o n selected pulmonary functions ( 1 9) . Pulmonary func tion tests were performed before and after each thoracic mo bil ization or restriction procedure. Her early findings indicated that thoracic mobilization techniques in healthy subjects tend to decrease the FRC and RY, while i ncreasing the total thoracic compliance. Restriction techn iques tend to decrease the F RC and total compliance. RV appears to be i ncreased, and it may be that ai r-trapping or uneven l ung ventilation distribution is responsible for this change. In further studies, M urphy found that there is an i ncrease in VT and respiratory rate after thoracic mobilization, wh ich results i n an increase in alveolar ventilation (20) . In a technique that restricts breathing and thoracic mobiliza tion, a decrease in Vr and an i ncrease in respiratory rate are noted. At times there are m i nute ventilation i ncreases, but overall alveo lar ventilation remains decreased. Looking at the effect of n itrogen clearance from the l ungs, thoracic mobilization clears n itrogen from the l ungs .faster. Any procedure that restricts breathing, cre ating a rapid shallow breathing pattern, reduces the clearance rate of this gas. Murphy used a subsequent mathematical model to analyze the various factors that may have influenced the clearance of nitrogen from the l ung. She concluded that, for n itrogen clearance to be enhanced, it is i m portant to i ncrease VT and improve the d istribution of gas i n a homogeneous fashion throughout both l ungs. This means that manipulation likely not o n ly improves movement but also may i mprove ventilation homogeneity. I n other words, O M T n o t o n l y m a y improve movement factors o f the thorax i ncreasing bulk airflow w i t h each breath but also m ay, with each breath taken, distribute air more evenly through the l ungs, i mproving ventilation-perfusion relationships. Finally, i n her effort to further study this observation, Mur phy used I - 1 3 1 -labeled human albu m i n to study the effect of thoracic mobilization o n pulmonary capillary circulation (2 1 ) . The method was used to look a t the distribution o f blood flow throughout the lungs. In healthy subjects, blood flow distribu tion may reflect the distribution of ven tilation, since perfusion usually matches ventilation in lung disease and in healthy sub jects. Murphy reported that thoracic mobilization i ncreases the density o f radioactivity throughout the l ungs. This fi nding sug-

gests that enhanced movement of the chest improves ventilation as suggested by these changes i n lung perfusion. This process leads to improved lung oxygenation since ventilation-perfusion relationships within the l ungs are enhanced. Doran and col leagues (22) studied the role of spinal curvature on resp iratory mechanics. They hypothesized that an alteration i n l umbar lordosis induces changes in respiration. Their experience had been that many patients in the i nitial physical examination have an i ncreased l umbar lordosis that manipulation can decrease. Experiments were performed to establ ish the reproducibility and variabi l i ty ofa table that they constructed to quanti fy the degree of l umbar lordosis. Once the reliability of their measurement table was determined, they recruited young adult volunteers. They assessed how OMT would affect respiratory function. The test was admi n i stered using h igh velocity, low amplitude ( HVLA) techn iques with emphasis placed on treatment of the transitional areas of the spine. Respiratory function was mea sured for 1 5 minutes using both a pneumotachograph and a respiratory plethysmography, which assessed thoracoabdom inal motion and timing. Following manipulative treatment, which often successfully decreased the l umbar lordotic curvature, there was a corresponding decrease in respiratory rate and an increase in VT• A larger abdominal component to each breath, as com pared with the thoracic component, was noted. The Doran group concl uded that one of the sign ificant fac tors that correlates with impairment of respiration is the lordotic curve, and that OMT can alter this curve and favorably affect the mechanics of respiration. These i nvestigations, reported i n abstract form , are hard to in terpret. Most of the conclusions are based on minimal published data. A need exists for extensive controlled stud ies exploring the effect of OMT on pulmonary mechanics and gas exchange.

THORACIC PU M P

The thoracic p u m p has been investigated for its effec;r o n res p iratory function and its immunomodulating effect by a vari ety of techniques. Since the early reports of M i ller in the 1 920s (23,24) , the thoracic lymphatic pump tech nique has been used as a research and treatment tool. More recently, Allen has been responsible for readdressi ng the potential value of the thoracic pump techn ique. He proposed a study to investigate the effects of this i n tervention on respi ratory function in healthy subjects (25). The results of this study have yet to be publ ished, but they have been obtained for some patients with respiratory disease who have received thoracic pump intervention. These patients have shown an improvement i n Vc, i mproved mobilization of the thoracic cage and spine, and more rapid clearing of ai rway secretions (26) . In a subsequent editorial, Allen and Kelso stated that patients who have been treated with the thoracic pump and mobilization of the thoracic cage and spine nearly u n i formly experience a sense ofwell being and relieffrom pulmonary congestion, dyspnea, and ' the m ilder forms of air h u nger (27) . They claim that physicians have also observed improved sputum expectoration. In this same editorial, the authors provoke the osteopathic profession's inter ests i n establishing a national cli n ical trial to explore not only the

34. PuLmonoLogy physiologic changes that occur with this form of manipulative intervention but also how these changes improve the quali ty of care of our patients. Additional proposed mechanisms for the effectiveness of tho racic pump therapy center on an enhancement of immune func tion. In a preliminary investigation, Measel studied the effect of the thoracic pump on the imm une response of healthy male medi cal students by measuring how two serologic tests changed in response to a subcutaneous admi nistration of pneumococcal polysaccharide antigen, administered subcutaneously (28) . The students, once treated by the thoracic pump tech nique, had an increased immune response on the basis of testing for polysac charides 1 , 3, 4, 6, 8, 1 4, 23, 25, and 56 by passive hemaggluti narion . This study suggests that the thoracic pump had a signif icant effect on the humoral or B-cell component of the immune system. On follow-up Measel, in a double-bl ind study, evaluated the effect of the thoracic pump technique on peripheral blood, bone marrow, and thymic-derived cel ls, again in medical students (29) . Prel imi nary results indicare that white cel l counts rose and lym phocyte numbers decreased following lymphatic pump interven tion. Additionally, the percentage of circulating T cells and B cells increased following therapy. It appears, therefore, that thoracic pump therapy significantly changes the peripheral leukocyte blood picture in heal thy indi viduals. In a pilot study, Paul and co-workers (30) attempted to determ ine whether i nterferon, an antiviral and antibacterial chem ical, could be released or induced by thoracic pump ma nipulation. Twelve heal thy adults were studied in a controlled fashion. Serum samples were drawn im mediately before and at different times during the 24-hour period after manipulative in tervention. Interferon levels were determi ned by a tissue culture technique that used a reduction of cytopathic effect as the end point variable. Mean pretreatment serum i n terferon levels were no different than the posttreatment levels in this acute study. This study does not discount the effectiveness of the thoracic pump maneuver in the treatment of infectious lung disease. I t is pos sible that the classic agents necessary for interferon production may be req ui red to initiate stimulation of interferon production and that the rhoracic pump served to augment or enhance the response. Further research is necessary to clarifY the usefulness of the thoracic pump tech n ique for the augmentation of body i nt e rferon production. A more recent study used a guinea pig model to explore the effect of thoracic pump techn ique on macrophage activity dur i ng lung infection with Streptococcus pneumoniae (3 1 ) . This study may or may not relate to humans, but the sequence of experi ments performed indicate that the thoracic pump technique has an effect on macrophage enzyme activity that could be impor tant for the control of pneumonia with this organ ism in humans. Agai n, fu rther controlled studies are necessary.

PREVENTION AND TREATMENT OF LUNG D I SE ASE

Osteopathic physicians typically treat respiratory disease by con ventional means, but their options expand to a new level and

51 1

intensity with the appropriate use of OMT. As discussed earlier, a variety of manipulative techniques are useful in relieving tho racic cage discomfort, in faci litati ng i n halation and exhalation , a n d in i mproving overall ventilation a n d perfusion oft h e lungs. I n addition t o techniques that concentrate on paravertebral m uscle disease, other techniques concenuate on i mproving rib motion and enhancing the performance of the secondary muscles of res piration , such as the cervical strap muscles and the superficial muscles of the thorax. Thoracic pump techniques have been used to enhance the elimination of airway secretions and perhaps even increase the movement of fluids from l ung parenchyma and pleural space. The thoracic pump techniques are often employed with rib elevation techniques. This combination of techniques has been proposed to prevent venous stasis throughout the body and to enhance fluid movement from the parenchyma of the l ung. Most osteopath i c physicians do not treat specifically for the thoracic problem that is present but expand their therapy to treat the entire body. Although special attention might be directed at the cervical and h igher thoracic area, for patients with respi ratory d isease it is not unusual to also treat somatic dysfunctions found in the lower thoracic, lumbar, and sacral areas. Treati ng the lower thoracic and l umbar areas can favorably influence ab dominal muscle performance, which, at times, is essential in res piration. The patient's condition and response to manipulation should govern the frequency and i ntensity ofeach osteopathic ma nipulative intervention. Optimal timing has not been established. Clin ical studies of the effectiveness of the use o f OMT in visceral diseases have been anecdotal, with small numbers of pa tients. The use of manipulation has been explored for patients with a variety of i n fectious diseases o f the airways and lu ngs and with COPD, i ncluding asthma and emphysema. Limited infor mation is available on using mani pulative techniques in the man agement of respiratory distress syndrome and for the prevention of postoperative pulmonary complications.

RESPIRATORY IN FECT I O N

The early osteopathic l i terature is full of anecdotal case reports and information discussing the use of OMT in the treatment of acute and chronic pneumonia. From the begi n n i ng of the 1 9th century to the middle of the 20th century, pulmonary tuberculo sis was o ften treated adj unctively with manipulative intervention (32-38). The older l i terature also has many articles focusing on us ing manipulative treatment in the management of patients who had bacterial pneumoniae other than tuberculosis (39-6 1 ) . Most notably, several articles taught the effectiveness of osteopath i c manipulative support for patients suffering from influenza pneu monia during the great flu epidemic of 1 9 1 8 (48-53). These older studies are primarily anecdotal; no data are presented but there are eloquent descriptions of the benefits of OMT. Nonetheless, osteopathic physicians at that time and even roday are convinced that manipulative treatment improves the course and outcome of patients with both acure and chronic infections o f the chest. The l i terature cited in this chapter contains excellent descriptions of the techn iques of manipulation used i n treating pneumonia.

512

V I. Osteopathic Considerations i n the Clinical Specialties

I n i tial manipulative treatmenc in pneumonia has three main goals: l.

Reduced parenchymal l ung congestion

2 . Reduced sympathetic hyperreactiviry the lung

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3 . Increased mechanical thoracic cage and diaphragmatic motion An explanation of the rationale (62,63) for OMT and how OMT should be used in the creatmenc ofpneumonia can be found elsewhere ( 5 8-6 1 ,64-66). Clinical scudies o n the effectiveness of OMT in visceral d isease are limited. Data concerni ng the use of this therapy in the treatmenc of lower respiracory tract disease are few. An early study by Kurschner (67) compared chlorampheni col therapy with combined chloramphenicol and OMT i n the treatment o f children with whooping cough. This scudy was poorly controlled and the number of patiencs enrolled was small, but the use of OMT was associated with a lower daily cough average and a q uicker recovery and return co school compared with those who had not received manipulation. Purse performed a retrospective analysis o f manipulation in the treatment o fupper respiracory tract i n fection in children (68). Purse reviewed 4,600 cases of upper respi racory tract infection, in which 780 incidences of complications were found. These compl ications ranged fro m simple conjunctivitis and acute oti tis media to acute pneumonia and bronch itis. The nearly 1 7% complication rate was below the 33% to 50% rates commonly associated with standard medical treatmenc at that time. Schmidt (69) reported her anecdotal experience in treating 1 00 cases of up per respiracory tract disease using OMT. The majoriry of patiencs had pharyngitis, rhinitis, o r si n usitis. The investigacor concluded that manipulation reduced duration of symptoms and compli cations, but the data presenced were unconcrolled and encirely anecdotal. Nevertheless, the study's greatest value is the detail in which patienc managemenc is described. Kline studied 2 5 2 children who had been hospitalized for respiratory infection over an 1 8-monch period (70). All pa tients received supportive therapy. One group received OMT, another group received ancibiotics without manipulation, and a third group received a combination of therapies. The investigator found that patients who received supportive therapy, manipula tive treatmenc, and antibiotics recovered faster than the patients who received manipu lation o r antibiotics alone. The efficacy ofOMT in older adu l t hospital ized patiencs with acute pneumon ia has also been reported (7 1 ) . I n a small group of patiencs older than 60 years of age with acute pneumonia, OMT was effective in reducing the duration of antibiotic use and the duration of worrisome leukocytosis. Based on the re sults of this in itial small trial, a larger, more comprehensive study (72) clearly demonstrated that patiencs with pneumonia who were treated with O MT and appropriate ancibiotic therapy had a shorter course of therapy and hospital stay. Patients who were at least 60 years old, hospitalized with pneumonia, and treated with antibiotics were randomized to receive OMT or light touch as a concrol incervencion. Patiencs who received OMT received it from an accompl ished specialist. Seven standard and some non standard osteopathic manipulative techniques were administered.

Bilateral paraspinal i nhibition, bilateral rib raising, diaphragmatic myofascial release, condylar decompression, soft tissue techn ique to the cervical m uscles, myofascial release CO the ancerior thoracic i n let, and the thoracic pump were the standard incerven tions that were employed. Duration of antibiotic therapy was 2 days shorter for patiencs who received OMT. Additionally, they were discharged from the hospital 2 days earlier (6.6 versus 8.6 days) than patiencs who did not receive OMT.

CHRONIC OBSTRUCTIVE PULMON ARY DISEASE

The use of OMT for the treatmenc of asthma and other forms of COPD has been suggested in the osteopathic li terature from as early as 1 902, when the journal ofthe American Osteopathic Association fi rst appeared (73,74). One of the 1 902 articles (72) stresses the relevance of envitonmencal control measures as part of the treatmenc plan for asthma, a unique concept for that time. The importance o f manipulative incervention was also stressed. In 1 9 1 2, Louisa B urns, DO, publ ished her experiences in diag nosing and treating asthma in patiencs at the Pacific College of Osteopathy (75). She reviewed 2 1 cases of asthma and also care fully described a multitude of structural fi ndi ngs associated with reactive airway disease, the importance of avoiding irritanc gases and dusts, and how OMT is effective in attenuating the chronic symptoms of this disease. Perhaps the first clinical study of mani pulation and pulmonary disease was that by Wilson (76). Publ ished in 1 92 5 , his study included 20 patiencs with asthma who had received a rype of vac cine treatmenc and who were given manipulative intervention. This study, albeit poorly controlled, showed that 1 5 of these patients had some temporary relief; 1 0 patiencs had 50 fewer asthmatic attacks over an extended time period. Additionally, the study demonstrated the reproducibil iry of certain palpatory findi ngs in patients with asthma. Wilson concluded that "this study tells a cold, hard, cash story to employers and insurance companies" about the benefit of this form of therapeutic inter vention. Wilson's specific manipulative techniques for asthma were evencually published the following year (77), and an even more in-depth treatise of his techniques was published several years later (78) . One of the most concise descriptions of the osteopath ic management o f asthma was published in 1 9 5 9 by Kline (79). H is management plan was based on personal experience with patients having acute asthma and others with a variery of chronic lung diseases. During acute asthma, somaric dysfunctions will always be found in the 2nd CO 4th thoracic vertebrae and the 4th rib on the right side will always be elevated. The only other constant fi nding is a lesion of the 3rd cervical vertebra with rotation to the left. Kli ne's manipulative intervencions were active, involving treatmencs that focused on im proving cervical and thoracic mobiliry and on using the thoracic pump. Kline emphasized re laxation of the thoracic cage and improvement of diaphragmatic function. He strongly urged physicians co concinue manipulative treatmenc on a regular basis, even during periods of asthma stabiliry. Length of hospital stay is reported to be reduced by nearly one day when OMT is used as a treatmenc modaliry for acute asthma

34. PuLmonoLogy exacerbation. It has been suggested that substantial cost savings would occur as well (80) . Belcastro and colleagues ( 8 1 ) hypothesized that OMT may be effective in the treatment of bronch iolitis. To investigate this theory, they studied 1 2 infants between the ages of 2 and 1 1 months with a clinical diagnosis of bronchiolitis. They ran domly assigned each infant to a treatment scheme, comparing OMT with postural drainage and bronchodilator therapy with placebo. A sequence of OMTs was developed. Outcomes were measured by the number of hospital days and the daily respira tory rate. Although data were i nconclusive because of the small number of patients, this study did establish a research protocol and discussed the treatment of bronchiolitis fro m a n osteopathic standpoint. Other forms of airway disease have been treated by OMT. Over a 9-month period, Howell and associates (82) evaluated 1 7 patients with COPD who received OMT. Measuring pul monary fu nction tests and arterial blood gases assessed the effect ofOMT. Improvement was shown in the arterial CO2 tension, in arterial oxygen saturation, in TLC, and in RV, especially in those patients who were hyperinAated and barrel-chested (typical fea tures of emphysema) . However, in another study (83) i nvolving patients with COPD, manipulation did not change VC or RV Nonetheless, manipulation may have improved work capacity and dyspnea, both at rest and during exertion. The patients who received O MT also had fewer upper respiratory tract i n fections than did the patients who did not receive manipulation. In a case report by Howell and Kappler (84), OMT was di rected toward mobil ization of a COPD patient's rigid thoracic spine and chest cage. During 1 6 months of therapy, thoracic cage mobility improved. Specifically, high thoracic paraspinal tissue re activity diminished. Clinically, walking tolerance i ncreased and episodes of difficult breathing became less frequent. Additionally, the oxygen saturation of arterial blood improved bur hyperinAa tion as determined by pulmonary function testing increased. The increase in TLC in this patient l i kely represents progressive em physema, a process that would be difficult to inAuence with any therapeutic intervention. More relevant, these authors discussed the importance of exploring new clin ical end-point variables for evaluating OMT. These include: Parameters of functional performance Compliance and distensibility of the thoracic cage Lung ventilation and perFusion relationships Spinal and thoracic cage mobil i ty Finally, at least twO authors have outli ned many of the factors that must be taken into account when a clin ical study exploring the eFfects of manipulation on patients with COPD is being considered (85,86). The role of O MT in treatment algorithms for acute and chtonic asthma and For the management of other COPD needs to be better defined by well-controlled clinical i nvestigations. Manipulative treatment should be beneficial for these groups of patients. An intervention that improves thoracic mobility and Favorably aFfects the regulatory mechanisms of the autonomic nervous system should be beneficial for patients with asthma and COPD. The clinical experience of some osteopathic physicians

513

appears encouraging ( 8 7 ) , b u t careFully designed clinical i nvesti gation is needed.

RESPIRATORY D I STRESS SYN DROME

Only one study exists in which OMT was used in the treatment of respiratory distress syndrome in the newborn (88) . A rib-raising tech n ique was used and a variety of treatment end-point variables were assessed. This study lacked proper control but i t suggested that the use of OMT could Favorably affect outcome, mainly by reducing deaths. The death rate in the study group was lower than that found using historical controls.

PREV E N T I ON OF POSTOPERATI V E PULMON ARY COM P L I C ATIONS

Generally speaking, pulmonary complications are the most Fre quent cause of postoperative morbidity. Atelectasis, a collapsed or airless segmental l ung condition, is the most common pul monary complication. Surgeries commonly associated with the development of lung atelectasis include high abdominal surgery and thoracic surgery. Aggressive pulmonary toilet measures, in cluding patient-generated incentive spirometry, have been im portant in reducing the incidence of this complication postoper atively. Ftom an osteopathic standpoint, it is important to point out that these surgeries often have a m usculoskeletal component, even when postoperative pulmonary complications do not ex ist. The existence of a pulmonary complication enhances the probability of developing a musculoskeletal component. Osteo pathic physicians have been treating patients with manipulative treatment, both preoperatively and postoperatively, to prevent respiratory complications from occurring (89) . Dickey (90) has carefu l ly described numerous postoperative complications asso ciated with median sternotomy and the value of a large number of osteopathic interventions that he has had an opportunity to per form, both p re- and postoperatively. Rib fractures, brachial plexus inj uries, and fascial and diaphragmatic restrictions often compli cate coronary bypass surgery. Emphasis on early lymphatic and tissue drainage techniques is suggested. Attention is paid to in terventions that can enhance diaphragm Function. Additionally, thoracic somatic dysfunction in the postoperative chest surgery patient is associated with abdominal visceral problems, such as ileus and all of its complications. These complications can be helped by OMT. Henshaw (9 1 ) not only defined the presence of postoperative somatic dysFunction but also clearly pointed out the high inci dence of preoperative somatic dysfunction in patients undergoing either low or high abdo mi nal surgery. Less postoperative respi ratory complain ts and complications were reported in the O MT group as compared to the control group. Sleszynski and Kelso (92) have studied the effects of thoracic pump adm i nistered on the fi rst postoperative day in patients who had undergone chole cystectomy. They compared this manipulative modality with the use of i ncentive spirometry in the prevention of atelectasis. In pre venti ng atelectasis, the thoracic pump-treated patients had similar occurrences to those patients treated with incentive spirometry.

514

V I. Osteopathic Considerations i n the Clinical Specialties

However, the patients treated with thoracic pump had an ear lier recovery and a quicker return toward preoperative values for FVC and forced expi ratory volume- l than did patients rreated with incentive spirometry. Finally, it has been shown that OMT can actually enhance the effecrs o f incentive spirometry following abdominal surgery (93).

6. Hansen K, Schliack H. Segmental Innervation. Stmtgan, Germany: G Theime; 1 962.

7. Beal Me. Viscerosomatic reAexes: a review. jA OA. 1 98 5 ; 8 5 : 7 86-80 1 . 8 . Kelso AF. A double-bli nd clinical swdy o f osteopathic findi ngs i n hos pital patiems. Progress repon. jA OA. 1 97 1 ;70:570-592.

9. Kelso AF, Larson NJ , Kappler RE. A clin ical i n vestigation of the osteo pathic exam ination. jAOA. 1 980;79:460-467.

1 0. Long FA. Swdy o f the segmemal i ncidence of certai n spinal changes in various d i sorders. Osteopathic Digest. 1 940;6: 1 1 - 1 3 .

1 1 . Deming G S, Kruener Ve. Srudy of rhe segmemal incidence of certain

CONCLUSION

The respiratory sysrem is a beaurifully designed pump whose chief purpose is to exchange CO2 for oxygen in the respiratory process. A disease that affecrs any component of this physiology generally disruprs the entire pump system . Whether the disease affects the lung parenchyma, vascular circulation, lymphatic cir culation, or a neuromuscular component, alterations of the m us culoskeletal system will be found in the physical examination. These alterations cannot be ignored. They provide readily avail able, noni nvasive clues to help the physician detect the presence of visceral disease. These alterations must eventually be treated to enhance the likelihood of cure and i mprove the time to com plete disease resolution. Proper medical care and O MT should be combined to support the respiratory sysrem . The osteopathic physician's knowledge and skills in providing effective manipu lative treatment often optimize thoracic cage motion, improve diaph ragmaric function, enhance lymphatic drainage, and stabi lize autonomic infl uences. Osteopathic physicians are convinced of the efficacy o f manip ulative treatment. O ur experience has been thar OMT is helpfu l for our patients. There are l i mited data demonstrating t h e clini cal efficacy of manipulative intervention in certain disease states. It is imperative that further clin ical investigation be pursued to advance the science of osteopathic medicine.

spinal palpawry fi nd i ngs i n disorders o f the respirawry tracr. jAOA.

1 943;43:264-267. 1 2. N icholas NA. Correlation of somatic dysfunction with visceral disease. jA OA. 1 97 5 ; 7 5 :425-428. 1 3 . M i ller WD. Treamtent of VisceraL Disorders by Manipulative Tberapy. The Research Status ofSpiual Manipulative Therapy. Bethesda, M D : U S Depanmem of Healt h, Education, a n d Wel fare; 1 97 5 .

1 4 . M illard F P. Applied lymphatics of r h e chesr. jAOA. 1 9 1 2;2 1 :22-23. 1 5 . M illard F P. Drainage o f the in tercostal spaces. jA OA. 1 923;22 :262-265.

1 6. Eggleswn AA. The effect o f man i pularive rreatmcm on body funcrion. A prel i m i nary repon. jAOA. 1 940;39: 279-284.

1 7. Derwiler ES. Some i m mediare effecrs of osreoparhic manipularive rrear menr. Swdies on fou r hundred cases. jA OA. 1 9 50;49 :39 1 -395.

1 8 . Onley G R, Sam wick RD, Dahle RE, er al. Recordi ng of physio logic changes associared with mani pulation i n healrhy subjects. jA OA.

1 980;80:228-229. 1 9 . Murphy Aj. Preliminary swdies o f rhe i n A uence of pulmonary and thoracic mobilization

procedu res on

pulmonary fu nnion. jA OA.

1 965;64:9 5 1 -952. 20. Murphy AJ. Comparison of nitrogen washout curves from human experimems and from a mathematical model o f rhe lung. jA OA.

1 967;66: 1 023-J 024. 2 1 . Murphy AJ. Conrinuation of the srudy of rhe effen of rhoracic mobi lizarion o n the disrribmion of 1 3 1 - 1 i n the lungs. jAOA . 1 97 1 ;70: 1 057-

1 05 8 .

2 2 . Doran J , Freiburger L, Z i n k G , Kil more M . Relationship o f osteopathic manipulative rreatmem, lordosis, and resp i ration. jA OA. 1 982;82: 139-

1 40. 23. Miller CEo Osteopathic princi ples and thoracic p u m p therapeutics proved by scienrific research. jA OA. 1 927;26 :9 1 0-9 1 4.

24. Miller

CEo

T he

mechanics

of

lymphatic

circulation.

jAOA .

1 923;22:397-398.

25. Allen T. A pilor swdy on rhe effect o f the thoracic pump on respiratOry

ACK N OWLEDGMEN TS

We would like to rhank rhe journal o/the American Osteopathic As sociation staff for helping us in our search for the older osteopathic l iterature. Kim Williams was invaluable in her efforrs in prepar ing this manuscript. Finally, William Kuchera, DO, FAAO was invaluable to us in accelerating our understanding of osteopathic medicine and we are thankful .

funcrion. jA OA. 1 963;62:839.

26. Allen TW, Pence T K. The use o f rhoracic pump i n rreatmenr of lower respiratOry tract disease. jA OA. 1 967;67:408-4 1 1 .

27. Allen TW, Kelso AF. Osteopath i c research and respiratOry d i sease. jA OA. 1 980;79:360. 28. Measel jW. The effect o f the lymph3fic pump on the i m m une response: I . Preli minary srudies o n rhe anribody response

w

pneumococcal polysac

charide assayed by banerial agglminarion and passive hemaggl minarion.

jA OA. 1 982;82:283 1 . 29. Measel J W. The effecr o f the lymphatic pump o n the B and T cells i n peripheral blood. jA OA. 1 986;86:608.

30. Paul RT, StOmel Rj , Broniak FF, Williams BB. I n rerferon levels i n hu

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2. Beal Me. Palpawry test i ng for somatic dysfunction in patiems with cardiovascular d isease. jA OA. 1 98 3 ; 8 2 : 822-83 1 .

3. Beal Me, Morlock J S . Somatic dysfunction associated with pulmonary d isease. jA OA . J 984;84: J 79- J 83.

4. Ponenger F M . Symptoms of Visceral Disease. Sr. Louis, MO: CV Mosby Co; 1 93 8 .

5 . Bhagat BD, Young B A , B iggerstaff DE. Fundamentals of Visceral Inner vation. Springfield, I L: Charles C Thomas; 1 977.

man subjects throughour a 24-hour period following thoracic lymphatic pump manipulation. jAOA. 1 986;86:92-95.

3 1 . Boyer jM, Davis M, Cashon G , er al. Effecrs o f thoracic pump technique on macrophage acriviry during i n fection of gui nea pigs with Streptococcus

pneumoniae. jA OA. 1 987;87:698-699. 32. Keene WE. Some possibilities i n the rreatmenr and prevenrion of ruber culosis from an osteopathic standpoint. jAOA. 1 904;4: 1 47- 1 54.

33. Meacham WB. On pul monary ruberculosis. jA OA . 1 905;4: 3 1 5-322. 34. Bolles NA. The osreoparhic and physical examination o f a case of pulmonary ruberculosis. jA OA. J 906 ; 5 : 2 83-288.

35. Hayden

W].

Tuberculosis. jA OA. 1 906;5:288-293.

36. Meacham WE. Pulmonary tuberculosis. jAOA . 1 908;7: 20 1 -205. 37. Terrell AP. Tuberculosis: a s rudy. jA OA. 1 9 1 0;9:332-335. 38. Johnson F E. Osreopathy and ruberculosis. jA OA. 1 936;3 5 : 3 1 9-327, 34 1 .

34. Pu!mono!ogy 39. Hulett MT. Osteopathic lesions in acute respiratory diseases. jA DA. 1 907;6:38 1 -384. 4 1 . Link E C Osteopathic care of pneumonia. jADA. 1 9 1 0; 9 : 5 2 1 -527.

42. Overton JA. The treatment of pneumonia. jADA. 1 9 1 2; 1 1 : I 033-

1 96 5 ;65:278-28 1 . 7 1 . Noll DR, Bryman P N , Gebhatdt GP, Masterson EV. The efficacy of OMT in the elderly hospitalized with acute pneumonia. jA DA .

1 992;92: 1 1 79 .

1 037. 43. Webster Gv. The treatment of pneumonia. jA DA. 1 9 1 4 ; 1 4: 1 2 8- 1 3 1 . GM.

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RF.

Treating

72. N o l l D R , Shores J H , Gamber R G , et a l . Benefits of osteopathic ma nipulative treatment for hospitalized elderly patients with pneumonia.

jADA. 2000 ; 1 00:776-782.

1 9 1 6; 1 5 :27 1 -276. 45. Connor

70. Kline CA. Osteopathic manipulative therapy, antibiotics, and supportive therapy i n respiratory i n fections i n children: comparative s tudy. jADA.

40. Ivie WHo The treatment of pneumonia. jA DA. 1 909;8:279-2 8 1 .

44. Laughlin

51 5

and

aborting

lobar

pneumonIa.

jA DA.

1 9 1 6; 1 5 :336-343. 46. Fulham cv. Pn e u m onia. jA DA . 1 9 1 7; 1 6:9 1 7-92 1 . 47. LaRue J B . Pneumonia. jA DA. J 9 1 9; 1 8:206-208. 48. Tuttle LK. I n A uenza and pneumonia treatment. jADA. 1 9 1 9 ; 1 8 :2 1 12 1 4. 49. Fullum Cv. Treatment of pneumonia. jA DA. 1 920;20: 1 75- 1 77 .

5 0 . Burns L, Perry A E . Osteopathic treatment a n d laboratory findi ngs. jA DA. 1 920;20: 1 79- 1 8 1 . 5 1 . Crane RM. Experiences with pneumonia. jA DA. 1 92 2 ; 2 1 :347-350. 52. Miller CEo The specific cure of pneumonia. jADA. 1 924;24:99- 1 0 1 . 53. Death statistics reveal comparative values o f osteopath and drug treat ments. Dsteopath Physician. 1 9 1 8(Dec);34: 1 2.

54. Peckham FE Osteopathic care and management of lobar pneumonia. jADA. 1 927;27: 1 80- 1 8 1 . 5 5 . Fischer RL. Treatment of lobar pneumonia. jADA. 1 929;29:354-3 5 8 . 5 6 . Conley. GJ. Treatment. jADA. 1 937;36:3 1 6-3 1 8 . 57. Watson J O , Percival E N . Pneumonia research in children a t Los Angeles County Osteopathic Hospital. A preliminary report. jADA.

J 939;39: 1 53- 1 59. 58. Horton ER . Osteopathic manipulative treatment in pneumonia. jADA. 1 940;39:5 1 1 -5 1 3. 59. Litron HE. Manipulative treatment of pneumonia. Yearbook AcadAppl Dsteopathy. 1 96 5 ; 1 : 1 36- 1 38. 60. Medaris CEo Th e osteopathic treatment for lobar pneumonia. Yearbook Acad Appl Dsteopathy. 1 947: 1 24- 1 30. 6 1 . Facto LL. The osteopathic treatment fo t lobar pneumonia. jADA. 1 947;46:385-392.

62. Burns L. Osteopathic pathology of the lungs. jADA. 1 933;32:474-478. 63. Grainger HG. Lobar pneumonia and the segmental plane. jADA. 1 95 1 ;50:25 5-263. 64. Frymann VM. The osteopathic approach to cardiac and pulmonary problems. jADA. 1 978;77:668-673.

65. D'AJonw AF, Evans DJ . Disorders of the respiratory system. In: Hoag J M , ed. Dsteopathic Medicine. New York, NY: McGraw-Hill; 1 969: 465. 66. Heilig D. Iffustrative Points in Technique. New York, NY: McGraw-Hill; 1 969: 1 97-203. 67. Kurschner OM. A comparative clinical investigation of chlorampheni col and osteopathic manipulative therapy of whooping cough. jADA.

1 9 5 8; 5 7 : 5 59-56 1 .

73. Forbes HW Bronchial asthma. jADA. 1 902; 1 : 1 06- 1 09. 74. Coffman KW Asthma. jADA. 1 902; 1 : 1 88- 1 90.

75. Burns L. Clinic reports fro m the Pacific College of Osteopathy. jA DA. 1 9 1 2 ; 1 1 : 1 0 54- 1 056.

76. Wilson PT. Experimental work i n asthma at the Peter Bent Brigham Hospital. jA DA. 1 92 5 ; 2 5 : 2 1 2-2 1 4 .

7 7 . Wilson P T. Specific technic for asthma. jA DA. 1 926;25 :473. 78. Wilson PT. The osteopathic treatment of asthma. jA DA. 1 9 59;45:49 1 492.

79. Kline JA. An examination of the osteopathic management of bronchial asthma. Yearbook Acad Appl Dsteopathy. J 9 5 9 : J 27- 1 3 J

•

80. Fitzgerald M, Stiles E G . Osteopathic hospitals' solution to DRGs may be OMT. The DO. 1 98 4 ; 2 5 : 97- 1 0 1 .

8 1 . Belcastro MR, Backes CR, Chila AG. Bronchiolitis: a pilot study o f os teopathic and manipulative treatment, btonchodilators, and other ther apy. jADA. 1 984;83:672-676.

82. Howell RK, Allen TW, Kappler RE. The inAuence ofosteopathic manip ulative therapy in the management of patients with chronic obstructive l u ng disease. jADA. 1 97 5 ; 74 : 757-760.

83. Miller WD. Treatment of Visceral Disorders by Manipulative Therapy. The Research Status ofSpinal Manipulative Therapy. Bethesda, M D : U S Department o f Health, Education, an d Welfare; 1 97 5 : 295-30 1 .

84. Howell RK, Kappler RE . The inAuence o f osteopathic manipulative therapy on a patient with advanced cardiopulmonary disease. jA DA.

1 973;73:322-327. 85. Hoag J M . Project in the study of chronic obstructive l u ng disease. jA DA. 1 970;69: 1 03 1 - 1 033. 86. Mall R. An evaluation of routine pulmo nary function tests as indicators of responsiveness of a patient with chronic Obstructive l u ng d isease to osteopathic health care. jA DA. 1 973;73: 327-333.

87. Hoag J M . Musculoskeletal involvement in chronic lung disease. jA DA. 1 972;7 1 :698-706. 88. Bailey WP Evaluation of rib raising technique in respiratory distress syndrome. jA DA. 1 963;62:924-928.

89. Still GA. Advantages and necessity of osteopathic post-operative treat ment. jADA. 1 9 1 9; 1 8:48 1 -486.

90. Dickey J L. Postoperative osteopathic manipulative management of me dian sternotomy patients. jADA. 1 989; 89: 1 309- 1 322.

9 1 . Henshaw RE. Manipulation and postoperative pulmonary complica tions. The DO. 1 963(Sep) : 1 32- 1 33.

92. Sleszynski SL, Kelso AF. Comparison of thoracic manipulation with in

68. Purse FM. Manipulative therapy of upper respiratory infections in chil

centive spirometry in the prevention o f post-operative atelectasis. jA DA .

69. Schmidt I C Osteopathic manipulative therapy as a primary factor in

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the management of upper, middle, and pararespiratory infections . jADA.

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1 993;93:834-845.

OSTEOPATHIC PHYSIC AL MEDICINE AND REHABILITATION J. MICHAEL WIETING JAMES A. LIPTON

KEY CONCEPTS • • • • • •

Definition of the specialty of Physical Medicine and Rehabilitation (PM&R) History of osteopathic PM&R Patient evaluation by the osteopathic PM&R specialist Use of osteopathic manipulation by PM&R physicians Research concepts and status Illustrative cases in osteopathic PM&R practice

DEFINITION OF THE SPECIALTY OF PHYSICAL MEDICINE AND REHABILITATION

Physical methods of healing have been practiced since prehis toric time; however. the specialty of physical medicine and re habilitation (otherwise known as physiatry) did not become a recognized medical specialty until 1947. Most widely known as physical medicine and rehabilitation. this specialty is also known as rehabilitation medicine. physical and rehabilitation medicine. and as physiatry. The specialty today comprises the disciplines of physical medicine. rehabilitation medicine. and e1ectrodiagnostic medicine. Osteopathic physicians (DO) and allopathic physicians (MO) who specialize in physical medicine and rehabilitation (colloqui ally known as "PM&R") are called physiatrists. Physiatrists are specialists in the diagnosis and treatment of patients of all ages in three major subspecialty realms: 1.

11.

Physical medicine: diagnosis and treatment of musculoskele tal injuries and pain syndromes. including acute and chronic musculoskeletal diseases. sports and occupational injuries. and degenerative diseases including low back pain. Rehabilitation medicine: comprehensive rehabilitation of neurologic and musculoskeletal conditions. such as stroke. brain injury. spinal cord injury. amputations. burns. sports injuries. and others. The physiatrist often practices rehabili tation medicine while directing a team of medical rehabil-

111.

itation professionals including. but not limited to. physi cal and occupational therapists. rehabilitation nurses. reha bilitation psychologists. speech-language pathologists. social workers/discharge planners. recreation therapists. vocational rehabilitation counselors. case managers. and others. Electrodiagnostic medicine: physical medicine and rehabil itation is the only specialty in medicine in which training in electrodiagnosis (nerve conduction studies. electromyog raphy. and evoked potentials) is required.

Physiatrists are physicians who use physical agents and other medical therapeutic methods to assist in the healing and reha bilitation of patients. Treatment involves the entire person and addresses the physical. social. psychological. and emotional needs of the patient to achieve optimal restoration of quality of life so that potential for recovery is reached. Osteopathic physiatrists incorporate fundamental concepts of the body as a unit. the body's capability of self-healing/health maintenance. the inter relationship of structure and function. and the basis of treatment on understanding of body unity. self-regulation. and structure function interdependence. Additionally. osteopathic physiatrists incorporate the use of osteopathic manipulative medicine (in cluding structural diagnosis and osteopathic manipulative treat ment) in their approach to treating patients. After graduation from medical school, a minimum of 4 years of postdoctoral graduate medical education is needed for train ing as a specialist in physical medicine and rehabilitation. One year of this training. the internship. is devoted to the develop ment of fundamental clinical skills; this year includes experi ences in family practice. internal medicine. pediatrics. and gen eral surgery or other critical care medicine. The remainder of the year may include any combination of a multitude of specialty experiences. including. but not limited to. neurology. orrhope dic surgery. psychiatry. radiology. rheumatology. sports medicine. urology. or subspecialties of internal medicine (such as cardio logy. pulmonology. nephrology. or oncology). On completion of the internship. an additional 3 years of residency training are needed in PM&R. which includes training regarding electrodiag nostic medicine. and the diagnosis. etiology. treatment. preven tion. and rehabilitation of neuromusculoskeletal. cardiovascular, pulmonary. and other system disorders in patients of all ages.

35. Osteopathic Physical Medicine and Rehabilitation

Board certification may be awarded to physicians who complete a comprehensive written examination at the end of (or after com pleting) residency training and a rigorous oral examination after at least 1 year of full-time clinical practice, fellowship training, or an acceptable combination of these experiences.

HISTORY OF PHYSICAL MEDICINE AND REHABILITATION

[t is well established that the use of manual procedures and ma nipulation'dates back several centuries. Evidence exists to place the use of manipulation and manual procedures in Thailand over 4,000 years ago. The use of the hands to treat injuries and dis eases was practiced by the ancient Egyptians, and the writings of Galen, Oribasius, and Celisies refer to manual procedures in med ical practice. The 18th and 19th centuries saw renewed interest in the use of manual procedures. Dr. Edward Harrison, a 1794 graduate of the University of Edinburgh, developed a reputa tion in London for using manual procedures. Bonesetters became popular in England and the United States in the 19th century. Skilled bonesetting practitioners, such as Hutton, led the renowned Drs. James Paget and Wharton Hood to report in The Lancet and the British Medical journal that medicine of the day should pay attention to the successes of contemporary bone setting practitioners. The disenchantment of A. T. Still with the medical practice of his day led to the formulation of his new medical philosophy, which was called osteopathic medicine (1). Physical medicine also dates back to ancient times. Hip pocrates used rraction and leverage to treat spinal deformities. He liotherapy and hydrotherapy were recognized and used in Roman times. There was a void in the reported use of manual procedures that seems to correspond to the time of the split between physi cians and barber surgeons. The role of manual techniques in patient care declined as physicians became less involved in pa tient contact and hands-on care was allocated to barber surgeons. This was also at the time of the bubonic plague, and it is possible that physicians were reluctant to have close personal contact with patients. In the late 18th and early 19th centuries, applications of gal vanic and faradic currents were prescribed as valuable therapeu tic procedures for a variety of diseases and conditions. Around 1890, high-frequency currents from spark-gap diathermy ma chines were introduced to medical practice by d'Arsonval in France. In the early 1900s, the profession of physical therapy was developing along with new increased interest on the part of allopathic physicians who began to see the value of the approach to patient care that had been promulgated by the osteopathic pro fession for over a quarter of a century by then. The early 1900s was also a time of increased empirical trials, which provided evidence that physical medicine and manipulation were effective methods of intervention in musculoskeletal and other disease and injuries. The osteopathic profession was the source of many of these ef forts, including the pioneering work of Dr. Louisa Burns and others. Osteopathic physicians, for example, were noted to ap ply the principles of hyperemia (stimulating blood flow to the spinal cord) in the treatment of infantile paralysis (2). During World War I, diathermy, electrical stimulation, heat, massage, and

517

exercise were increasingly used as therapeutic tools in the U.S. (3). The early 20th century also saw proponents of electromagnetic therapy for musculoskeletal conditions. Allopathic physicians of that time began to join osteopathic physicians in the practice of "physiotherapy," using techniques gleaned from literature and from demonstrations in the U.S. and Europe. Col. Harry Mock of the U.S. Army medical corps referred to the importance of the use of physical and occupational therapies in the rehabili tation of wounded and other disabled persons in World War I (4). This was echoed after World War I I by Dr. John Coulter, also of the Army medical corps (5). After World War 1, empirical trials provided evidence that physical methods were useful to aug ment traditional medical care (6). Additionally, physicians were pioneering new medical applications of radiographs and other therapeutic methods. I nvestigations were initiated regarding the effectiveness of using functional activities to provide exercise and retrain coordination. In the early 1920s, medical organizations, such as the Amer ican Medical Association Council on Physical Therapy and the American Society of Physical Therapy Physicians, were formed (6). These organizations (whose names were later changed nu merous times) included physicians who practiced in the areas of physical medicine, physical therapy, radiology, and rehabil itation. The major organizations for physicians in the field of physical medicine and rehabilitation today include the American Osteopathic College of Physical Medicine and Rehabilitation, the American Academy of Physical Medicine and Rehabilitation, the Association of Academic Physiatrists, the International Soci ety of Physical and Rehabilitation Medicine, and the American Congress of Rehabilitation Medicine. These organizations col lectively represent approximately 75 years of development of the field of physical medicine and rehabilitation. Additionally, two major American medical journals have been developed to pub1ish research in the specialty, the Archives ofPhysicaL Medicine and Rehabilitation and the American journal ofPhysical Medicine and Rehabilitation. Journals are also published in Europe, the Middle E ast, and Asia. Formal education for allopathic specialists in physical medi cine and rehabilitation began in 1926 with short courses, 3 to 6 months in duration, in physical medicine at Northwestern University Medical School; these were later extended to 1 year. Before those courses, training in physical medicine was ac complished by preceptorships with experienced practitioners. Formalized training programs for physicians subsequently began to develop, initially under the auspices of the American Registry of Physical Therapists. In 1936, Dr. Frank Krusen established the first 3-year physical medicine residency program at the Mayo Clinic (6). Dr. Krusen, who coined the word "physiatry" to de scribe physicians who were dedicated to adding physical medicine to traditional medical therapeutics to treat neuromusculoskeletal disorders, is considered the " Father of physical medicine" (6). After World War II, with the advent of antibiotics and the ad dition of new medical technology, the awareness of American society of the need for more advanced treatment and rehabili tation care for disabled persons became heightened due to large numbers of soldiers returning from war with injuries and dis abilities that had previously proved fatal. Additionally, the po liomyelitis epidemic received extensive publicity in the media of

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VI Osteopathic Considerations in the Clinical Specialties

the day. These events created an increased demand for physi cians who were trained in comprehensive medical and physical rehabi I i tation. An interesting parallel event added to the demand for the specialty of physical medicine and rehabilitation. After World War II, Dr. Howard Rusk, a traditionally trained internist and military physician, noted that inactive, non-physically involved rehabilitation in convalescence resulted in functional deteriora tion in soldiers who were recovering from trauma or disease. As a result, the military had unprecedented numbers of soldiers who were not allowed to return to active duty. Dr. Rusk carried out a controlled experiment that demonstrated a dramatically im proved return of strength, endurance, and overall function with an aggressive, patient-centered approach to rehabilitation. Sub sequent to his military career, Dr. Rusk began private medical practice and made initial efforts to train physicians in the spe cialty of physical medicine and rehabilitation. As the specialty of physiatry grew, the need for ongoing re search and training programs became evident. Bernard Baruch, a noted philanthropist, chaired a committee that awarded grants to hospitals and medical schools to establish physical medicine and rehabilitation teaching and research programs. By the mid-1940s, numerous postdoctoral training programs in physical medicine and rehabilitation were established through this funding. In January of 1947, the advisory board of medical specialties (the precursor of the current American Board of Medical Specialists) formally recognized the American Board of Physical Medicine as a credentialing organization (6). In 1949, the name was changed to include rehabilitation to recognize that phase of the specialty. Early after the specialty was organized under one governing body, electrodiagnosis was introduced to the field for the purpose of evaluating neuromusculoskeletal pathology. It became evident that elecuodiagnosis allowed physicians to more efficiently eval uate, from a qualitative, as well as a quantitative standpoint, pathology of the neuromusculoskeletal system. After the 1950s, the specialty of physical medicine and re habilitation grew rapidly. I ncreased research showed throughout the latter part of the 20th century that comprehensive rehabili tation decreased dependency and increased functional indepen dence and quality of life for disabled persons. This created new demand for physiatrists and pointed to a need for additional training programs. Physical medicine and rehabilitation became a "shortage specialty" and remains so at this time. The specialty grew at unprecedented rates in the 1980s and the 1990s, and has continued to grow; however, as with other numerous other med ical specialties, an inconsistent distribution of physiatrists from a geographic standpoint has developed. Today, the specialty of physical medicine and rehabilitation is a vibrant, thriving, ex citing group of physicians who practice physiatric medicine in a variety of settings with a wide scope ofinterests and p ractice styles. There are currently over 80 accredited residency programs gradu ating over 300 physicians annually. The sole osteopathic program is at Michigan State University College of Osteopathic Medicine (and is dually/allopathically accredited as well). It is anticipated that the future will see additional osteopathically accredited res idency programs in physical medicine and rehabilitation. The 21st century brings many new challenges to physical medicine and rehabilitation. Much research is ongoing and many

medical advances are anticipated. With these advances come new issues that bring technology to bear on medical ethics and the appropriate use of technology. In the osteopathic profession, the specialty of rehabilitation medicine began in the late 1940s in response to osteopathic physi cians who were interested in structural diagnosis and manipula tion and the rehabilitation process. It became evident that an additional level of care was needed, and the osteopathic profes sion developed the practice affiliate, the American Osteopathic College of Rehabilitation Medicine, in 1954. The American Os teopathic Association added physiatry as a specialty in 1954. The prevailing attitude within the osteopathic profession at chat time was that specifying "physical medicine" was a redundancy, as os teopathic training at that point emphasized physical medicine oriented treatment, as opposed to allopathic medical schools, which neglected it. Thus, the osteopathic profession elected to designate the specialty as rehabilitation medicine. (This organiza tion was renamed the American Osteopathic College of Physical Medicine and Rehabilitation in 200 l .) The American Osteo pathic Board of Rehabilitation Medicine (also recently renamed the American Osteopathic Board of Physical Medicine and Reha bilitation) was organized in 1954 to provide a credentialing mech anism for osteopathic physicians in the specialty of physiatry. The specialty of physical medicine and rehabilitation is very compatible with the basic tenets of osteopathic medicine, which place emphasis on the concept based on the linkage of the science and art of medicine. Osteopathic physiatrists naturally embrace the concept of the body as a unit of the person-the body, mind, and spirit, the body's capability of self-regulation, healing, and health maintenance, the inter-relationship of structure and func tion, and the basis of treatment on these concepts. An essential activity of the physiatrist is to establish lines of communication among members of the comprehensive rehabil itation team, which includes the patient, family and significant others, employer, and third-party payers, as applicable. Physia rrists evaluate disability using the concept of structure/function relationship, as patients must be actively involved in their own rehabilitation program.

PATIENT EVALUATION BY THE OSTEOPATHIC PHYSIATRIST

The osteopathic physiatrist practices from the perspective of the osteopathic philosophy of health enhancement and preventive health care with the belief that structure and function are inte grated in healthy and diseased states. The osteopathic physiatrist makes use of the physical and biologic sciences related to health maintenance and disease prevention, and typically looks beyond the patient's presenting complaint in specific diagnosis and treat ment. Biologic, psychological, behavioral, sociocultural, occupa tional, and environmental factors related to the patient's life are explored (7). These factors may have significant effect on the pa tient's illness and disability and may preclude maximal physical and psychological recovery. This broad-based approach to treat ment addresses the body as an entire unit and from a functional point of view. As osteopathic physicians use manipulative proce dures in the context of total patient care along with other accepted


modaliries, a sysremaric approach ro medical problems has devel oped, which is properly designared as "manual medicine" (7). The physiarric hisrory and physical examinarion is rhe basis for all subsequent therapeutic decisions. The osteoparhic physia rrist may encounrer patients through referral from primary care, via secondary or rerriary specialists, or, as in many military and civilian sertings, direcrly via an inirial patienr-physician contacr. The parienr's needs are variable-a simple, new diagnosis, a re habilirarion program for a well-esrablished diagnosis, or perhaps an addirional srructural evaluation. Although any physiarrist can prescribe medicarions, modaliries, or orher rherapies, rhe osreo parhic physiatrist can provide a disrinctive evaluarion rhar is well grounded in manual medicine. There are some diagnoses that are parricularly amenable ro such care. A good example would be the common condirion of inrerscapular rib resrriction. Although anriinflammarory medications can be used, experrly applied os teopathic manipulative medicine can immediarely and safely ad dress rhe roor cause of rhe pain in a cosr-effecrive manner. In ad dirion ro rhe convenrional hisrory and physical examinarion, rhe physiarric evaluarion is somewhat differenr. The physiarric evalu arion is based on a convenrional hisrory and physical examinarion; however, [he physiarrisr railors rhe procedures of rhe convenrional process ro furrher clarify rhe functional problems of the patienr. The physiarrist emphasizes functional capacity in the home and community throughout the evaluation. The osteopathic physia rrist derermines nor only physical deficits but also the functional impacr of rhose deficits, because identification of functional prob lems allows determination of funcrional goals rhat become rhe basis for developing a therapeutic managemenr strategy. Evaluarion by the osteoparhic physiarrisr idenrifies patienr im pairmenrs (losses or abnormality of psychological, physiologic, or anaromical srrucrure or funcrion), disability (a resrriction resulr ing from an impairmenr of the ability ro perform an activity in rhe manner rhar is considered "normal"), and handicap (disad vanrage resulring from rhe fulfillment of a socieral role rhar is considered "normal" for an individual). Though parients may have mulriple impairmenrs, rhese might not cause disabilities or handicaps unless rhey affecr rhe parient's ability ro funcrion in rhe home or community. The physiarric hisrory generally includes chief complaint, his rory of presenr funcrional problem, and funcrional hisrory. The funcrional hisrory typically will include assessmenr of mobility activities, acrivities of daily living (dressing, barhing, and hy giene acriviries), household and community acriviries, assessmenr of cognirion, communicarion, vocational and avocarional srarus, and rhe need for assistive devices. Psychosocial hisrory will usu ally include assessment for subsrance abuse, psychiatric, or sexual hisrory, and an evaluation of rhe parienr's currenr living situarion, vocarional, and financial status. Medicarions, allergies, dier, pasr medical and surgical hisrory, family hisrory, and review of systems will also be included. In addirion ro rhe rradirional examination, physiatric physical examinarion will focus on assessing funcrion in rhe areas of mobility, acriviries of daily living, household acriv iries, and driving. The examinarion will be focused on the neu romusculoskeleral system using inspecrion, palpation, evaluarion of range of motion and conrractLIres, assessmenr ofjoinr stability, and manual muscle resring. Neurologic examination will evaluate the parient's overall cognirive srarus (including level of conscious-

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ness, menral status, and communication) and will also include as sessmenr of sensation, cerebellar function, cranial nerves, muscle srretch reflexes, manual muscle tesring, and speech and language function. The osteopathic physiatrist is rrained ro make unswerv ing use of a comprehensive hisrory, physical examinarion, and diagnostic evaluarion for even the most rourine-sounding com plainr. As an example, assessmenr of how the forces of gravity and impaired coping skills can affecr a patienr's overall funcrion may need ro be considered in developing a risk-benefir ratio associated wirh a proposed treatmenr regimen. A parient wirh low back pain may nor achieve symprom relief unless both somaric dysfunction and concomitanr gair dysfuncrion are addressed; if rhe patient also smokes as a reaction ro stress, this may affect the number, types, and locations of other somatic dysfunctions (as in the rib cage) thar can interfere with the primary complaint of interesr. After collection of data and physical examination, the osteopathic physiatrist will formulate a problem-oriented summary that iden tifies the patient's major problems, which will include perti nent impairmenrs, functional deficits, and medical and surgical issues. From this, the osteopathic physiatrist formulates a problem list wirh recommendations regarding rehabilitation issues along wirh a subsequent management plan noting rrearment options for rehabiliration, as well as medical and surgical problems. The physiatric management plan is typically inrerdisciplinary and ad dresses functional deficits, physical impairmenrs, psychosocial, medical, and surgical issues. Therapeutic precautions and appro priare treatmenr settings are also identified. Treatmenr goals are determined based on a realistic appraisal of rehabilitation and medical status and what is attainable after completion of rhe pro posed treatment plan. Potential obstacles ro achieving functional goals and rhe estimated time ro achieve goals are also determined.

THE USE OF MANIPULATION IN PHYSIATRIC P RACTICE

The physiatrist is usually able ro identify, through focused mus culoskeletal examination, patients who are most likely ro bene fit from manipulative care. Although some manipulation tech niques have applicability ro hospitalized patienrs, most patienrs in physiarric pracrice who are appropriare for manipulation are en counrered in the outpatienr setting. This constituency includes patients with structLIral problems, such as vertebral rotations, pelvic asymmetry, sacral rorsion, or other enrities in which diag nosis relies on palparory skills. After performing a general physiatric examination, the osteo pathic physiatrist will idenrify and treat any underlying pathology, including fractures, herniated discs, sprains, srrains, hemaromas, joinr injuries, and peripheral and central neurologic injuries. Ad ditional diagnostic stLIdies will be employed as necessary. The physiarrisr contemplating manipulative intervention performs a focused detailed hisrory and structLIral examination in the area suggested by the symproms or by rhe general examination. This typically involves observation, active gross and fine motion assess menr, and general palparory/motion examination. The srructutal and functional evaluation should begin from the moment the physician's senses contact the patienr. Listening ro and observing ambulation patterns, measuring symmerry of paired srructures

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(such as malleoli, anterior and posterior superior iliac spines, in ferior lateral sacral angles, and sacral-sulci), and observing trans fers, dressing, and so on, may provide indispensable insights into the cause and treatment of multifaceted clinical presentations. Success of manipulative therapy in physiatric practice, as in other specialties, often depends on accurate palpatory diagnosis. Palpa tory and segmental autonomic changes may be significant com ponents of structural diagnosis. Bony structure asymmetry, restrictive vertebral motion rela tive to adjacent vertebrae in Aexion, extension, side bending and rotation, tissue texture changes, local tolerance to palpation or induced motion, and tenderness elicited over vertebral processes or by induced motion are generally included in evaluation of ver tebral or segmental levels. Evaluation of passive motion for range, symmetry and amount of force needed to achieve full range is as sessed in terms of quality or "end-feel" motion (1). Evaluation of combinations of vertebral motions are also included. The osteopathic physiatrist will often "spring" vertebrae and examine for areas of tenderness or local pressure on interspinous ligaments; these techniques are useful in determining muscu loskeletal function and loss of joint mobility (8). Subcutaneous tissue texture changes, such as edema or fibrosis, may also be noted on palpation and may indicate musculoskeletal pathology with associated segmental autonomic changes (8). Examination of the ribs, occiput, and pelvis in the structural examination is often included. The osteopathic physiatrist may determine that hypermobile musculoskeletal segments may not be amenable to manipulative intervention, but may indicate the presence of hy po mobile segments in other locations and, if nontender, may be amenable to manipulation to resolve distant hypermobility (1). Thorough structural examinations, as noted, may add 5 to 10 minutes to an initial visit and less than 5 minutes to sub sequent examinations. The osteopathic physiatrist choosing ma nipulation is advised that they should possess a relatively high de gree of basic palpatory skills so that referral to another physician or a non physician manipulative practitioner can include specific identification of structural dysfunction. In addition, palpatory ex amination allows the osteopathic physiatrist to determine areas needing manipulative treatment and to establish a potential end point of manual care. The osteopathic physiatrist who possesses expertise in manipulative care has the ability to provide the pa tient (or referral source) a "one stop shop," at which a compre hensive evaluation, diagnosis, and nonsurgical treatment regimen can be provided. Osteopathic physiatrists who use manipulation have a variety of approaches available to them for manual treat ment. Their individual armamentarium of treatment techniques depends on their training, their study with mentors, and the in tegration of and comfort level with particular techniques. Choice of technique may also depend on the patient being served. Many different treatment approaches are available; the interested reader is referred to numerous selected references for further inquiry in this particular area. The availability of manipulative care depends significantly on geographic location and regional practice patterns. Osteopathic physiatrists who wish to use manipulation but do not provide it themselves generally refer patients to either a physician or licensed non physician provider. Referral to another physician practitioner generally works well, but potential problems exist, especially re garding referral of that patient. This issue can be satisfactorily

addressed through a specific referral that states the exact nature and scope of evaluation and treatment requested, encouragement of discussion with the referring physician, and a statement thar makes clear the intent of rhe physiatrisr to resume rhe remain der of the patient's care. When referring to another physician (physiatrist or otherwise) for manual care, consideration should be given to how to recognize appropriare skill and training. Pos sible avenues to obtain skill in manipularion include certificarion by an osteopathic specialty board (which requires evaluation of capability in osteopathic principles and practice), attendance ar postdoctoral courses offered by numerous osteoparhic and allo pathic sponsors, and certification of ptoficiency for comperence in a particular manipulative approach (such as cranial osreopa thy). The American Osteopathic Board of Neuromusculoskeleral Medicine (NMM) provides full board certificarion in osreoparhic manipulative medicine and the American Academy of Osteopa rhy confers Fellowship on physicians certified in NMM who have undergone further tesring in manipularive medicine and who have contributed in a significant way to rhe body of knowledge related to manipularion. If referral is to a licensed non physician practirioner, the problem to be rreated must firsr be accurately diagnosed and a specific prescription musr be written for manip ulative care. Manipulative care can also be provided as part of a comprehensive therapy program; however, the physician should write a detailed prescriprion for rhe specific area to be treared and idenrifY the diminished motion to be restored, as well as frequency and length of trearment. This enables rhe physician to monitor parient progress objectively and determine the end point and benefit of manipularive treatment. Three main obstacles have been identified for physiatrists interested in performing manipularion: skill acquisirion, skill maintenance, and economic considerarions. Manipularive techniques are best learned on colleagues and fellow learners under close supervision. Studies suggesr rhat rhe minimum learning time required may vary from 3 to 12 months depending on the modality (9,10). This extended period has significant ramifications for the practitioner. Because of enhanced safety and small potential for harm, sufficient skill can be acquired by most practitioners in 1 to 2 weeks of formal training in each of rhe types of manipulation, including isometric/muscle energy, countersrrain, myofascial release, and articulatory techniques. Training rime for these approaches is shorter because inap propriare or nonindicared indirect rechnique, unless repeated frequently or over a prolonged period of rime, rarely causes detrimental effects. These rime frames are predicared on the osteoparhic physiatrisr having achieved basic skill proficiency in manipulative care during rheir inirial medical training.

RESEARCH REGARDING MANIPULATION IN PHYSIATRIC PRACTICE

In recent years, scientific evidence for the efficacy of manipularion has been mounting in the treatment of numerous clinical enr ities that are commonly addressed by physician specialists in physi cal medicine and rehabilitation. Most inquiry has been aimed at acute musculoskeletal conditions and pain syndromes (11). The process has been somewhat slower in the area of chronic pain; however, objective evidence is becoming more apparent. The


efficacy of manipulation for low back pain, for example, has been addressed in many previous studies and reviews. Manipulation was one of the recommended treatments for acute low back pain in the 1994 Agency for Health Care Policy and Research (now the Agency for Health Care Research and Quality) guidelines. Koes et al. (12) reported a randomized, prospective clinical trial of manipulative therapy for persistent, nonspecific back and neck pain. In this study, one group of patients with nonspecific back and neck pain complaints of at least 6 weeks duration received chiropractic spinal manipulative therapy and a second group re ceived only exercise. Improvement in pain complaint was greater in the group receiving manipulative therapy than the other group after 12 months of follow-up. Vernon et a1. (13) reported that manipulation was able to increase local paraspinal pain threshold levels in patients with chronic mechanical neck pain syndromes. Hurwitz (14) did an extensive review of randomized clinical trials of manipulation for persons with neck pain and headaches. Many high-quality studies demonstrated at least short-term benefits of manipulation. Gross and Fiechrner (15,16) demonstrated that the effectiveness of manipulation is enhanced when used with other concurrent treatment approaches, such as exercise and er gonometric adjustments. Winters showed that manipulation was very efficacious in treating shoulder disorders based on complaint, duration, and rate of treatment success (17). Few studies have been reported that evaluate the efficacy of manipulation of sports injuries in controlled interventional trials. Cibulka and Delitto (18) have reported a statistically significant difference berween hip mobilization versus sacroiliac manipula tion in 20 runners with hip pain and sacroiliac dysfunction. Sev eral studies have attempted to clarify the relationship between lower extremity function, lumbopelvic mobility, and sacroiliac and low back pain. Although these studies are primarily descrip tive, they do have clinical relevance. Muscle imbalances, with re sultant pain and dysfunction, have been described by Janda (19) and others (20). The collaborative efforts of Greenman, Janda, and Bookhout have provided a working clinical paradigm that, when used diagnostically and as a basis for exercise prescription, enhances manual medicine treatment (1). The exact physiologic reasons for the efficacy of manual treatments are not often well understood. There are theoretical constructs that address, among other things, a bony alignment, muscle link, muscle and spindle tone, neurologic and nociceptive input, central nervous system processing, psychological factors, and others (21). The actual act of human touch undoubtedly contributes to the patient's expe rience (21). This is a complicated issue that incorporates many aspects of the human experience, including pain, function, phi losophy, psychology, and social milieu (21). It is hypothesized that if these issues are more rigorously researched, it is likely that the efficacy of manual therapy (as is true in many other aspects of medicine) will be multifactorial in nature. In the area of chronic pain, Greenman and associates (1) found that manipulation can be quite effective in not only relieving acute musculoskeletal pain caused by manipulable somatic dysfunction, but also may occasionally help in reducing reported pain levels in the chronic pain population (7). Manual medicine has recently been shown to be useful for chronic neck and low back pain (22,23). The most valuable purpose of manipulation in the chronic pain population is to assist in increasing physical activity to productive levels. These researchers

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have rwo hypotheses regarding the relationship berween chronic pain and somatic dysfunction: 1.

11.

The somatic dysfunction may have been a primary pain gen erator during the acute stage (which had not yet completely resolved), and this unresolved dysfunction had been an on going source of nociception responsible for causing changes in the central nervous system (functional pathology), which perpetuates pain perception. The somatic dysfunction may have continued or recurred as a pain responder and may have developed into a secondary pain generator. Had this dysfunc tion been treated in a timely fashion (during the acute phase), central changes may not have occurred and the chronic pain syndtome would not have developed. The somatic dysfunction may primarily be a response to an already altered central nervous system output (pain respon der) caused by a nonrelated source of nociception, such as degenerative disc disease.

Because of the vicious cycle that is established in both of these hypotheses, treatment could result in improved motion, but pain relief may not occur, or be short-lived, even if the somatic dysfunc tion can be corrected. Dependency on manipulation (as with any other passive modality) could quite easily occur because of tem porary pain relief. In their chtonic pain population, Greenman, Stanton, and Wieting found that maximal benefit was usually obtained with eight to ten sessions of manipulation over a 2 to 3 month period (7). The judicious, periodic use of manipulation to maintain achieved levels of musculoskeletal function is often necessary over longer periods of time. Exercises prescribed specif ically for persistent or recurrent somatic dysfunction have been found to be effective by Bourdillon et al. (24). These exercises can be easily learned and performed independently by the patient. Regular daily physical activity (e.g., work) has also been shown to be effective in maintaining restored musculoskeletal function. Numerous studies have shown that rest and sedentary activities are counter-productive. An additional benefit is obtained by body conract thtough the application of hands directly on the areas of complaint. Symp toms can often be reproduced during the palpatory structural examination. This evaluation facilitates trust in the physician by demonstrating arrenrion to those specific areas that have been perceived by the patient as being a causative factor of pain. This is consistent with the patient's expectations for evaluation and treatment. Further, the manipulative process by the astute physi atrist may, on occasion, facilitate an emotional response on the part of the patienr that is manifested by voluntary disclosure of personal information, and which allows the physician and patienr to gain insight into the stressors and suffering that often are a sig nificant part of a chronic pain syndrome. Healing is facilitated by creating an effective connection berween mind and body, thus rejecting the Cartesian theory of mind/body separation (7). It is felt that this connection must be augmented through a coopera tive effort berween the physician, the patient, and other members of the treatmenr team. The chronic pain patient is best served by assisting with restoration of normal physiologic movemenr patterns and with the development of health-promoting thought patterns and beliefs. The patienr regains physical and psycho logical "normalcy," and the cenrral nervous system "resets" and readapts to a more physiologic mode. To achieve desired total

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outcome, Functional restoration must also include social and vo cational integration within the Family and community. Physiatrists see a preponderance of individuals with "failed low back pain syndrome." The goal of rehabilitation is to achieve Functional restoration with return to Full activity, including work, on a long-term basis. Greenman (25) reported the incidence of sacroiliac dysFunction, for example, in a population of 183 such low back pain patients. An increase in the incidence of restricted motion in the sacroiliac joint and symphysis pubis was noted. These dysFunctions (lesions of skeletal, arthrodial, myofascial, or related structures) included pelvic obliquity and sacral base unleveling (short leg/pelvic rilt syndrome), pubic dysFunction, anterior nutational restriction of the sacrum, innominate sheer dysFunction, non neutral lumbar dysFunction, and muscle imbal ance of the lower extremities and trunk. Two or more of these aForementioned dysFunctions were found in 86.3% of patients, and only five patients had none (25). Diagnosis was made with a thorough history and physical, including palpatory structural examination. Indicated imaging and laboratory studies were also recommended to rule out other causes. The patient's usual pre sentation was with a history of low back pain, usually unilateral, overlying the sacroiliac region and radiating to the buttock and lower extremity, usually involving the posterior and posterior lateral thigh. Seven ty-five percent of patients were able to re turn to Full premorbid activity, including work For those who were employed, after completing a manual medicine and Func tional restoration rehabilitation program lasting approximarely 7.8 months (with the majority completing this program in less than 6 months) (2 5). It would seem that the vast majority of persons with chronic pain adapt, compensate, and continue to Function well without incapacitating distress. There are, however, many who, for what ever reason, have extreme distress, sufFer significantly, and are unable to maintain their usual roles within the family and com munity. A clear distinction should be made between the physical impairment, the suFFering, and the disability. It generally makes no diFFerence whether or not there is demonstrable evidence of injury (i.e. , verifiable anatomic change); the net efFect is the same. Those who become dysfunctional are dependent on their Fam ilies, the healrh care system, and the social welFare system (in cluding worker's compensation) in varying degrees. Successful treatment approaches must address this dependency. Psycholog ical variables have been shown to be related to both chronic pain and the transition From acute to chronic pain (26). Ten percent of chronic back pain individuals in the worker's compensation system, For example, aCCOUJ1( For 80% of the cost to that system (27). Much of the dependency seen in the chronic pain popu lation is iatrogenic with all specialties and treatment approaches implicated. Manipulation is no exception. Any treatment ap proach must help patients understand their situation, promote a healthy Functional belieF system, encourage physical activity, promote social and vocational reintegration, restore self-esteem and confidence, and teach strategies to allow patients to control their pain rather than the pain controlling them. The job of the osteopathic physiatrist in this case is to help patients conquer the chronic pain syndrome, not to blame them for it. The successFul outcome of any procedure depends on the expectation for it. The osteopathic physiatrist, in approaching

chronic pain patients, acts consistently as iF the persistent pain is caused by functional pathology within the central nervous sys tem, which cannot be objectively identified by currently available methods. Regardless of proven or suspected initial etiologic no ciceptive sources, the objective is to treat with the hope of pain relief but not to expect it. As Wall (28) eloquently stated, "Our task is not so much to cure pain as to aid recovery."

RETURN TO WORK/DUTY ISSUES

The cost-avoidance and potential savings experienced through a fiscally responsible evaluation and treatment program is of inter est to both allopathic and osteopathic physicians. The osteopathic physiatrist can, and oFten does, diagnose, treat, and resolve many simple and complex issues through eFFective use of osteopathic principles and manipulative care. This is particularly valuable in the instance of patients in military and critical nonmilitary Func tions. In these cases, the return to Full dury of a person with work restrictions results in significant recovery of lost productive time and cost savings. Maximal operational efficiency of military per sonnel m ay, in fact, be essential to national security. There are many specific diagnoses where osteopathic care (including ma nipulation) may offer the Fastest, safest, most specific treatment course possible. [n a nation faced with staggering losses of produc tivity and associated cost from musculoskeletal conditions, spe cific, efFective care using osteopathic principles oFFers an especially attractive option to improve health and work Force eFFectiveness.

ILLUSTRATIVE CASES OF OSTEOPATHIC PHYSIATRIC PATIENT CARE Low Back P a i n

Low back pain is second only to headache as a cause of pain in the industrialized world, and it is the leading cause of financial expenditure For worker's compensation (29). [n the U.S., the annual cost of low back pain is approximately 16 billion dollars per year (30). Studies have suggested that 25 million Americans have lost one or more days of work annually because of low back pain, and approximately 2% of workers each year submit disability claims attributed to low back pain (31). It is estimated that 50% to 80% of adults will have low back pain in their lifetime (32). A 1985 telephone survey of 1,254 Americans revealed that 56% of the adult population of the United States had some low back pain in the year preceding the survey, and that 3% of those had low back pain For more than 1 month (31). Studies have suggested a lifetime low back pain rate of about 60% to 90%, and an annual rate of about 5% (33,34). Low back pain is commonly addressed in physiatric practice. To evaluate low back pain, the osteopathic physiatrist must understand pertinent risk Factors (which include occupa tional, patient-related (such as age, gender, postural, mobility, strength and fitness considerations), and the anatomy and kine siology of the lumbosacral spine. The evaluation of the patient with [ow back pain begins with history but also includes physical examination (via inspection, palpation and percussion, and as sessment of range of motion) a neurologic evaluation (including


gait, station, coordination, muscle srretch reflexes, muscle bulk and srrength, and sensation), and appropriate diagnostic srudies (including, but not limited to, imaging srudies and electrodiag nosis) as appropriate. Structural and manual medicine evaluation should include motion testing (of the thoracolumbar region) with emphasis on forward and backward bending, side-bending, and rotation. [n trasegmental motion testing should be accomplished in positions of rotation, flexion, extension, and side-bending. Additionally, evaluation for scoliosis is also indicated. Both direct and indi rect manipulative techniques can be brought ro bear on low back pain. Muscle energy techniques can address both type I neutral (group) curves and type II somatic dysfunctions (involving sin gle segments). Counterstrain can be employed ro treat anterior tender points, (especially in the supine position) and posterior tender points (with the patiem prone). Common tender points include L l , L2, abdominal L2, L3, L4, and L5 anteriorly, and Ll and the posterior points of L l -5, L3-5 upper pole, and L5 lower pole. High velocityllow amplirude thrust can also be used effectively to treat somatic dysfunctions of the lumbar spine. An apparently healthy aviaror in his early 40s presented with a complaint oflumbar pain that prevented him from flying, pre sumably from the forces encountered during take off. None of his fellow aviators had complained of back pain, although they experienced the same schedule of flight operations. The patient was reluctant to complain of pain and would rather have de felTed seeking medical attention. He did his best ro downplay his pain, yet his seeking medical care was significant. The pa tient's medical hisrory was completely unremarkable except for awaking at night to note low back pain. Nonstructural physi cal examination was unremarkable until srructural components were examined. The patient was noted to have a physiologic short right leg, elevated right anterior superior iliac spine, and a right-on-right (forward) sacral torsion. Although diagnosis of gait dysfunction and sacral somatic dysfunction was considered and addressed, it is important to also consider other etiologies of this musculoskeletal presentation. Additional diagnostic studies were ordered, including complete blood count, erythrocyte sed imentation rate, blood chemistry, urine analysis, and plane films ofthe lumbosacral spine. The patient was noted to have markedly elevated urine protein. An orthosis and manipulation reduced the patient's back pain by two-thirds within 3 days and completely eliminated it within 1 week. On repeat testing, urine protein con tinued to be markedly elevated. After referral to a nephrologist, the patient eventually underwent renal biopsy confirming the additional diagnosis of focal glomerular nephrosis. The patient was subsequently placed under treatment with an angiotensin converring enzyme inhibitor and scheduled to receive appropriate physiatric and nephrologic follow-up. After additional care, the patient ceased to have nocturnal awakening, his back pain did not rerum, and he resumed normal flight status. [n addition to manipulative care, a comprehensive approach also includes rherapeutic exercise that is designed to establish and maintain musculoskeletal structural integrity. Evaluation oflum bar lordosis and the muscles that act to attain and maintain it is indicated. Strengthening of the upper and lower abdominal mus cles, stretching of low back and gluteal muscles, as well as pelvic tilt to decrease lumbar lordosis and exercise to increase lumbar

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flexibility are also appropriate. Stretching of back extensors and anterior pelvic muscles, as well as hip flexors and hamstrings is a part of manual care. Maximizing the patient's involvement in a therapeuric exercise program is needed ro optimize functional outcome.

Carpal Tu nnel Syndrome

Carpal tunnel syndrome is one of the most common forms of repetitive stress injury. It is a condition that can be caused by repetitive motion, often in the workplace or during leisure activ ities. This painful condition is caused by swelling of the flexor tendons of the hand. The flexor tendons, median nerve, and deep radial anery and vein pass from the forearm to the hand through the narrow carpal runnel, which is composed of bones and ligaments in the wrist. When these tendons and surround ing membranes swell, pressure is exerted on the median nerve, causing pain, numbness, or tingling. Repetitive srress injuries, such as carpal tunnel syndrome, are some of the fastest growing workplace injuries. Carpal tunnel syndrome is one of the leading causes of lost work days, with employees averaging 30 days away from work. Repetitive stress injuries often rop the list of lost time injuries and illnesses reponed by American employers. Treatment of carpal tunnel syndrome by the osteopathic physiatrist can be simple or complex depending on the severity and frequency of symproms. Treatments can include physical therapy, stretching, special braces or splints, ice, strengthening exercises, and antiin flammarory medications or steroid injections. Surgery is usually a last resort for patients who do not respond to conservative treat ment. Early diagnosis and treatment improves the chances for successful functional recovery. Sucher (35) demonstrated that physician-applied, three-phase soft tissue myofascial release, in combination with self-stretch of the carpal canal, is very effective in the rreatment of mild to moderately severe cases. This manipulative approach involves: I.

11.

111.

"Opening" the carpal canal with stretching and release of the transverse carpal ligament to increase space within the canal, thereby decreasing pressure on the median nerve. This procedure reverses the natural tendency toward flexion of the carpal canal and subsequent narrowing of the carpal space. Release of the true myofascial component of the carpal canal, the attachment of the abductor pollicis brevis muscle. Indirect srretch of the distal carpal canal with internal distention/dilation of the canal.

Through magnetic resonance imaging analysis of the cross sectional area of the carpal runnel and e1ectrodiagnostic study, this technique has been shown to produce clinical improvements in the form of reduced distal latencies and increased motor re sponse amplirudes (36). Additionally, the antero-posterior and rransverse dimensions of the carpal canal were shown to sig nificantly increase after this rreatment (36). Further studies by Sucher and Hinrichs (37) have shown that osteopathic manipu lative techniques show promise for nonsurgical relief of pressure on the median nerve in patients with carpal tunnel syndrome through lengthening the distal rransverse carpal ligament.

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vr. Osteopathic Considerations in the Clinical Specialties

Cervica l Sprai n/Stra i n

Perhaps the most commonly encountered cervical disorders in physiatric practice involve sprain and strain trauma to the cer vical spine. A sprain is a tearing or stretching of ligament or tendon structures due to joint trauma; a strain is a muscular in jury. The most Frequent cause of cervical sprain/strain in the U.S. is "whiplash," with greater than one million cases reported per year (38). The classical mechanism of injury involves cervical spine hyperextension as the result of a motor vehicle collision From the rear, or iF the patient is in a moving vehicle that strikes a nonmoving object. Although such injuries may involve liga ments, tendons, and muscles, the osteopathic physiatrist must also consider potential injury to the nerve roOt, cranial nerves, or associated joints (such as the temporomandibular joint). A diagnosis includes history of neck and headache pain and possibly associated stiffness and fatigue. Physical examination fre quently reveals dim inished range of motion of the neck, tender ness to palpation (both anteriorly and posteriorly), and facet joint tenderness. Special attention should also be given to structural ab normalities and somatic dysfunctions involving cervical and other areas of the spine, as well as assessment of areas of sympathetic hyperactivity. Treatment should be individualized for the patient and may include medications (such as nonsteroidal antiinflam matory drugs and other analgesics) for pain or sleep disturbance and physical therapy modalities (such as massage, ultrasound, electrical stimulation, and any therapeutic exercise program that focuses on appropriate neck muscle position and posture). Manipulative treatment should be used to decrease edema and acute tissue reaction. Generally, gentle indirect approaches using myofascial or facilitated positional release or counterstrain are most helpful in acute injury to the cervical and upper thoracic region. Passive range of motion exercises and lymphatic drainage can also be used. Subsequently, muscle energy and/or myofascial release can be used to restore respiratory motion in the cranium and sacrum and to restore motion in the pelvis and sacrum. Pa tients with more long-term symptoms may require manipulation of other areas of the body in addition to the cervical region. Begin ning with soft tissue techniques, the osteopathic physiatrist can then employ direct or indirect techniques along with a vigorous active range of motion program.

M a n i p u l ation in Sports Rehab i l itation Med i c i n e

The purpose of using manipulation in the practice of sports re habilitation medicine is to provide an adjunct in the treatment of many nonsurgical musculoskeletal mobility impairments result ing from injury or, occasionally, ro provide primary treatment to decrease pain and speed return to activity. The global objective is to restore normal pain-free motion with the highest level of motor control and coordination in a state of postural balance that allows the athlete to perform at the highest level of his or her ability. Manipulation is an appropriate adjunct to the rehabilitation of sports-related injuries. Timing, however, should be appropriate. li'eating an acutely inflamed area with direct techniques may ag gravate inflammation and increase pain. Indirect techniques (such as counterstrain and myofascial release) may help to decrease

inflammation. A manual medicine approach should be consid ered an integral part of comprehensive sports rehabilitation. In addition to the PRlCE (protection, rest, ice, compression, eleva tion) prococol, nonsteroidal and other antiinflammacory medi cations, muscle relaxants, analgesic medications, as well as physi cal and occupational therapy and physiatric-directed therapeutic exercise can also be employed. Because of the benefits of manipu lation and pain relief resulting from muscle relaxation, the use of medications can often be minimized. This is helpful co athletes in sanctioned sports, as well as recreational athletes, who avoid medication because of the side effects and disallowance of com petition. Many medications (including narcotics, analgesics, and some muscle relaxants) are banned by athletic organizations. As an example, the knee is the most frequently injured joint in sport activity (39). Diagnosis and management of knee in juries requires a detailed knowledge of functional knee anacomy, mechanism of injury, the pertinent Sport, and the most com mon sport-related knee injuries. Structural examination of the knee m ust certainly include evaluation of patellar tracking, tib ial head motion, assessment of any effusion, edema, pain, pop ping, locking, or "giveaway," as well as range of motion and leg length symmetry. Evaluation of a knee injury should also include assessment of the hip, ankles, feet, and lumbar spine, as well as the function of pertinent muscles in other structures of the knee joint. Patellofemoral dysfunction, iliotibial band syndrome, patellofemoral dislocation, tendonitis, and anterior cruciate lig ament trauma should also be evaluated. In an osteopathic manual medicine approach co knee injury, evaluation and treatment of acute fractures and other serious in juries is accomplished first, with soft tissue and other structural problems being treated secondarily. Knowledge of the pertinent sport, as well as its associated equipment, will give the osteopathic physiatrist insight inco the effect that these faccors may have on injury co the knee. Classically, shoe spikes, playing surface, and other faccors may affect the likelihood of injury. Manipulative treatment may be used co regain or maintain range of motion while the knee is healing and co correct or prevent con.tractures associated with the healing process. In the initial manipulative approach co rescoring motion of the knee and its associated com ponents, a passive indirect technique, such as myofascial release, counterstrain, and soft tissue, may be employed. These can be later followed with more direct approaches, such as muscle energy and high velocity/low amplitude thrust. As in previous examples, manipulative treatment should also have, as an adj unct, an appro priately directed therapeutic exercise program that will generally involve stretching and strengthening of knee flexors and exten sors, paying special attention to the medial quadriceps. Prokop and Wieting (40) describe stretching and articulacory technique approaches co increase joint play in patellar restriction. These techniques are often helpful for treating knee injuries co football players, runners, and athletes participating in other sportS. Many patient complaints co osteopathic physicians in all spe cialties are musculoskeletal in nature and may be ideally treated by physical rather than pharmacologic or surgical approaches. The osteopathic approach involves a comprehensive, patient centered system of health care with manipulation as a useful adjunct. Manipulation and manual medicine are natural compli ments co other methods of musculoskeletal care. Palpacory skills

525


are an essential aspecr of parient examinarion and evaluarion, and manipularion is very useful in improving range of morion and decreasing pain, rhereby increasing funcrional benefirs ro rhe parienr. Manual medicine, and more specifically manipularion, have benefired from rhe rehabilirarive conceprs offuncrional reac rivarion and rransirioning from parienr-passive ro parient-acrive care, as promulgared by Sranron and Mein (41). Alrhough rhe use of manipularion is nor inrended as an al1-inclusive rrearment approach, ir is a valuable sysrem of parient care when used in rhe conrexr of roral care inregrared wirh orher appropriare proce dures. Ir is our hope rhar rhis chaprer will srimulare rhe interesr of rhe reader in rhe valuable role of manual medicine and ma nipularive procedures in physiarric pracrice, and rhar rhe reader's apperire ro learn more abour manual medicine and rhe specialry of physical medicine and rehabilirarion will be srimulared.

1 6. Fiechmer J J , Brodeur RR. M a n ual and manipu larion tcchn i q ucs fo r rheumatic d isease. Rheum Dis Clin North Am. 2000;26( I ) :83-96. 1 7. Winters J C , Sobel J S , Groenier K H , et al. Comparison of physiother apy, manipulation, and corticosteroid injection for treating shoulder complaints in general practice: Randomized single blind study. BM). 1 997;3 1 4 : 1 320- 1 3 2 5 . 1 8. Cibulka M 0, Delirro A. A comparison of twO d i ffe rent mcthods t o !Tcat h i p pain in run ners. } Orthop Sports Phys Tim: 1 993; 1 7: 1 72. 1 9. J and a v. Muscle Fimction Tming. London, England: Buncrworrh Heineman; 1 983. 20. Geraci Me. Rehabilitation of pelvis, h ip, and thigh i n j u ries in Sports.

Phys Med Rehabil Clin N Am. 1 994 ; 5 : 1 57.

2 1 . Sch l i nger M , Andary M T . M assage and M a n ual Medicine. In: 0'

o n nor

FG , Wilder RJ� eds. Textbook 0/ Running Medicine. N ew York, N Y: McGraw-H il i ; 200 1 : 56 1 . 22. Rogers RG. The effects of spi nal manipulation on cervical ki nesthesia i n patients with chronic neck pain: A p i lot study. J Manipulative Pbysiol

Ther. 1 997;20:80-85. 23. Triano JJ , McG regor M , Hondras MA, et al. M ani pulative therapy versus education p rograms for chronic low back pain. Spine. 1 99 5 ;20:948953.

AC KN OWLEDGMENTS

24. Bourdillon J F, Day EA, Bookhout MR. Spin/If Manipulation, 5th ed.

The aurhors appreciare and acknowledge rhe assisrance of Debra Summers, Curarorial Assisrant ar rhe Srill Narional Osreoparhic Museum', and rhe Narional Cenrer for Osreoparhic Hisrory in Kirksville, Missouri, in researching rhe early hisrory of osreo parhic physical medicine.

2 5 . Greenman P E . Sacro i l iac Dysfunction i n thc Failed Low Back Pain Syn

Oxford, UK: Butterworth- Heincman; 1 99 2. drome. I n : Vleeming V, Mooney C, et ai, cds. Conference Proceed ings of the First I nterdiscipl i nary World Congress In Low Back Pain and I ts Relation to the Sacroiliac Joint. Netherlands: European Conference Organizers; 1 99 2. 26. L i nto n SJ. A review of the psychological r i s k factors i n back and neck pain. Spine. 2000 ; 25(9 ) : I 1 48- 1 1 56. 27. Battie M L, Bigos SJ . I nduStrial Back Pain Complai nts: A Broadcr Per

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1 984. 3 1 . Taylor H, Curran N M . TlJe Nuprin Pain Report. New York, NY: Louis Harris and Associates; 1 98 5 . 32. Biering-Sorensen F. A prospective study of low back p a i n in a general

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Hunt; 1 999: 1 1 2- 1 1 3 . 8. Rech tien JJ, Andary MT, Holmes TG, et al. Manipulation, Massage, and Traction. I n : Delisa J A, cd. ReiJabilitation Medicine: Principles and Prac

tice, 3rd cd. P h i ladelphia, PA: lippi ncorr-Raven Publ ishers; 1 998:523. 9. Lewin K. Manipulation Therapy in the Rehabilitfllion o/the Motor System. london, England: Bu rrerworrh- Heineman; 1 98 5 .

back trouble over a one year period. Spine. 1 984;9: I 06. 34. Frymoyer J W, Pope M H, Clements J H , et al. Risk factors in low back pain: An epidemiological su rvey. } BoneJoint Stlrg Am. 1 983;65 : 2 1 3. 3 5 . Sucher B M . Myofascial release of carpal t u n nel syndrome. J Am

Osteopflth Assoc. 1 993;93( I ) : 92- 1 0 I .

1 0. Maigne R. Diagnosis and Treatmem o/Pain o/Vertebral Origin. Baltimore,

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MD: Williams & Wilkins; 1 996. I I . U .S. Deparrment of Health and Human Services. Acute low Back Prob

Docu mentation with magnetic resonance imaging.} Am Osteopflth Assoc.

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U . S . Governmcnt Printing Office; 1 994. 1 2. Koes BW, Boutcr lM, Van Mamereu H, et al. Random ized clinical trial of manipulative therapy for persistent back and neck complailHs: Results of one year follow-up. 8M). 1 992;304:60 1 -605. 1 3. Vernon HT, Aker P, Burns S, et al. Pressu re pain t h reshold evaluation of the effect of spinal manipulation in the treatment of chronic neck pain: A pilot study. } Manipulative Physiol Ther. 1 990; 1 3( I ) : 1 3- 1 6.

1 993;93( 1 2): 1 273- 1 278. nel syndrome: Biomechan ical and osteopathic i n tervention to increase the length of the transverse carpal ligamcnt. J Am Osteopath Assoc. 1 998;98:( 1 2 ) : 679-686. 38. Evans RW. Some observations on whiplash i n j u ries. Neurol Clin. 1 992; I 0:975-997. 39. Mellion MB. Sports MedicirJe Secrets. Philadelphia, PA: Hen lcy and Belfus; 1 994.

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I 996:XV.

RHEUMATOLOGY J. MICHAEL FINLEY

KEY CONCEPTS • • • • • • • • • • • • •

Frequency, impact, and costs of rheumatic diseases Inflammatory arth ritides Osteoarthritis Soft tissue injury and fibromyalgia History Physical examination Specific rheumatologic examination Differential diagnosis Inflammatory arthritides Degenerative arthritis Nonarticular rheumatism Management Osteopathic Principles

Rheumarology is defined as the subspecialty of internal medicine that deals with the medical evaluation and rreatment of the musculoskeletal system. R heumatologists are specialists who de vote themselves to the diagnosis and management of the both r heumatic and non-rheumatic soft tissue and joint-related medi cal problems. Musculoskeletal complaints affect approximately 33% of the North American population, and are frequently cited as among the most common reasons for patient visits to physicians. The social and economic impact of these conditions is enormous. T he Arth ritis Foundation reports that there are more than 100 different forms of arthritic diseases (1). Clini cally, they account for more impairment and functional limita tion among middle-age and older adults than any other disease category (2). Prevalence is highest among older adults, but all age groups are affected. Impairment, disability, and job loss are frequent. In a North American study of patients over age 65, musculoskeletal symproms, including knee trouble, back trouble, and unspecified joint pain, were more common in this population than in any other group (3). Prevalence rates increase with age, and are rare under age 18 (4). Among those over age 65, arthritic diseases are among the leading causes of physician visits. Patient surveys document that a majority of individuals aged 75 and over report having arthritis (5).

Self-reported arthritis is more common in women than men. Among racial and ethnic groups, it is more prevalent in American Indians, and slightly more so in blacks. It is less prevalent in Hispanics than w hites. In general, arthritis is more likely to cause activity limitation in older persons, women, and nonwhites. In 1992, the last year available, rotal expenditures for musculoskeletal-related problems were $118.5 billion per year, excluding fractures and acute injuries. Costs continue ro increase due ro both population aging and better overall survival rates. In the 1960s and 1970s, overall COStS accounted for approximately 0.7% of the gross domestic product. By the late 1980s, they had increased ro 2.5%, and even more dur ing the 1990s. Work loss and rehabilitation costs add to indirect costs, accounting for anywhere from 50% ro 76.5% of all medical costs. Studies of costs incurred by patients with the most com mon rheumatic diseases, rheumaroid arthritis (RA), osteoarthritis (OA), and fibromyalgia (FM) have documented that these dis eases have much higher than expected direct medical costs when compared with patients of similar ages without arthritis. Not sur prisingly, those with the most severe and disabling diseases incur the highest costs (6). T his review of rheumarology is in no way exhaustive. Drawing from Bernard Rubin's material in the first edition of this text (7), this chapter highlights the integration of osteopathic principles with management of rheumatic and non rheumatic problems.

PATIENT EVALUATION AND PROBLEM-SOLVING (SEE CHAPTER 19) Because of their ability ro use palparory skills, osteopathic physi cians ate uniquely qualified ro evaluate patients presenting with musculoskeletal complaints. Along with empathetically sensitive interview and other examination methods, this particular skill is useful for establishing rrusting relationships. More precisely de fined and described patient problems are often identified with these special skilis. Younger patients often assume that rheumatic diseases are af Aictions of older patient. T hey are also apt ro assume that their problems are self-limited or curable when they are nor. On the other hand, even roday, many physicians either miss or delay a diagnosis of rheumarologic disease, sometimes with devastating long-term consequences. Establishing a precise hisrory is vital for a correct diagno sis. [n general, patients seek help for pain, pain equivalents,

36. RheumatoLogy

depression, and anxiery. Painful sensations have many e1emenrs. Some are physiologic, but many are perceptually driven, i.e., they are learned behaviors. Feelings of helplessness and hopelessness are common in this population, particularly among those who make frequenr physician visits. (See Chapters 6, 8, 15, 17, and 19.) Pain equivalents include unpleasanr (not necessarily painful) sensations, such as itching, aching, stiffness, and nausea. The his tory should include detailed inquiry about the patient's motiva tion for coming to the doctor, especially in the absence of pain or pain equivalenr (8). As a consequence, successful treatmenr depends on pain relief and its inrerpretations. Clearly stated and understandable explanations are the keys for long-term success.

History Taking (8) (See Also, Chapter 19) In general, do the symptoms raise the possibiliry of systemic disease(s), or local conditions? A localized condition may affect multiple sites. What joinrs or other structures are involved? What is the pattern of involvement? In what order does joint involve ment occur? How fast does it occur? At what time of the day does it start? If joint involvement is painful, severity is estimated by whether it interferes with function of the affected extremity, or with sleep and work. Is involvemenr self-limited, migratory, or progressive? If limited, how long do episodes last? Are they migratory or progressive? Migratory means that the process subsides completely before moving to another apparently normal joint. Progressive means that the first joint stays afflicted as the pathologic process moves on to additional joints. Has this problem been treated previously? What was done and for how long? Was disease progress affected? What was its effect on the disease? Were there any drug side effects? The duration ofmorning stiffness serves as a convenient, non specific index of inAammatory activiry. Typically, it is directly ptoportional to the severiry of the inAammatory process. Varia tions in duration are readily used to evaluate inAammation and responses to treatment. For example, the duration of morning stiffness is a more precise assessment than the erythrocyte sedi mentation rate for rheumatoid inAammation. If a structure is severely inAamed, motion usually causes pain unless there are neurologic problems that interfere with nocicep tion. In general, pain arises from stimulation of synovial, capsular, periosteal, ligamentous, or tendinous free, unmyelinated nerve endings. Mechanical irritation and inAammation are common causes. Both pain and numbness occur in association with nerve entrapments in the carpal tunnel, for example. Other common sites are the suprascapular nerve in the shoulder and radicular syndromes arising from arthritic and degenerative changes in the neck. Intermittent muscle spasm and chronically increased mus cle tone are common in this group of patients. As joinr involvement advances, disuse muscle atrophy occurs rapidly in afef cted systemic rheumatic diseases may also demonstrate characteristic muscle pathology. For example, upper-limb involvement com monly causes clumsiness of varying rypes, with loss of hand strength as a common complaint. Difficulry in rising from a chair or climbing and descending stairs signals both hip girdle and lower limb involvement (9). Depression is common in individuals with chronic arthritis. Two rypes are common, primary and reactive. Primary depression

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occurs particularly frequently in fibromyalgia patients, over 95% of whom are women. Living alone, having maladaptive thoughts, and expressing more functional limitations arc particularly com mon in about half of these patients (10). Some (11) believe this common, ambiguous diagnostic category has a significant lim bic nervous system and neuroendocrine componenr that affects specific aspects of brain, brainstem, and spinal cord function ing. "Some scientists believe . . . the syndrome may result from a trauma affecting the central nervous system . . . Others believe the syndrome may be triggered by an infection, such as a virus." No one knows for sure (11). R heumatic diseases, on the other hand, tend to create long term problems as a consequence of mounting frustration with loss of personal autonomy. Reactive depression is common in this group (See C hapters 15 and 17). The problem frequently arises or is aggravated with the onset of pathologic fatigue. Emo tional labiliry, including crying, morbid thoughts, temperamen tal outbursts, and withdrawal are common under these circum stances. These symptoms often disappear as the disease remits (8). A number of questionnaires are available for long-term eval uation: the Stanford Health Assessment Questionnaire, Func tional Disabiliry Index, and Arthritis Impact Measurement Scales. These instruments document the patient's functional status with results comparable to traditional measures of disease-related joint activiry, such as tender point count, radiographic joint erosion score, and erythrocyte sedimentation rate (12). Other historic cues, such as chorea or "growing pains" in childhood may aid in differentiating rheumatic fever or juve nile rheumatoid arthritis URA) in an adult patient. A history of recent exposure to ticks or viral illness may clarify an otherwise obscure arthritis. Even more important is a sexual history in a patient suspected of having gonorrheal arthritis or reactive arthritis, such as Reiter syndrome. Diabetes is often associated with adhesive capsulitis of the shoulders, Dupuyrren contracture, and OA. A family history of arthritis may or may not be helpful. The stability offamily life and the stabiliry and type of job are impor tant points to establish (11). Avocations should also be recorded because these, too, must often be dealt with in designing a treatment program. Current drug inrake should be listed here, including alcohol and tobacco. A mental status examination is important to establish the pa tienr's level of emotional maturiry and realiry testing. Organic brain disease, including the late effects of brain injuries, demenria, and Alzheimer disease, is particularly important when assessing treatmenr compliance issues (8).

PHYSICAL EXAMINATION Palpation A standard, disciplined routine examination of the musculoskele tal system is essential. A number of excellent monographs are available to provide more detailed descriptions (13,14). The physician's hands and fingers are important physical ex amination tools. Although various mechanical devices are useful for quanrifying tenderness, joint swelling, and skin temperature, none are as useful as the fingers. A rypical peripheral joint and

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spinal screening examination should take 5 or 6 minutes, on average. Osteopathic physicians, with their special backgrounds us ing palpatory diagnosis, are particularly suited for this work. A working knowledge of both topographic and functional anatomy is essential to know which structures lie under the palpating hand. Joint and muscle tenderness are nonspecific, but very sen sitive signs of trouble. Some experts use a great deal of force, although other clinicians are gentler. In general, inexperienced practitioners tend to use too little force when evaluating superfi cial structures. On the other hand, some experts, such as McCarry (15,16), recommend force sufficient to blanch the thumbnail to rule out active disease (when examining areas that are not obvi ously inflamed). If tenderness is present, then either a low pain threshold or pathologic change may be responsible. Fortunately, most tenderness due to an organic cause is accompanied by more specific findings, such as swelling, crepitus, and increased local hear. Classic fibromyalgia tender point sites s hould be routinely evaluated on every patient (17). Areas of tenderness can be "controlled" by applying similar pressure over nearby areas. A neurotic patient may be tender everywhere on the body. Tender bones should be distinguished from aching soft tissues. For example, the anterior tibia is often tender in older subjects for unknown reasons. Bone tenderness may also present in severe osteoporosis and other forms of systemic bone disease.

Range of Motion Passive joint motion testing embraces a set of common and fa miliar osteopathic palpatory procedures. It is used to evaluate all peripheral, spinal pelvic mechanics for alrered tissue tension, asymmetry, restricted motion capabiliry, and tenderness (TART). (See Glossary and Section V I I, C hapters 38 th tough 73.) It is also a method for eliciting pain and joint conrractures.

Swelling Swelling of joints, bursae, and tendons is always abnormal. Un like tenderness, swelling specifically indicates organic disease. Swelling is most often due to underlying inflammation and can be due to synovial thickening, increased volume of joint fluid, or local edema. If thickened tissue is felt, particularly in multiple areas, synovium is probably thickened, owing either to inflam matory proliferation or to storage of abnormal material, such as amyloid. Synovial thickening in a tendon sheath, common in Reiter syndrome or psoriatic arthritis, produces a "sausage finger" or "sausage toe" appearance. In general, synovial swelling is most pronounced on extensor surfaces of joints, where the capsule is more distensible. Effusions are particularly common in large weight-bearing joints. Thus, fluid is often found in the knee, and is less com mon in the hip. It is even less common in ankles, upper limbs, hands, and wrists because of their tighter capsules. Nodular swellings over peripheral joints commonly signal osteophytes and osteoarthritis. Less frequently, they mark the presence of r heuma toid nodules. A number of less common conditions also occur. Clinically, a pathologic nodule cannot be accurately identi fied without a biopsy. Most turn out to be synovium herniated

through defects in the joint capsule, and are most commonly associated with RA, or systemic lupus erythematosus.

Other Clinical Findings Increased skin temperature is a common and usually nonspe cific finding. See TART, above. Sometimes crepitus ( joint noises) occurs during passive range of motion testing. Generally, the finer the crepitus, the more clinically significant it is. Some times tendons will snap over joint surfaces and bony promi nences. Typically, the noise is due to tendons snapping over bony promlllences.

DIFFERENTIAL DIAGNOSIS AND USE OF DIAGNOSTIC TOOLS The general category in which a problem falls is usually obvi ous from the history and physical examination. To pinpoint the diagnosis, however, laboratory examination, including gross and microscopic joint fluid analysis, radiologic study, specialized tests, and occasionally, biopsy for ordinary or special microscopy, are often indicated (18). Routine laboratory tests include complete blood count, chem istry panel, and urinalysis. Synovial fluid examination in selected individuals commonly provides useful diagnostic information. Autoantibody and immune complex assays are indicated when specific inflammatory r heumatic diseases are suspected. One must be alert to a number of diagnostic pitfalls. Patients with r heumatoid arthritis can have a positive antinuclear anti body titer. Persons over 60 years old can have rheumatoid factor in the absence of rheumatoid arthritis. An elevated sedimenta tion rate indicates the presence of any rype of inflammation or infection, even unrelated to a rheumatic disease, and an abnormal creatine phosphokinase (CPK) value is not necessarily diagnostic of polymyositis (7). Radiographic examination is important for differentiating in flammatory from non-inflammarory disorders. X-ray imaging is often used ro stage disease progression and to follow progress once therapy has been instituted. In general, joint inflammation, whether from long-term infection or an autoimmune process, leads to osteopenia and joint erosions. On the other hand, non inflammatory rheumatic diseases frequently cause an increase in bone as a result of subchondral sclerosis, osteophyte formation, and bridging of joint spaces. The laner are commonly seen on plain spinal films. Local ultrasound (US), magnetic resonance imaging (MRJ), and computerized tomography (CT) are also helpful.

INFLAMMATORY ARTHRITIDES Rheumatoid Arthritis R heumatoid arthritis (RA) is a systemic inflammatory disease with its primary manifestation in the synovium that results in substantial morbidiry and premature death (19-21). The diag nosis of RA should be considered in any patient with polyalTicular inflammatory arthritis of greater than 6 weeks duration, especially if the hands and feet are involved (22).

36. Rheumatology

The hallmark of the disease is a chronic, symmerric pol yarthritis (synovitis) that typically affects the hands, wrists, and feet initially, and later may involve any joint lined by a syn ovial membrane, most frequently the knees, ankles, hips, elbows, and shoulders (22). Although RA primarily involves the syn ovium, features of systemic disease are also present in almost all patients, ranging in severity from fatigue, low-grade fevers, and mild to moderate anemia, to serositis (pleural or pericardial ef fusions) and severe multisystemic vasculitis. Fortunately, recent pharmacologic advances with disease-modifying antirheumatic drugs (DMARDs), slow-acting antirheumatic drugs (SAARDs), and TNF-a inhibitor therapy is significantly improving treat ment outcomes (23). Four of seven distinct criteria establish the diagnosis of RA (24). They include at least 6 weeks of: Morning joint stiffness for at least one hour. Simultaneous soft tissue swelling in three or more joint groups. Ill. Hand involvement for the previous. IV. Symmetric involvement, i.e., same joints on the right and left.. v. Rheumatoid nodules. VI. Serum rheumatoid factor (RF). VII. Radiographic evidence of typical RA bone erosions of the hands and wrists.

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patients and probably represent sacroiliac involvement. Often these symptoms are incorrectly ascribed to hip disease or sciatica. Because low back discomfort is such a common malady in the population at large, much attention has been directed at at tempting to differentiate inflammatory from non-inflammatory back pain (25). Characteristically, inflammatory back symptoms are suggested by prominent stiffness and pain in the morning or after other periods of rest (gel phenomenon) that improve with exercise. Such symptoms are most likely to reflect AS in a person younger than 40 years. Additional historic data suggesting AS include back pain that forces the individual out of bed at night or is not relieved by lying down, as well as concomitant chest-wall pain (26). Enthesitis, especially involving Achilles or plantar ten don insertions and causing heel pain, may appear alone or with arthritis (29,30).

I.

II.

The 6 week requirement for diagnosis is necessary, because there are many other causes of symmetric polyarthritis (viral and others) that often mimic RA but are of shorter duration (22). During both acute and chronic phases of the RA process, osteopathic physicians can offer patients range-of-motion exer cises. The use of any of several indirect osteopathic manipulative procedures is also helpful.

Seronegative Spondyloarthropathies A patient presenting with an asymmetrically distributed inflam matory arthritis, with or without spinal joint involvement, a di agnosis of seronegative spondyloarthropathy. The seronegative spondyloarthropathies are characterized by sacroiliitis, peripheral inflammatory arthritis, and the absence of serum rheumatoid factor (RF) (5). There is an assoCiation with the HLA-B27 allele in many cases, although, the pres ence of this genetic marker is neither diagnostic nor predic tive of spondyloarthropathies. Examples of seronegative spondy loarthropathies include juvenile and adult ankylosing spondylitis (AS), Reiter syndrome, spondylitis associated with chronic in flammatory bowel disease, or psoriatic arthritis. Some forms of teactive arthritis follow enteric infection, with such organisms as Yersinia. Shigella, Salmonella, and Campylobac ter. All share similar clinical manifestations. The prevalence of sacroiliitis is high, along with extraarticular manifestations, in cluding uveitis and, occasionally, oral ulcers (5). Chronic low back pain and stiffness are typically the first symp toms of AS (25-27). Onset is usually insidious rather than abrupt, and patients often cannot date when symptoms first began or pre cisely localize the areas affected (28). Complaints of alternating pain, first in one buttock and then the other, occasionally with radiation down the posterior thigh, can be elicited from some

Juvenile Rheumatoid Arthritis Juvenile rheumatoid arthritis ORA), known outside of North America as Juvenile Chronic Arthritis, occurs in patients younger than 18 years of age. Approximately 250,000 children in the United States have JRA (31). JRA takes many forms, including systemic-onset JRA, also known as Still disease. Still disease is associated with negative rheumatoid factor, negative antinuclear antibody, high fevers, and a rash. A small percentage goes on to have chronic desrructive arthritis. Pauci-articular JRA occurs in half of all patients with juvenile rheumatoid arthritis, with four or fewer joints affected; pauci means few. Young girls with positive antinuclear antibody and pauci-articular JRA are at risk for iri docyclitis, which can cause potentially serious eye inflammation. Regular ophthalmologic visits with thorough slit lamp examina tions are necessary until they reach adulthood. Older boys with pauci-articular JRA who are HLA-B27 positive might also have a form of juvenile ankylosing spondylitis manifested by sacroiliitis and asymmetric lower extremity arthritis (7).

Crystal-Induced Arthritis Crystal-induced arthritis primarily includes gout and pseudo gout. The latter is classified as calcium pyrophosphate deposi tion disease. Gout, itself, is probably the second most common inflammatory arthritis in the United States. Both are monoar ticular, and polarized microscopy of synovial fluid identifies the crystals (7,32,33). Gouty arthritis, recognized since antiquity, remains common. It mainly affects middle-aged and older men, in contrast to RA, OA, and most other connective tissue diseases that seem to occur more often in women (5).

DEGENERATIVE ARTHRITIS Osteoarthritis Osteoarthritis (OA) is a slowly evolving articular disease charac terized by the gradual development of joint pain, stiffness, and limitation of motion (34). At present, the terms OA, osteoarthro sis, and degenerative joint disease are used interchangeably. It is the most common of all joint diseases. Its importance de rives from its economic impact, in terms of both productivity

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(si ngle greatest cause of days lost From work) and cost of treat ment (chronic use of analgesics and antiinflammatory drugs) (35). Degeneration of cartilage is the most prominent patho logic change. Both experimental (36) and clinical (37) studies have shown mild-to-moderate synovitis, although inflammatory changes may be absent early (38). Although OA is oFten benign, severe degenerative changes often cause serious disability. Although the etiology of the disorder is still not clearly under stood, osteoarthritis has been shown to be a family of disorders with cartilage as a target organ. Biomechanical Factors play a cen tral role, with risk factors, such as age, weight, and occupation acting as major variables. With more severe disease, pain may be persistent and interfere with normal activities of daily living. A chronic loss of restorative sleep with attendant increases in pain reports is common in this group. Pain is the predominant symptom and initially oFten involves only one joint. Others tend to occur as time passes. The pain is most often described as a deep ache that is frequently accom panied by joint stiffness aFter periods of inactivity, such as on rising in the morning and after sitting. Pain is aggravated by using the involved joints, and may radiate or be reFerred to sur rounding structures. In the early stages it is commonly relieved by rest. Because no treatment can currently prevent or ameliorate the basic disease process, medical treatment is aimed at relieving pain, with orthopedic intervention largely reserved For situations that cannot be controlled with more conservative therapy (35). Newer concepts of pathogenesis suggest that OA is not an inevitable se quence of aging itselF and raise the possibility of rational preven tive and therapeutic approaches in the future (34). The most effective symptomatic therapy combines several approaches and is oFten more efFective if a multidisciplinary approach is Followed. Typical participants are the primary care physician, rheumatologist, physiatrist, orthopedist, physi cal therapist, occupational therapist, psychologist, psychiatrist, nurse/nurse coordinator, dietitian, and social worker.

NONARTICULAR RHEUMATISM Fibromyalgia Primary fibromyalgia (FM) has been defined as chronic, widespread musculoskeletal pain and tenderness at 11 of 18 spec ified sites established by the American College of Rheumatology (39). Qualitatively, the FM tender point count has been referred to as a "sedimentation rate" for distress (40). The absence of signs of connective tissue or other muscu loskeletal disease is implicit in this definition. Because of its subjective nature and its frequent association with disturbed sleep, chronic Fatigue, headaches, and irritable bowel syndrome, the validity of classifying FM as a (rheumatic) disease rather than a "syndrome of being out of sorts" has been challenged (41-48). Patients often appear anxious and depressed, and studies have shown that they may Feel dissatisfied with all aspects of their lives. Strong evidence has been given For an association berween FM and major depressive disorder. Nevertheless, the specific charac-

teristics of anxiety and depression have not been identified con sistently on psychological testing. On the other hand, it has been suggested that chronic pain and fatigue of any cause regularly engenders anxiety and depression (49,50). Despite their subjectivity, symptoms of FM tend to be con stant over many years. Decreased threshold to pain on pressure over certain sites and increased skin fold tenderness have led to nu merous attempts to demonstrate localized peripheral abnormali ties and to speculation that FM is a disorder of pain modulation (40). There are no irrefutable biochemical, immunologic, or anatomic abnormalities detected in FM. However, studies of biopsied muscle samples have Found decreased levels of adenosine triphosphate and phosphocreatine both at rest and after exercise (51). These findings have been confirmed by magnetic resonance spectroscopy in a small number of patients (52). Other findings, such as decreased regional cerebral blood flow with low cere brospinal fluid metabolite levels, have been cited as evidence For functional dysregulation of central pain pathways (53-55).

RHEUMATIC DISEASE MANAG EMENT Management of rheumatic diseases is predicated on an accurate diagnosis. Once a diagnosis is established, interventions and rec ommendations should be based on evolving evidence that most rheumatic diseases are neither benign nor inevitably disabling. As with many other chronic conditions, such as diabetes mellitus and hypertension, treatment focuses on quality-of-life issues with strategies designed to prevent adverse outcomes to the extent pos sible. Fortunately, both medical personnel and the public-at-Iarge have a much better understanding of these situations than they did only a few years ago. The good news is that, with proper care, most can function at quite high levels with ol;ly minor impact on their daily lives.

Nonpharmacologic Treatments (7) Nonpharmacologic therapies For rheumatic diseases are oFten re warding, generally providing an assistive role. Along with improv ing general physical fitness, both physical therapy and occupa tional therapy are fundamental components of treatment for both rheumatic and nonrheumatoid disorders. (Also see Chapter 35, Osteopathic Physical Medicine and Rehabilitation.) No single modality has proven to be most successful. However, treatment of the somatic component of any arthritic process by administration of appropriately chosen manipulative treatment is often helpFul in relieving both pain and emotional distress (56,57). Manipulative techniques also supplement other adjunc tive measures. Indirect approaches are particularly useful, using strain and counterstrain, myofascial release, and Functional tech niques. (See Chapters 58-66.) Exercise, muscle strengthening, weight and nutrition management, along with general home and workplace considerations, are also factored in, including appro priate ergonomic advice. Both OA and FM have proven to be particularly responsive to osteopathic manipulative methods. Medical management gener ally focuses on symptom management because, unril recently, no

36. Rheumatology

single inrervenrion has been proven to cure the primary disease processes, including DMARDs and SAAMARDs. Nonsteroidal antiinAammatory drugs (NSAIDs) are particularly useful, and their generic forms are inexpensive. A carefully graded, incremenral exercise program is essenrial. If the regimen advances too quickly, symptoms may worsen, threat ening compliance. Importantly, the patienr should be advised that worsening pain is a warning sign that exercise tolerance has been reached (58). Symptomatic relief commonly also occurs using both heat and cold.

MEDICATIONS Pharmacologic therapies are generally nonspecific, although re cent research has focused on underlying cellular physiology and targeting specific parts of the immune response.

Antiinflammatory Drugs (59) NSAIDs are fundamental to the treatment of most rheumatic diseases. They are useful as both analgesic and antiinAamma tory agents, and are generally inexpensive when generics are p rescribed. Salicylates are also inexpensive and generally well tolerated. In general, larger doses are required than those used for primary analgesia. A constant blood level of 20 to 30 mg/dL is needed, which for most patienrs, requires between 3 and 6 grams of as pirin daily. All patients should be monitored for toxic blood levels and side-effects, including tinnitus, deafness, and gastrointesti nal intolerance. Recent evidence suggests that the latter occurs more often when Helicobacter pylori infection is present. E radi cation of the H. pylori then allows for safer use of these products (60). Overt gastrointestinal tract hemorrhage or ulceration is infre quent, but when it occurs, it dictates discontinuation of the drug and exploration for H. pylori infection (60). In most cases, con comitant administration of proton pump inhibitors significantly reduces NSAID-induced gastrointestinal toxicity (59).

Corticosteroids Local injection of corticosteroids into affected joints and my ofascia I trigger points often produces dramatic symptomatic and functional improvements. Unfortunately, long-term side effects make them unrealistic choices except for the unresponsive patient with aggressive joint disease that th reatens loss of functional abili ties. Oral prednisone, given every other day, is commonly helpful in this group of patients. Higher doses are necessary for patients with neuropathy, vasculitis, pleuritis, pericarditis, scleritis, and related conditions (59).

53 1

gold salts, penicillamine, sulfasalazine, and minocycline. Anti malarials are usually given as hydroxychloroquine (Plaquenil), 200 mg once or twice daily. This drug may cause retinal lesions and loss of vision, making regular annual ophalmologic evalua. . (Jons a necessity. Currently, the most widely used and effective form of long term therapy for RA appears to be methotrexate. An oral dosage of 7.5 to 25 mg one time per week is usually effective. A therapeutic response usually occurs within several weeks. Side effects include hepatotoxicity with a possibility of cirrhosis, bone marrow sup pression, oral ulcers, and potentially life-threatening pneumoni tis. Methotrexate may also cause a leukocytoclastic vasculitis that promotes formation of more rheumatoid nodules. This condi tion is called systemic nod ulosis. Simultaneous treatment with folic acid 1 mg per day reduces methotrexate toxicity without impairing efficacy. LeAunomide (Arava), a pyrimidine antagonist that selectively inhibits activated T lymphocytes, has been recently inrroduced for long-term treatment of RA. Sulfasalazine in large doses is effective in some patients. Minocycline has also been found to be effective in RA (6 1 ). Gold salts, rarely used, are given in weekly intramuscula r in jections. It produces remission in many cases. Common side ef fects include pruritic skin rashes and painful mouth ulcers. Se vere manifestations include bone marrow suppression (usually leukopenia or thrombocytopenia), renal damage with protein uria, and rarely, nephrotic syndrome. Frequent urinalyses and blood counrs must be performed, especially during the early phases of treatment. In general, gold salts have fallen out of favor as more effective and better tolerated treatments have become available. Penicillamine is also effective. Like gold salts however, its ef fects begin slowly. Bone marrow and kidney toxicity are more common side effects. It also has the potential for inducing other autoimmune diseases, such as myasthenia gravis, Goodpasture syndrome, and lupus erythematosus. As a result, both gold salts and penicillamine are rarely used today. Immunosuppressive agents, such as azath ioprine, cyclophos phamide, chlorambucil, and cyclosporine have been used to treat especially severe, unremitting RA. Etanercept (Enbrel), a soluble recombinant TN F-a receptor inhibitor, has recently been introduced for severe RA manage ment. To date, it has proven to be highly effective at controlling symptoms and, seemingly, disease progression, in many patients. Toxicity appears to be low, but concerns about potential cancer induction and infectious complications resulting from TNF-a blockade remain to be determined. High cost is a particular dis advantage along with the need for twice weekly injections. InAiximab (Remicade), a chimeric TNF-a receptor anrago nist is also available via intravenous infusion every 6 to 8 weeks. Concerns also exist about potential long-term side effects.

Surgery DISEASE-MODIFYING THERAPIES Disease-modifying antirheumatic drugs (DMARDS) (59), the more slowly acting drugs, include antimalarials, methotrexate,

Surgical joint replacement has been a major benefit for thousands of disabled arthritis sufferers. Prosthetic devices for hip and knee joinrs generally give excellenr results, and devices for ankle, elbow, and shoulder replacement are improving.

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Vi. Osteopathic Considerations in the CLinical Specialties

OSTEOPATHIC MANIPULATIVE TREATMENT: EFFICACY AND RESEARCH

REFERENCES J . Decker J L, Glossary Subco m m i nce of rhe ARA Comm i nee on

Arthritis patients appear to experience improved q uality of life when offered OMT, as opposed to more traditional pharmaco logic therapy. Research studies involving large numbers of patients followed for months or years have not yet been done. The long-term bene fits of OMT are unknown in these conditions. A study examining the use of OMT as an adjunct in the management of systemic lupus erythematosus has begun (62), but results are not yet available. Tucker (63) examined the treatment of osteoarthritis using manual therapy. His work, published almost 30 years ago, has conclusions that are valid today regarding the early use of p hysi cal measures for the treatment of osteoarthritis followed by more traditional pharmacologic therapy (7). He believed that the early use of manipulative treatment might be beneficial, but if symp toms persisted after 6 months, more aggressive traditional therapy should be considered.

rheumarologic pracrice. American Rheumarism Associarion nomencla rure and classifica rion of arrhriris and rheumarism. Arthritis Rheum. 1 983;26: 1 029-1 032. 2 . Haber L D . Disabl i n g effecrs of chronic disease and impairmenr. I I . Funcrional capaciry l i m i tations. j Chrollic Dis. 1 973;26(3): 1 2715J. 3 . Vcrbruggc L M . From sneezes ro adieux: stages of health for American men and women. Soc Sci Med. 1 986;22( 1 1 ) : 1 1 9 5- 1 2 1 2. 4. Lawrence RC, H e l mick CG. Arnerr FC, er al. Esti mates of the prevalencc of arrhriris and selecred musculoskeletal disorders in rhe U n i red Stares.

A rthritis Rheum. 1 998;4 1 (5) :778-799. 5. Felson D . Epidemiology of the Rheumaric Diseases. I n: Koopman WJ, ed. Arthritis (mdAllied Conditions. 1 4th cd. Philadelphia. PA: Lippincorr Will iams & Wilkins; 200 J . 6 . Yel i n E , Callahan L F. Thc economic cosr and social and psychological i m pacr of musculoskeleral conditions. National Arthritis Data Work Groups. Arthritis Rheum. 1 996;39( 1 1 ) : 1 93 1 . 7 . Rubin B . Osreoparhic Considerarions i n rhe Cl i nical Specialr ies Rheumarology. I n : Ward R. cd. Foundatiol'lS of Osteopatbic Medicine. I sr ed. Philadelphia. PA: Lippincorr Williams & Wilki ns; 1 99 5 . 8 . McCarry OJ. D i fferenrial Diagnosis of RJ,eumaric Disease: Analysis o f S i g n s and Symproms. [ n o Koopman W J . e d . Arthritis and Allied Condi

tions. 1 4rh ed. Philadelphia, PA: Lippi ncon Williams & Wilkins; 200 1 . 9 . Csuka M E. McCarry OJ. A rapid merhod for measurcment of lower

CONCLUSION Osteopathic principles and concepts are particularly useful when working with arthritic patients of all types. Palpatory diagnosis and manipulative treatment are particularly applicable for this population. With the possible exception of infectious arthritis, no rheumatic disease can truly be cured. By combining appropriate neuromusculoskeletal and laboratory diagnoses with carefully se lected pharmacologic therapy and manipulative treatment, the patient can experience both symptomatic and functional im provements, including an improved sense of well-being. Clinical research will answer lingering questions regarding the benefits of osteopathic manipulative treatment in this pop ulation. Recent studies dealing with fibromyalgia and systemic lupus erythematosus are among the first efforts to examine osteo pathic manipulative treatment in a defined population (64,65). More controlled studies of this nature are planned for the future.

exrremiry muscle strengrh. Am j Med. 1 98 5 ;78:77-8 1 . 1 0. Okifu j i A . Tu rk DC. Sherman JJ . er al . Evaluarion of rhe relarionship berween depressi o n and fibromyalgia syndrome: Why aren'r all patienrs depressed? j Rheumatol. 2000; 1 : 2 1 2-2 1 9 . 1 1 . N I AM S/ N I H Websire. Fibromyalgia Research: Challenges and Op pOrtu n i ties. Imp:/ /www. n iams. n i h . gov/hi/ropics/fibromyalgia/fibromya. h rm. Accessed May 1 5 . 2002. 1 2. Gordon DA. Approach ro the Parienr wirh Musculoskeletal Disease. I n : Goldman L. Bennerr J C , eds. Cecil Textbook of Internal Medicine. 2 1 sr ed. Philadelphia. PA: WB Saunders; 2000. 1 3. Polley H F. H under GG. Rheumatologir inten;iewing andphysical exami

nation ofthe joints. 2 n d ed. P h i ladelphia. PA: WB Saunders; 1 97 8 . 1 4 . Dohcrry M . Doherry J . Clinical Examination ill Rheul1Iatology. London. England: Wolfe; 1 992. 1 5 . McCarry OJ, Ganer RA. Phelps P. A dolori mercr for. q uanri fication of articular tenderness. A rthritis Rheum. 1 965;8 : 5 5 1 -5 5 9 . 1 6. McCarry O J . Ganer R A . Steele AD. A rwenry-pound dolorimetcr for quanrification of articular tenderness. Arthritis Rheum. 1 968; 1 1 :696698. 1 7. Wolfe F. Smythe H A , Yunus M B, er al. The American College of Rheumarology 1 990 crireria fo r the c1assificarion offibromyalgia. Rcporr of the m ulticenrer crireria commi rrcc. Arthritis Rheum. 1 990;33: 1 601 72 . 1 8 . Shmerling R H . L i a n g M H . Laborarory Evaluarion of Rheumaric Dis eases. I n : Primer on the Rheumatic Diseases. 1 Orh ed. Arlanra. GA: Arrhri ris Foundarion; 1 993:64-66.

ACKNOWLEDGMENTS

1 9 . Scorr D L. Symmons D P M . Coulron

B L. er al.

Long-rerm our

come of treating rheumaroid arthriris: Resulrs after 20 years. Lallcet. 1 987; 1 : 1 1 08- 1 1 1 1 .

This chapter is dedicated to my wife, Michelle Miller, and sons Richard and Casey. Their support and indulgence allowed me to complete this project. The intellectual support and patience of my co-workers, who helped me find the time in an overworked schedule to complete this project is appreciated. Not to be for gotten are the other members of the Western University College of Osteopathic Medicine of the Pacific staff, Drs. Michael Seffin ger and Ehab Tuppo, and Christine Jacobson, MA, who offered important suggestions. I thank each of you for your support in helping to bring forth this chapter.

20. Pi ncus T. Brooks R H . Callahan LF. Prcd icrion of long-term mortaliry in parienrs with rheumaroid arr h ri t is according ro s i mple quesrionnaire and j o i nt cou n r measu res. Ann Intern Med. 1 994; 1 20 ( 1 ) : 26-34. 2 1 . Wolfe F, M i rchel l O M . Sibley JT, er al. The morraliry of rheumaroid arthriris. A rthritis Rheum. 1 994;37(4 ) : 4 8 1 -494. 22. O'Dell J R. Rheumaroid Arthritis: The Cl i n ical Picrure. In: Koopman WJ . ed. A rthritis and A llied COl7ditions. 1 4 rh ed. Lippi ncorr Williams & Wilki ns; 200 1 . 23 . American College of Rheumarology Ad Hoc Commi rree on Clin ical G u ideli nes. G u idelines for the managemenr of rheumaroid arrhriris.

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AN OSTEOPATHIC APPROACH TO SPORTS MEDICINE P. GUNNAR BROLINSON KURT HEINKING ALBERTJ. KOZAR

KEY CONCEPTS • • • •

• •

Appreciate the unique role ofosteopathic medicine in sports medicine Understand the roles and responsibilities of the sports medicine team Understand the pathomechanics of sport and exercise-related disease and dysfunction Describe the relationship between somatic dysfunction and common sportS-related injuries and how osteopathi c manipulative treatment i s integrated i n the treatment ofthe injured athlete Understand the unique challenges associated with sideline coverage and event management medical issues Understand the rational behind treatment and what factors need to be considered prior to returning the athlete to play

1 2 million. Due to the affects of Title IX, and the Amateur Sports Act of 1 978, there has also been a major impact on the field of sports medicine for young women. Now more than 55 million women participate in recreational SPOrtS annually (2) . Growing numbers of senior athletes are exercising routinely and partic ipating in competitive sports. By the year 2030, 20% of our population will be over the age of sixty-five. It is also encourag ing to see that 2 to 3 million people with disabiliries participate in sports each year in the United States (3) . It is this diversity that makes the field of sports medicine so exciting and challenging. However, this rise in physical activity has been accompanied by an increase in the number of sports-related injuries. It is es timated that over 1 7 million Americans seek medical care each year because of athletic and recreation-related problems (4) . Due to the enormous volume of participants and numbers of injuries, medical practitioners of all fields need to be educated on the diagnosis and treatment of athletic injur ies.

WHY IS THERE SUCH AN "EXERCISE BOOM?"

Sports medicine is the branch of the healing arts profession that uses a holistic, comprehensive approach to the prevention, di agnosis, and management of sports and exercise-related injuries. Osteopathic sports physicians apply their medical and scientific knowledge with a philosophy that the athlete's structure and func tion are interrelated. Osteopathic physicians must look at the en tire scope of an athlete's problem, including the mechanism of injury, environmental inAuences, inherent postural and muscle imbalances, the psychological effects of injury and rehabiliration, and finally, to the athlete's safe return to play. The osteopathic primary care physician can also play a key role in sports medicine. Although only 20% of the American population regularly participates in an exercise program, our population is becoming more active, health conscious, and physically fit (I). This increase in athletic participation does not only include the younger ath letic male. Participation in sports by children and adolescents has dramatically increased over the last few years. The number of ado lescent athletes involved in formal sports participation continues to increase yearly in the United States and now totals more than

Over the last 2 to 3 decades, hundreds of studies delineating the beneficial effects of exercise have emerged. National recommen dations advocating the development and mai ntenance of life long patterns of physical activity have been published. Many serious health problems can be controlled, improved, or el imi nated through moderate, consistent physical activity. Consider able evidence suggests that regular exercise in conjunction with other risk-reducing behaviors, will protect against an initial car diac episode (primary prevention) ; will aid in the recovery of patients with myocardial infarction, coronary bypass surgery, or angioplasty; and will reduce the risk of recurrent cardiac events (secondary prevention). Due to the beneficial effects of exercise and dietary modification, coronary artery disease has decreased 30% in the United States since 1 960. Aerobic exercise and en durance training can also lead to numerous favorable metabolic effects. These include but are not limited to: a more favorable lipid profile, control of obesity, decreased blood pressure, improved glucose tolerance, higher bone density, and improved self-image (3, 5 ) .

3 7.

Improving physical health also improves emotional health. I t has been known for many years that chronic psychological and emotional distress is associated with a deterioration of health. When comparing exercise programs with relaxation techniques and psychotherapy, exercise was proven to be more effective at decreasing depression than relaxation techniques and was equally as effective as psychotherapy. There is a high correlation between regular exercise and intellectual function, memory, and improved self-concept (6). Regular exercise and appropriate t raining in older adults increases physical safety, reduces susceptibility to acute and chronic disease, and improves psychological outlook (7).

PRACTITIONERS

Ideally, the field of sports medicine consists of health care providers who work in synchtony to provide a "team approach" ro achieve better health for the patient. At the head of this team of professionals is the physician who diagnoses the condition and directs the tr�tment plan. The team physician must have an un restricted medical license and be responsible for treating and coor dinating the medical care of athletic team members. The primary responsibility of the team physician is to provide for the well being of the individual. The team physician should possess special pro ficiency in the care of musculoskeletal injuries and medical condi tions encountered in sports. The team physician also must actively integrate medical expertise with other health care providers, in cluding medical specialists, athletic trainers, and allied health pro fessionals. The relationship of the physician and athletic trainer is critical, as is the link between the coach, physician, athlete, and family members. This "team approach" helps to motivate the dis couraged player, evaluate the injured player, and eliminate risks to the player who is coming back from an injury. The athletic trainer not only carries out the physician's treatment plan, but is a highly skilled practitioner. The team physician must ultimately assume responsibility within the team structure for making med ical decisions that affect the athlete's safe participation. The team physician is the "final authority" to determine the mental and physical readiness of athletes in organized programs (8). The osteopathic physician has a unique role in the total care of the athlete or active patient. Our philosophic approach is patient, not disease, oriented. This philosophic approach lends i tself to this population, because athletic patients are generally healthy and motivated to return to better health. Palpatory skills pro vide osteopathic physicians with a distinct advantage over other health care practitioners in determining the location, extent, and associated manifestations of athletic injury. Finally, osteopathic physicians who effectively use OMT have another "tool in the toolbox" with which to treat an important component of athletic injury-somatic dysfunction.

An Osteopathic Approach to Sports Medicine

535

this is the case, a common approach is to do a Sports medicine fellowship after an orthopedic surgical residency. Some neurosur geons also practice sports medicine. I f a primary care emphasis is sought, then a sports medicine fellowship can be completed after a family practice, pediatrics, emergency medicine, or internal medicine residency. For those interested in a purely manipulative practice, a sports medicine fellowship can follow a residency in osteopathic manipulation. Not all practitioners of sports medicine have postgraduate or fel lowship training. However, it adds exposure, extra training, and confidence, and is now a requirement to sit for the certification examination of added qualification in sports medicine offered by the American Osteopathic Association (AOA). The American Osteopathic Academy of Sports Medicine (AOASM) is the pro fessional organization of the AOA in which osteopathic sports medicine professionals meet, exchange ideas, and develop new knowledge.

HISTORY OF SPORTS MEDICINE AND OSTEOPATHIC SPORTS MEDICINE

Physicians have been caring for athletes since ancient times. Herodicus, the teacher of Hippocrates, was the most well known Greek physician around 400 B.C. In those days, they supervised the training and care of Olympic athletes. In the second century A.D., Galen, the fi rst to be called team physician, served as the physician to Roman gladiators. His knowledge of exercise phys iology greatly influenced the practice of medicine for the next millennium. A. T. Still's teachings on the importance of structure and func tion and the significance of the musculoskeletal system in the maintenance ofhealrh were keys to his philosophy. It should sur prise no one, that Still and the administration of American School of Osteopathy (ASO) encouraged new students, both men and women, to join the Athletic Association (9). Professional and collegiate sports were just becoming popular at the turn of the 19th century. As Still's reputation grew as a highly skilled prac titioner in providing relief of sprains, strains, and dislocations, many injured athletes came to him to be treated. Accordingly, Still became known as a pioneer in sports medicine ( 1 0). In 1 90 1 , the first athletic director was named at the American School of Osteopathy while both intramural and intercollegiate sportS, in cluding football, baseball, and basketball, prevailed in Kirksville. The ASO teams were charter members of the Missouri r ntercolle giate Athletic Association. The Osteopaths, as they were known, took on major universities including Notre Dame and Nebraska. ASO teams were often very good and gained so much reputation for the school that many famous athletes later came back to at tend. Forrest "Phog" Allen, an illustrious coach whose teams won 77 1 basketball games during his long career at the University of Kansas, was probably the best known sports figure to attend ASO.

TRAINING PRE-PARTICIPATION PHYSICAL

SportS medicine physicians can enter this field of medicine through numerous pathways. The physician must decide early on if he/she wants to practice surgically oriented medicine. I f

One of the most important functions of a sports medicine pro fessional is to perform a thorough pre-participation physical

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Osteopathic Considerations in the Clinical Specialties

examination (PPE). The pre-particIpation history and physi cal examination has numerous functions, with the screening for life-threatening conditions at the top of the list. This ex amination may be the only time the athlete will have contact with a medical professional during the teen years. The PPE was originally designed to clear those athletes who were eligible for competition and hold out those who were not. In 1 992, the American Academy of Pediatrics (AAP), the American Academy of Family Practice (AAFP) , the American Medical Society of Sports Medicine (AMSSM) , the American Orthopedic Society for Sports Medicine (AOSSM) and the AOASM, published Pre participation Physical Evaluation ( 1 1 ) , in an effort to provide a common format for practitioners to use. In 1 996, the American Heart Association produced a document entitled Cardiovascular Preparation Screening ofCompetitive Athletes at the 26th Bethesda Conference on Cardiovascular Health ( 1 2, 1 3) . [n the challenge t o decrease the risk o f sudden cardiac death, they determined the following: A complete medical history, physical examination, and brachial artery blood pressure should be performed before par ticipation in organized high school (grades 9 through 1 2) and college sports. • Screening should be repeated every 2 years; in intervening years, a history should be taken. • A national standard for pre-participation examinations should be developed. • A health care worker with the training, skills, and background necessary to reliably obtain a detailed cardiovascular history, perform a physical examination, and recognize heart disease should perform athlete screening. •

Although these guidelines are clinically useful, there is no na tionally accepted form for completing the pre-participation phys ical exam ination. However, the following are goals and objectives that should be considered during the pre-participation examina (Ion: • • • • • • • • • • •

Screen for life-threatening conditions Decide eligibility or restriction of play (based on classification of sport: contact, limited contact, non-contact) Determine disqualifYing medical conditions for sport partici pation Evaluate the function of the musculoskeletal system and prior lll Junes Record a baseline mini-mental status examination Check for communicable diseases Counsel/educate on athletic injury prevention and cancer screening examinations based on the population Establish rapport with athletes Evaluate for the potential of injury and areas of performance enhancement Educate the athlete on closed head injury, used of ergogenic aids, and proper protective equipment

Osteopathic physicians should perform a screening musculoskele tal examination with emphasis on evaluation for the presence of somatic dysfunction

The pre-participation physicals should take place at least 6 to 8 weeks prior to the sports season. The history is the primary fo cus for all athletes. An athlete who reports syncope or chest pain

during exertion is waving a "red flag" during the examination. It is also crucial to inquire about any alterations in consciousness or concussions during sports, asthma, recent history of mononucle osis, and menstrual history. All athletes should be asked if they are using any medications, OTC preparations, or performance enhancing drugs. Family history should elicit if there has been a cardiac-related death in a fi rst-degree relative under the age of 5 0 , and any known congenital heart disease. The physical examination is a screening examination only, but should include a thorough cardiac evaluation in at least two posi tions carried out with maneuvers. The musculoskeletal screening should include not only evaluation of symptomatic joints, but also a general screening examination, a focused palpatory exami nation, and motion testing of body areas that contain significant tissue texture abnormality. Osteopathic physicians have unique palpatory skills. These skills can be very useful in determining if there is a somatic com ponent to a patient's medical condition or somatic dysfunction that may lead to overuse injury. Consider an asthmatic patient with upper thoracic and rib dysfunction. Palpating for these vis cerosomatic reflexes gives the clinician useful information regard ing management and sports participation. This approach allows the osteopathic physician additional structural and functional information. The following clinical examples highlight the importance of an osteopathic examination during the pre-participation physical: A baseball pitcher with significant thoracolumbar motion re striction may not transfer the ground reactive force through his legs and trunk to the upper exrremity. Because of this, he tries to throw harder with his arm, producing an overuse syndrome of the upper extremity. 11. A female tennis player with a history of dysmenorrhea de velops central low back pain during her season. This may be treated symptomatically or prevented if related somatic dysfunction is diagnosed and/or addressed during the PPE. Ill. Consider a patient with posterior and lateral knee pain, yet a normal orthopedic examination. It is not uncommoli to find somatic dysfunction of the ilium and fibular helld. Treatment of the ilium, hamstring, and fibula prior to the season may decrease the incidence of a hamstring strain while competing. 1.

Osteopathic physicians have unique skills to offer our com petitive young athletes. Ie is important to use these skills right from the beginning of care-integrated into the PPE.

THE OSTEOPATHIC APPROACH TO THE INJURED ATHLETE History

osteopathic approach to the injured athlete is a unique ap proach that is important because many musculoskeletal injuries or athletic-based illnesses have a somatic component. History taking in the athletic population should include all of the com ponents of the routine history, yet also cover questions regarding the athlete's level of play, type of sport(s) , positions, and prior in jury or illness. These questions will help the physician determine the mechanism of injury, whether the injury is an exacerbation of

An

37.

a pre-existing illness, or ifit is perhaps a new, undiagnosed medi cal condition. One must not settle on the obvious diagnosis based on the chief complaint; the history must be focused to probe for factors contributing to the cause of the obvious diagnosis. Many times, an athlete will see a physician not because they are in pain but because of a decline in their athletic ability or performance. It is important to find out if the symptoms are progressing, stay ing the same, or improving. I f progressive symptoms are presem, how has the athlete changed their activity or lifestyle to cope with this? What is the athlete's emotional state? Young athletes may not give a reliable history. Obtaining the history from family members can sometimes be beneficial. Parems of athletic children may have a different viewpoint of the evems surrounding the injury or illness. Parents or family members are a more reliable source of how the patiem is psychologically re sponding to the situation. Obtaining this information will allow you to also make return-w-play recommendations and, if indi cated, what type of restriction is necessary. From the history, a differential diagnosis is produced; the physical examination and diagnostic tests help narrow the focus. Physical Examination

The appreciation of tissue texture abnormality is fundamental to the evaluation of the patient. The experienced osteopathic physician uses palpation and a detailed functional biomechani cal evaluation to make an assessment that is not limited to the patient's subjective complaint. Osteopathic physicians also examine not only the injured re gion but also distant, potemially related sites. Often, there is a direct anatomic correlation. The body is interconnected through various complex fascial, neurologic, reflexive, and metabolic re lationships. Athletes especially rely on the transfer of energy be tween these different regions of the body. Osteopathic manipula tive therapy can correct these segmental and regional dysfunctions and thereby improve the transfer of energy that is required for various athletic demands. Osteopathic sportS physicians develop both their hands and minds and are trained to evaluate injuries differently. Consider a common sports medicine "itis," such as tendonitis, periostitis, or bursitis. I t is commonplace to quickly diagnose an "itis" in an athlete. An osteopathic physician can use palpatory skills to determine where the "itis" is located, its severity, and chronic ity. They also look for the "why" behind the injury. Was there a predisposing structural or functional imbalance between the muscles, joints, or connective tissues? Was it just a situation of too much, too soon, or too fast ? If so, what are the psychological or social factors motivating the patient? Lastly osteopathic doctors (DOs) do not have to rely solely on the prescription pad to relieve pain, decrease edema, or improve performance. Many athletic injuries can be treated effectively using osteopathic techniques. Standing Screening/Scanning Examination

The standing screening examination in the athlete is performed in the same fashion as for the general population; however, it is not uncommon to find some differences. Consider the evalua tion of spinal A-P curves. Athletes may develop unique postural


537

characteristics associated with their particular sport, which must be taken into account. On forward bending, asymmetry of muscle mass in the paraspinal muscles is not uncommon. This paravertebral muscle "humping" or p rominence may be related to spinal idiopathic scoliosis, functional group curve mechanics, or as a developmen tal response on the dominant hand side. This is especially true in athletes who predominately use one extremity (quarterback or place kicker). Athletes who perform repetitive motions (like golfers) can have lateral spinal curves due to muscle tightness from the patterned repetitious movement. Volleyball and basketball players (especially tall, thin females) are commonly found to have general ligamentous laxity and re curvatum at the elbows and knees. Arm span longer than height, arachnodactyly (long, thin fingers) , and kyphoscoliosis may tip off the doctor to Marfan syndrome. Because of potential aortic and cardiac structural abnormalities, these patients need a thor ough cardiovascular workup prior to competition. Runners may have a variety oHoot p roblems, including asym metric pes planus, which can present as a short leg on struc tural examination. In this situation, the iliac crest and greater trochanter may be low on the same side. Pelvic side shift will be away from the short leg side. A lumbar spinal convexity is commonly palpated on the short leg side. Asymmetric hamstring tension can affect posture and the standing flexion test. A tight hamstring muscle may hold the innominate inferiorly, giving a false negative test on the same side. A tight iliopsoas muscle may produce pelvic side shift away from the psoas spasm. A tight iliopsoas affects the standing ex amination. The patient may appear bent over forward and to the side of the spasm. Their belt line may appear low on one side. I n weight lifters, protracted shoulders may lead to rotator cuff impingement syndromes. This is usually attributed to poor posture, over-development of the pectorals, inhibited rhomboids and lower t rapezius muscles. T hese areas are prone to extended segmental dysfunctions that are painful and persistent. Treating these dysfunctions throughout the rehabilitation is crucial for restoration of a functional thoracic kyphosis (Fig. 37. 1 ). Evalu ating and treating these types of muscle imbalances is a key to preventing or treating shoulder complaints. Palpatory Examination

Athletic patients have an overall tone to their muscles and tis sues that is not found in the general population. Healthy muscle feels smooth and homogeneous, with taught fascia and less sub curaneous findings. The palpatory examination can determine the presence and severity of tissue texture abnormality, as well as the size, shape, and tone of the muscles. The extent and loca tion of muscle splinting (which is a common finding in athletic injury) needs to be determined with palpation. For example, mus cle splinting of the hamstrings can give a false negative anterior drawer test at the knee. Palpation can be used as part of the neurologic examina tion, because flaccid or attophic muscles may be related to a lower motor neuron lesion. Athletes with a herniated lumbar disc and radiculopathy may have palpable findings in the affected leg.

538

VI.

Osteopathic Considerations in the Clinical Specialties commonly becomes flaccid and attophic after knee arthtoscopy or injury. This is a neurologic inhibition, not a true weakness. This factor is important to determine and treat prior to prescrib ing more advanced therapeutic exercises. There are particular patterns of muscular contraction seen in various movements. Patients who have significan� muscular imbalances, somatic dysfunction, or injury are prone to having these abnormalities. Consider the low back pain patient who fi res their lumbar paraspinals instead of their gluteus with each hip extension. This pattern becomes learned and will persist and lead ro further injury or incomplete recovery if not corrected by appropriate neuromuscular retraining. Motion Testing

Motion testing should include joints, soft tissues, fascia, and cra nial motion. It is performed in areas that contain significant tissue texture abnormaliry. Prior to motion testing, it is important to understand that athletes may have very different qualities of mo tion, yet these are still "normal" findings. For example, motion testing in an athlete's innominates may reveal a symmetric yet fi rm compliance. A sedentary patient is typically found to have a soft compliant pelvis. Some athletes have significant flexibiliry of their ligaments and joints, yet this is not appreciated readily because of the generalized tone of the muscles. Clinically, it is more difficult to palpate areas of articular hypermobiliry than hypomobiliry. Adolescent females are commonly found to have ligamentous laxiry or hypermobil iry. This is commonly seen at the knees and shoulders. Sports that accentuate this laxiry include gymnastics and swimming. Other athletes appear to be stiffer. These differences in flexibiliry may be genetically related. Symmetric range of motion and an appro priate range of motion for a given activiry are important factors in motion testing and later on during rehabilitation. FIGURE 37.1. Flat Back Posture. (From Kendall FP, McCreary EK, Provance PG. Muscles Testing and Function with Posture and Pain, 4th ed. Baltimore: Williams & Wilkins; 1 993:76, with permission.)

Palpation may also reveal injury to ligamentous structures, such as in the acute ankle sprain. Torn ligaments are locally tender and may have a palpable defecr. Rents (tears) in the fascia with or without muscle herniation can also be palpated. In children, a frequent area of injury is the apophysis (where the tendon inserts on bone) , which can be palpated. In compartment syndtomes of the extremities, increased tissue tension, muscle fi rmness, fullness, and pain to applied pressure are common palpatory findings. It is imporrant to palpate the injured area (and sometimes distant areas) when the athlete is performing a particular motion, such as performing a sit-up. Tenderness, muscular findings, or even a hernia may be accentuated at this time. Tenderness of muscle during a concentric or eccentric contraction may indicate a muscular strain. Scar tissue does not actively contract and may be locally tender during this examination. Observation and/or palpation of muscle fi ring patterns can also provide useful information. Palpation at this time also al lows the physician to determine if a particular muscle is "turning on" or if it is inhibited. Consider the vastus medialis muscle. I t

Articular Motion Testing

Motion testing includes an evaluation of the quantity and quality of motion. Articular somatic dysfunction rypically occurs in the joint's minor motions. A significant variable during motion test ing is the concept of "end-fee\." End-feel is a qualitative finding of reluctance or resistance to further motion. It is a qualitative de scriptor of the restrictive barrier. Microtraumatic injuries (repet itive overuse) may have a fi rm end-feel .clue to muscle tightness. Macrotraumatic injuries evaluated within the "golden hour" may produce a loose or sloppy end-feel, especially if ligamentous dis ruption occurred. After this, muscle splinting of the injured area occurs, and the end-feel may become fi rm. Viscerosomatic re flexes may produce a rubbery end-feel to the tissues. The rype of restriction found during motion testing helps guide the selection of manipulative treatment. The Functional Biomechanical Examination

Sport performance is primarily a function of the musculoskele tal system. The body economy (including the cardiovascular and pulmonary systems) is constantly tuned to the high and variable demands of the musculoskeletal system. The athlete is subject to

37.

the biomechanical strength and flexibility demands of his or her particular sport, as well as the gravitational challenges producing the ground reaction forces of the associated sports performance. W hen approaching the injured athlete, it is important to think of functional anatomy, understanding the joints are both me chanical and sensory organs that produce both proprioceptive and nociceptive information. The processing of this altered in formation may change moror patterns and produce dysfunction and/or injury. The most important symptom of disturbed motor function is usually pain. As sports medicine clinicians, we want to avoid falling into the trap of treating symptoms. We must learn ro identify dysfunctional patterns and seek to guide our athletic patients in neuromusculoskeletal behavioral patterns that are less costly biomechanically a,}d more favorable to health and efficient function. To treat dysfunction, we must first understand function. We often recognize athletes by characteristic movements, such as running gait, golf swing, pitching motion, or other particular sport-related movements. Every individual acquires highly char acteristic motor patterns during growth and development. There are no norms to movement patterns. As sports medicine clini cians, we sometimes identify "functional pathology," recognizing that characteristic motor patterns have been altered under the influence of injury, fatigue, and/or abnormal compensations. We must therefore develop the ability to be accurate in reproduc i ng a functional profile of the injured segments, as well as the relationships of the segments to the whole. Compensations that can occur to the neuromusculoskeletal system allow us to adapt to both internal and external stressors. Some compensation can be normal, whereas others are abnormal and can be indicative of or create functional pathology. Part of the difficulty in de termining which compensations are normal and which are not demonstrates one of the central challenges of sports medicine. Gravity, ground reaction, and momentum are the primary drivers for functional compensations that can be influenced by extrin sic environments, as well as intrinsic causes, such as structural malalignment, strength, endurance, and flexibility of the con nective tissue. It is important to remember that all motion at all joints involves three planes: sagittal, frontal, and transverse, with appropriate neuromuscular control. Generally, each joint will have a dominant plane of motion for a given activity; however, injury can occur in a non-dominant plane. A typical example is the knee joint, which is primarily a sagittal plane dominant joint, but is often injured in the transverse or frontal plane. To evaluate and rehabilitate athletic injuries with intelligence, we must think in terms of a functional kinetic chain. The in jured tissue response needs to be predicted and evaluated with reference to ability to decelerate, stabilize, and accelerate specific functional athletic motions. A non-functional approach may try to initially isolate the injured tissue with inappropriate stretching techniques, exercises, and non-physiologic application of stress in an artificially designed, non-functional environment. This may ultimately inhibit the ability of the involved tissue to heal suc cessfully. As a result, this allows us to understand the integrated ground reaction force, center of body weight, muscle move ments, and other complementary forces. We can then success fully integrate the involved tissue into the entire kinetic chain system.


Pars interarticularis (Isthmus)

539

i.:.cu:...la:...r+-��iffI�

Superior art process process

A. Spondylolysis

B. SpondylOlisthesis

FIGURE 37.2. A fatigue fracture to the pars interarticularis is called (A) spondylolysis. When the fracture occurs laterally, (B) spondylolisthesis develops. (From Hamill J, Knutzen KM. Biomechanical Basis of Human Movement. Baltimore: Williams & Wilkins; 1 995: 3 1 0 [Figure 7- 22]. with permission.)

Somatic Dysfunction and Sports-Related Injuries

The following clinical examples demonstrate the importance of diagnosing and treating somatic dysfunction that accompanies four common sports injuries. Back Pain and Spondylolysis

Back pain is commonly seen in adolescent athletes. A spondylol ysis is a stress fracture of the pars-interarticularis of the posterior elements of the vertebrae (Fig. 37.2). It is most commonly seen at the L5 level and produces localized pain, especially with ex tension of the spine. The mechanism of injury is typically one of repetitive hyperextension stress; however, macrotrauma can also produce this injury. Patients typically p resent with central low back pain, which does not typically radiate into their legs. Pain may be reproduced with the patient bearing weight on a single leg and backward bending. Initial radiographs may show the classic "collar around the Scotty dog's neck" on oblique views, or they may be initially negative. A SPECT bone scan helps to confirm the diagnosis. I t is common to find significant somatic dysfunction along with this injury. Common areas of somatic dysfunction in this injury include: Iliopsoas spasm Flexed upper lumbar dysfunction • Sacroiliac/sacral torsion dysfunction • Innominate dysfunction • •

Iliopsoas Spasm

During the evaluation of gait, if the patient walks in a forward bent position, they may have an iliopsoas spasm (Fig. 37.3) . The following specific findings on physical examination may indicate this somatic dysfunction. A beltline that is low on one side may indicate the presence of a psoas spasm or short leg. A tight psoas may be associated with a flexed dysfunction in the upper lumbar spine (Ll). Pelvic side shift frequently occurs toward the side

540

VI.

Osteopathic Considerations in the Clinical Specialties ment of the psoas hypertonicity typically helps sacroiliac dysfunc tion. If significant sacral dysfunction is still present after treating the psoas, muscle energy, myofascial, or indirect techniques for the sacrum are useful. Dysfunction of the in nominates or pubes may maintain sacroiliac dysfunction. Do not forget that the ilium is the other half of the sacroiliac joint!

Treatment

Psoas major Ilium

II..'-----'-�....'-:'--Psoas ..k. minor

tendon �""'";:----Inguinal ligament

-,M--- Femur

FIGURE 37.3. Attachments of the right psoas major, psoas minor, and iliacus muscles. The psoas major crosses many articulations, including those of the lumbar spine and the lumbosacral, sacroiliac, and hip joints. The psoas minor does the same, except that it does not cross the hip joint. The iliacus, on the other hand, crosses only the hip joint. Psoas. (From Greenman PE. Principles of Manual Medicine. Baltimore: Williams & Wilkins; 1996:462 [Figure 20.15bl. with permission.)

of the longer leg or opposite to the side of the tighter psoas muscle. A tight iliopsoas resists hip extension. In a patient with spondylolysis, decreasing psoas hypertonicity is a priority. Many times, a Aexed Fryette type II dysfunction is commonly found in the upper lumbar region. Treating the Aexed lumbar component followed by stretching the tight psoas muscle accomplishes this. Care must be taken as not to apply excessive forces through the area of spondylolysis in accomplishing this.

The first goal of manipulative treatment in the acute spondyloly sis is to do no harm. Do notforget that this is afracture andfractures are treated with immobilization not manipulation! However, it is of paramount importance to relieve as much of the associated somatic dysfunction as possible. Gentle indirect techniques or muscle energy techniques may be appropriate. Tenderness at L5 and the iliolumbar ligament responds well to counterstrain tech niques. Myofascial release of the lumbosacral area can decrease pain and improve motion. Orthopedic treatment may include the use of a custom neu tral lumbar orthosis. This brace is typically worn around the clock initially, and then tapered as the patient improves over the next 6 to 8 weeks. Some athletes may still be able to practice or compete in the brace. Each case needs to be treated indi vidually. Repeat x-ray imaging or a thin-cut computerized to mography (CT) scan can help determine healing; however, the patient's symptoms typically guide the treatment. Watkins ( 1 4) describes the orthopedic management of spondylolysis in a vari ety of sportS. Consider the osteopathic approach to the patient with spondy lolysis and psoas spasm. Achieving appropriate muscle firing dur ing hip extension prior to strengthening is crucial. According to Janda's research (described by Dr. Philip Greenman) ( 1 5), the muscle-firing pattern for hip extension is: hamstrings, gluteus maximus, contralateral lower lumbar erector spinae, and their ipsilateral lower erector spinae (Fig. 37.4). "The most common al teration of this pattern is failure of activation and weakness of the gluteus maxim us, with substiturion by the hamstrings and erector spinae musculature, particularly in the upper lumbar and lower thoracic regions." OMT is a crucial component as the athlete retrains weakened abdominal and paraspinal muscles. Treatment of the thoracic, lumbar, and pelvic regions with OMT improves the activation of these patterns and sets the stage for appropriate rehabilitation.

Hip Joint Extension

�

Sacroiliac/Sacral Torsion Dysfunction

Sacroiliac dysfunction is also commonly present. The type of sacroiliac dysfunction is variable. A sacrum that freely extends is typically more painful and harder to treat. It may be related to Hexed lumbar dysfunction or A-P curve problems. A bilaterally Aexed sacrum is seen with an increased lumbar lordosis. Treat-

Thigh toward pelvis FIGURE 37.4. Hip joint extension. (From Kendall FP, McCreary EK , Provance PG. Muscles Testing and Function with Posture and Pain, 4th ed. Baltimore: Williams & Wilkins; 1993:20, with permission.)

37.


541

Anterior Knee Pain

Anrerior knee pain is a common finding in the athletic popula tion. There are many enrities that are grouped in this category. These include: patellofemoral pain syndrome, chondromalacia of the patella, miserable malalignment syndrome, and patellar tracking abnormality, to name a few. This painful condition is a spectrum of overuse; however, occasionally there may be a trau matic insult that starts the process. Overuse may result from training errors or underlying malalignment. Overload is charac terized by abnormal tensions across the patellofemoral joint with resultanr inAammation and microinjury. As the p rocess conrin ues, the cartilage on the under surface of the patella becomes softened and somewhat eroded away. Patienrs complain of an terior pain around the patella with a variable amount of local swelling. A common complainr is that the knee is painful with activity, especially negotiating stairs or hills. The knee will lock temporarily if the patienr was sitting for a while and then stands up. This is called the "theatre sign," and it is pathognomonic ( 1 6). During examination of the patellofemoral joint, it is common to palpate crepitation when motion is introduced to the patella. The trad�tional orthopedic examination of the patella looks for ballotmem (effusion) , lateral laxity, and the "patellofemoral grind test." This test is performed by having the supine patient con tact their quadriceps while an inferior pressure is applied on the patella. This test generally hurts the patient. Skilled hands can pal pate subtle amounrs of crepitation, excessive motion, and tracking abnormalities throughout Aexion and extension. The osteopathic palpatory examination not only palpates for restrictions of patellar motion and crepitation but also for the abil ity of the vastus medialis oblique muscle to "turn on." Atrophy, Aaccidity, or inhibition of this muscle is common in this condi tion. The muscle may become neurologically inhibited from axial somatic dysfunction or inhibited due to pain or disuse. Whatever the cause, the first step in rehabilitating these patienrs is to gain the ability of this muscle to fire. Associated physical findings of this condition also include in creased hamstring tension, fibular motion restriction, and in terosseous membrane tension. Increased tension of the ham strings will increase pressure between the patella and femoral condyles (Fig. 37.5). This can aggravate inAammation and car tilage damage at the undersurface of the patella. Increased ten sion in the biceps femoris, iliotibial band (ITB), and lateral fas cia of the thigh can cause motion restriction of the fibula and interosseous membrane. This constellation of findings is com monly seen in patellar tracking abnormalities. Subtle restrictions of fibular motion can be appreciated by translating the proximal fibula or lateral malleolus anteriorly or posteriorly. Interosseous membrane tension can also be assessed through internal and ex ternal rotation of the tibia and fibula. OMT can be applied to these dysfunctions with retraining of the vastus medialis muscle, thus improving hamstring and ITB tension.

Rotator Cuff Tendonitis/Im pingement Syndromes

Rotator cuff tendonitis and subacromial bursitis are corrunon sports medicine diagnoses. The history can help pinpoint the

FIGURE 37.5. Patellofemoral compression. A functioning quadriceps mechanism is necessary for proprioceptive control of the knee. The static stability provided by the cruciate ligament protects the patellofemoral mechanism and the menisci, and stops the femur from being driven into the tibia in deceleration and descending movements. (From Baker Cl. The Hughston Clinic Sports Medicine Field Manual. Baltimore: Williams &Wilkins; 1 996: 228 [Figure 20-9]. with permission.)

diagnosis in upper extremity complaints. For example, pain into the deltoid insertion at night may indicate a rotator cuff tear. A clicking or snapping deep in the shoulder may indicate a labrum tear. Apprehension with external rotation may indicate instability. It is important to realize that although these are common con ditions, not all shoulder pain is due to rotator cuff problems. So matic dysfunction plays a major role in the pathogenesis of shoul der pain. In young healthy patiems, most shoulder complaims are due to abnormal muscular tensions or forces across the pec toral girdle. Occasionally, bony abnormalities, fracture, arthritis, infections, or tumors are diagnosed. Injuries to the glenohumeral joint almost always lead to a restriction of motion. Consider the entire pectoral girdle and axial spine when assessing these injuries and conditions. Impingement syndromes can occur due to multiple factors. The space between the undersurface of the acromion and humeral head is called the impingement interval. This space narrows with arm abduction (Fig. 37.6). Any condition that further narrows this space can cause impingement. Several classification systems have been described. Neer ( 1 7) described three stages of injury based on patient age and pathologic changes in the rotator cuff. Impingement syndromes can also be divided into external and internal impingement. In external impingement, there is not enough room under the acromion for the supraspinatus tendon to glide freely. An example of this is outlet obstruction, where an arthritic spur or anatomic variant at the acromion may narrow the space. This usually occurs in patients older than 35 years of age. Another factor may be postural, where protracted (rolled forward) shoulders, weak cuff muscles, and poor humeral head depression cause a limited subacromial space. A common internal factor that causes impingement includes instability of the glenohumeral j oint. This usually occurs in pa tients less than 35 years old, and may be associated with a su perior glenoid labrum tear (SLAP lesion), a fracture (Bankarr lesion), or a depression-type fracture of the humeral head

542

VI.

Osteopathic Considerations in the Clinical Specialties Acromion process

Clavicle

Subacromial bursa

A. Normal

Supraspinatus \

,, ;

B. Abduction

"

J I

, I I ,

I I I J

compressed between bone and soft tissue

FIGURE 37.6. Supraspinatus/Impingement. (From Anderson MK. Hall SJ. Fundamentals of Sports Injury Management. Baltimore: Williams & Wilkins; 1997:405 [Figure 11.16]. with permission.)

( Hill-Sachs deformity). This impingement occurs more distal to the acromioclavicular j oint. Overuse, instability, and micro trauma contribute to this condition. The most common form of instability is anterior and inferior. The deficiency is in the anterior inferior glenohumeral ligament complex. Posterior, inferior, and multidirectional instabilities also occur. T here are specific tests for each of these. Diagnosis of the Somatic Component W hether or not there is an axial (spine and torso) component to the patient's complaint, it is prudent to include evaluation of the upper thoracic and cervical spine, the costal cage, and internal organs of the chest and abdomen in each patient with an upper ex tremity problem. The patient's history will occasionally steer the physician to the workup of visceral disease referring pain to the upper extremity. The physical examination, including palpation of the upper extremiry for evidence of somatic dysfunction, will elucidate the diagnosis. Occasionally, cardiopulmonary disease may be the cause of the somatic findings and pain in the upper thoracic spine and upper extremity. It is not uncommon to find somatic dysfunction between T 5-9 due to a viscerosomatic reflex from stomach or duodenal inflammation secondary to the pro longed consumption of nonsteroidal antiinflammatory medica tions that are often used to relieve the pain in the upper extremity. Even after resolution of upper extremity pathophysiology, persis tence of upper extremity pain may be due to referred visceral

pain or upper and/or mid-thoracic viscerosomatic dysfunction. This, of course, requires further evaluation and treatment of the visceral component of the problem. In addition to the upper extremities, the upper thoracic and cervical spine are important areas to palpate and evaluate for so matic dysfunction. The upper thoracic cord, especially at levels T l -4, supplies sympathetic efferents to the head, neck, and up per extremities. These efferents are involved in the regulation of blood flow and also innervate the musculature, modulating muscle tone ( 1 8) . Additionally, afferent fibers from the cervical spine and paraspinal soft tissues synapse in the upper thoracic spinal cord (intermediolateral cell column) . Somatic dysfunction in the cervical region causes increased afferent input into the up per thoracic spinal cord. This can, in turn, facilitate upper tho racic sympathetic hyperactivity and contribute to upperextremity dysfunction. Most mechanical neck problems are accompanied by identifiable upper thoracic and upper extremity somatic dys functions that are partly through this mechanism. Upper tho racic sympathetic hyperactivity (often from levels T2 and T3) can refer pain, tingling, or abnormal temperature sensations to the arm. W henever there is a dysfunction in any one part of the neu romusculoskeletal system, it is imperative to evaluate the entire kinetic chain as a dynamic unit of function in posture and mo tion. Investigating along these lines would lead the osteopathic physician to ask: Are there abnormal neurologic reflexes or asymmetric muscle strength, tone or size? II. Is there evidence of joint dysfunction? 111. Is postural imbalance contributing to the problem or com plaint? IV. Is the painful extremity on the concave or convex side of a spinal dysfunction? v. Is there evidence of compensation contributing to spinal or extremity dysfunction? I.

Dysfunction in the upper extremity will also affect scapular position and motion (Fig. 37.7). Somatic dysfunction of the up per thoracic spine and ribs can also affect scapulohumeral rhythm and scapular position. Smooth, efficient movement of the scapula and coordinated strength of the scapular stabilizing muscles are necessary to prevent upper quarter dysfunction (including rotator cuff problems). Cervical spine diseases (i.e. , herniated disc, osteoarthritis, stenosis) may refer pain to the upper thoracic region, shoulder, arm, and hand. Somatic dysfunction of the lo'wer cervical and cervical-thoracic junction can produce arm symptoms through three mechanisms: Direct irritation of cervical spinal nerves Neurovascular compression (thoracic outlet syndromes) • Myofascial restrictions resulting in lymphatic obstruction

• •

OMT directed at somatic dysfunction of the upper thoracic spine and ribs, cervical spine, and then to the myofascial struc tures of the pectoral girdle and arm is an important component of treatment in patients with rotator cuff disease.

37.


543

MOVEMENTS OF THE SCAPULA

Elevation

� { ' _.

Anterior tilt

�

Upward rotation

� . �

noid cavity

Downward rotation

Medial rotation of inferior angle

/ �

Lateral rotation of inferior angle

FIGURE 37.S. Inversion Ankle Sprain. (From Baker CL. The H ughston Baltimore: Williams & Wilkins; 1996:240 [Figure 22-1 J. with permission.) Clinic Sports Medicine Field Manual.

Depression

FIGURE 37.7. Scapular Motion. (From Kendall FP, McCreary EK, Provance PG. Muscles Testing and Function with Posture and Pain, 4th ed. Baltimore: Williams & Wilkins; 1993:16, with permission.)

Inversion Ankle Sprain

Ankle sprains are the most common athletic injury. They make up 45% of all injuries in basketball, 3 1 % in soccer, and 25% in volleyball. I nversion-type ankle sprains make up 85% of all ankle sprains ( 1 9) . The ankle i s a hinge type of synovial joint. The distal ends of the tibia and fibula form a "mortise" into which the superior aspect of the talus fi ts. The talus is wider anteriorly than posteri orly (wedge-shaped) . Plantar Aexion decreases the stability of the ankle because the anterior aspect of the talus is no longer wedged between the malleoli . Because of this anatomy, most ankle in juries occur in the plantar Aexed position. Ankle injuries should be assessed as soon as possible after the injury befote swelling commences. Because less than 1 5% of ankle injuries are found to result in significant fracture, the Ottawa ankle rules were devel oped to guide clinicians as to when to obtain a radiograph (20). Supination (inversion) stresses the lateral ankle ligaments (Fig. 37.8). Most inversion sprains occur with the ankle in the plantar-Aexed position. Various physical tests are used for assess ing the ankle ligaments. Palpable tissue texture changes are usually found over the injured ligament(s). Palpation for tissue texture changes is very valuable, especially when the patient is experienc ing too much pain to tolerate stress testing for ligament integrity. Tears of the anterior talofibular ligament are very common and are likely if the talus may be moved forward (and into slight inter nal rotation) 4 mm or more on physical testing. This test is called

the anterior drawer test. The ability to tilt the ankle or invert it more than 25 to 30 degrees implies rupture of the lateral liga ments. Grading ankle sprains is based on clinically determining if a minor incomplete, moderate incomplete, or total rupture of the lateral ligaments has occurred. The medial deltoid ligament is strong and thick; injury to it usually results in a bony avulsion. Always palpate for bony pain, crepitation, or point tenderness when considering a potential fracture. Most ankle sprains will be associated with dysfunction of the lateral malleolus and, frequently, with restrictions at the fibular head. Restriction at either the proximal (head) or distal (lateral malleolus) end of the fibula can alter normal ankle motion and produce pain and dysfunction in both the ankle and the knee, increasing the amount of time to recovery. A key mobilization to help restore fuJI range of motion is the "Talar Tug," where the talus is distracted from the calcaneus, allowing a resetting of the articular facets. The venous and lymphatic drainage must travel through my ofascia I structures associated with the ankle, knee, and hip on their way back to the heart. Dysfunction in any of these structures can disrupt both lymphatic and venous drainage and interfere with healing. Prolonged swelling alters the proprioceptive ability of the ankle and may predispose this area to further injury. Address ing somatic dysfunction may assist in the removal of swelling from the area and may ultimately speed the recovery from such lIl)unes. Consider the individual's gait biomechanics in their ankle re habilitation. When the heel first strikes the ground, the foot is in the supinated (inverted) position. As the body's weight is trans ferred an teriorly, the foot pronates (everts) . A Aat foot is frequently associated with over pronation (foot eversion). This will place excessive stress on the ligaments of the medial ankle and may

544

VI.

Osteopathic Considerations in the CLinical Specialties

lead to pain in this area. An excessive range or rate of ptonation may also be associated with shin splints. A high arch is frequently associated with excessive supination (foot inversion). This will place excessive strain on the ligaments of the lateral ankle and may lead to lateral foot pain. A useful manipulative approach in the acute ankle sprain uses myofascial and indirect techniques. As the swelling subsides, mus cle energy, articulatory, or other direct techniques can be used. For persistent ankle pain after an inversion injury, a direct myofascial release of the medial deltoid ligament and fascial structures seems to work well. OMT is useful to decrease edema and pain, allow ing the patient to begin a functional ankle rehabilitation program sooner. It is also useful to treat secondary symptoms (such as low back pain) that can occur from a change in gait after an ankle IIlJury.

PRINCIPLE CENTERED REHABILITATION

Principles are natural laws that, for the most part, are intuitively obvious. We hope that by introducing you to principles rather than practices and describing the principles behind some of the practices, you will be better prepared to handle the current chal lenges of sports medicine rehabilitation, as well as the unknown challenges of the future (2 1 ) . We hope to be able to prepare you to handle each patient and the situations unique to each patient. This approach tends to orient you away from a particular treat ment protocol and will provide you with a philosophic approach that will hopefully allow your patients to have outstanding func tional outcomes. Inherent in this process is differentiating between "treatment" thinking versus "preventive" thinking. Sports medicine clinicians need to avoid falling into the trap of "treating symptoms" and initiate a reevaluation and reprogramming process that prevents the injury from recurring. IdentifY the root cause of the injury and orient the rehabilitative process to attack the root cause rather than simply treating the symptom of the injury. Be cognizant of the natural laws taught in the disciplines of anatomy and physiology, which includes biochemistry and the biomechanics that govern successful (Of unsuccessful) function of the neuromusculoskeletal system in the perfofmance of the sport being played. These natural laws usually cannot be violated with impunity, or dysfunction and/or injury will occur. The more physiologically aligned our athletes are with these basic principles, the less the opportunity for injury and the greater the chance for success. Albert Einstein once said, "The significant problems we face cannot be solved by the same level of thinking that created them." We must be able to transform our patients to a new level of func tion to successfully reintegrate them into sports-related activities and prevent reinjury. Functional Approach

As we begin to approach the strategy for the design of a func tional rehabilitative process for our injured athletes, it is useful to think of the locomotor system as a "kinetic chain." Some things that are part of this chain include, but are not limited to, the

joints, muscles, bones, and proprioceptors that help to guide our patients in successful athletic activities. As such, we must begin to appreciate that there is a strange relationship between the cause and the cure of injuries. The ultimate goal of rehabilitation of an injured athlete is to return the injured individual back safely to the activity that directly contributed to the injury! In general, athletes enjoy having the opportunity to return to the activity that originally caused their pain in a successful and pain-free manner. Therefore, a vital component of the functional rehabilitative environment will actually be the causative activity. Therein lies the challenge of rehabilitation . . . to transform the cause into the cure. This transformation is the rehabilitation. Through reha bilitation, we must transform the injured tissue into tissue that successfully deals with the loads and motions of the causative ac tivity. We must reintegrate the injured tissue into a more effective and efficient functional chain reaction system. For this transformation and reintegration to occur and be suc cessful, a logical progression of clinically controlled techniques that are symptom and performance directed must be accom plished. Intelligent management of these techniques requires and is based on a strong biomechanical understanding of the kinetic chain and the pathophysiology of injury. Central to the understanding of kinetic chain muscle func tion in the locomotor system is understanding the concept of an oxymoron-a unique combination of two incongruent qualities juxtaposed to form a more meaningful concept. To wit, the in tegrated use of opposite words provides an understanding syner gistically greater than the combined understanding of each word used in an isolated manner. " Functional oxymorons" provide us with the necessary foundation to design and manage biomechan ically reactive rehabilitative environments (i.e., "causative cure"). The isolation of a soft tissue in an integrated system begins to describe the concept of "integrated isolation" (another functional oxymoron). Initially, one must isolate the involved tissue to fully understand the site of injury, the extent of injury, and the effect of injury. Concurrently, one must appreciate the actual function of the involved tissue and how its integration into the functional compensation system allowed for the excessive mechanical load ing of the tissue and the resultant injury. To determine the integrated isolated function of this tissue in the kinetic chain, what this tissue does in real life must be com prehended in a practical sense. The following questions need to be addressed and answered to appreciate the causes and compen sations resulting in tissue failure: I. To what forces does the tissue react? II. What joints and motions does the tissue decelerate, stabilize, and accelerate? Ill. In what planes and with what other tissues does it function? IV. How does the tissue dynamically integrate its isolated function? •

Answering these inquiries will lead to the successful design of the appropriate functional environment for rehabilitation, help ing to transform the injured tissue into healthy tissue, and then reintegrate it into the functional system. Therefore, the rehabilitative strategy is to design the envi ronment to facilitate the appropriate reaction of the target tissue

37.

with functional, progressive exercises and appropriate therapeutic modalities. This is controlled clinically by modulating the stress and strain of the activity, controlling the joints that dominate the activity, and determ ining in what plane the reaction/action predom inantly takes place. Compensations

Compensatiol1 occurs in the neuromusculoskeletal system that allows us to adapt to both internal and external stressors. Some compensation can be normal; however, others are abnormal and can be indicative of or create functional pathology. Part of the difficulty in determ ining which compensations are normal and which are abnormal demonstrates the cause and effect relation ship between functional activity and the resultant compensations. Gravity, ground reaction, and momentum are the primary drivers for functional compensations. Footwear and various orthotic in terfaces are examples of extrinsic environments that a functional system can react with and compensate for. Compensations can be caused by interacting with various forms of equipment, ther apeutic or otherwise, as well as types of terrain (playing fields, etc.). Structural malalignment abnormali ties are examples of intrin sic causes of compensations. Intuitively, the strength, endurance, and flexibility of the connective tissue h ave a direct effect on the compensation of the linkage system. Additionally, balance and other neuromuscular considerations, such as proprioceptive ability and muscle tone, have a dramatic effect on function and functional compensation. Determining the actual cause or causes of the compensation and what relationship the compensation has to the contribution of excessive mechanical loads to the involved tissue is the major task of the biomechanical evaluation. Un derstanding the potential causes and resultant compensation is based on the biomechanics of function and the timing of func tion. This understanding allows for more effective treatment of the causes of the injury and the resultant compensations, as well as the symptoms (pain). Real World Muscle Function

Clinicians typically describe muscle function in three ways: con centric, eccentric, and isometric. We think of a concentric mus cular contraction as a functional shortening of the muscle while it contracts. Eccentric contraction is a functional lengthening of the muscle while it contracts. Isometric contraction is a stabiliz ing force during which neither shortening nor lengthening of the muscle occurs. As we begin to understand the real world function of muscles and gtoupS of muscles , we begin to understand that muscles may function concentrically at one joint , eccentrically or isometrically at another joint, or in another plane at the same joint at the same time. This occurs within the kinetic chain, reacting with and against gravity, ground reaction, and momentum, in multiple planes of motion. This concept of chain reaction muscle function is best summed up in the phrase "econcentric." This concept of econcentric muscle function allows clinicians to understand the causes and compensations of both acute and overuse injuries and gives us an enhanced ability to determine the appropriate


545

econcentric reaction of the injured tissue to facilitate healing and enhance function. To intelligently rehabilitate injuries, we must know not only what the affected tissue is doing during the activity that con tributed to i ts breakdown, but also what it does, when it does, and why it does. As previously noted, we must also know how the involved tissue is integrated into the entire kinetic chain system. Pronation and Supination

Understanding pronation and supination gives us a head start in our thought process to determine potential causes of dysfunction and the resultant symptoms. Understanding functional chain re action pronation and supination gives us the ability to begin to determine which dynamic compensations are normal and which are abnormal. This also allows us to understand the integrated isolated function of the involved tissue with the other tissues that synergistically work in the kinetic chain with the symptomatic tis sue. This understanding also allows us to begin to take advantage of the concept of econcentric muscle function. Pronation is a collapsing of the chain, while supination is a re girding of the chain. Pronation is shock absorption, while supina tion is propulsion. Pronation is a reaction caused by the effects of gravi ty and ground reaction forces. Supination is a reaction resulting from pronation. Pronation succumbs to gravi ty, while supination overcomes gravity. The transformation of pronation into supination is the key to the success of the locomotor system in sport movement. Pronation and supination occur at all joints and in all planes of motion of the locomotor system. Remember that pronation and supination many times have more to do with the timing of motions at certain joints and in certain planes than with the actual amount of motion of the joint. Pronation is dominated by eccentric (deceleration) muscle function. Supination is dominated by concentric (acceleration) muscle function. Therefore, the transformation of pronation into supination is dominated by isometric (stabilizing) and econcen tric muscle function-deceleration of motion at one joint and acceleration of motion at another joint or in another plane, all at the same time. Osteopathic Manipulative Therapy and Rehabilitation

Somatic dysfunction frequently develops in the human neuro musculoskeletal system in the course of adapting to the relent less force of gravity. The athlete's ability to adapt is additionally challenged by the particular demands of his or her sport. OMT is a vital step to restore balanced structure and function. Once structure and function have been improved, comprehensive neu romuscular retraining as previously described can be undertaken. The Success Imperative

Successful rehabilitation depends on the ability to take advantage of just the right amount of motion, at just the right joint, in just the right plane, in just the right direction, at just the right time. A basic principle of functional rehabilitation is to allow the patient ro be successful and ro allow this success to ultimately transform

546

VI.

Osteopathic Considerations in the CLinicaL SpeciaLties

into the ultimate goal of returning the athlete to his or her sport. However, we must remember that the health and safety of the athlete is our primary concern. Our ability to successfully return athletes to the environment of sport is based on the integrative findings of the comprehensive biomechanical examination and an in-depth understanding of the pathophysiology of injury, as well as the loads and motions of the particular sport. We must be always mindful that the examination, diagnosis, and treatment of an athletic injury include a dialogue between two human beings, involving physical, physiologic, and psycho logical linkages. Th is is a complex transaction that, when skillfully performed, can result in a profound and long-lasting effect. The clinician interested in neuromusculoskeletal medicine quite lit erally has at his or her fingertips an extensive document of the patient's history, including indications of general health and the extent of structural adaptation to the environment, as well as challenges produced in the pursuit of sport.

CONCUSSIONS, HEADACHES, AND NEUROLOGIC DEFICITS IN ATHLETES

Headache is the most comrpon neurologic disease. Hippocrates was the first physician to describe a sports headache. The inter national headache society describes 1 3 categories of headaches and about 1 50 headache syndromes. In the young athletic pop ulation, there is about a 35% incidence of headache. A slightly greater incidence ofheadache (46%) is described in young athletic males. This is li kely secondary to higher numbers of males partic ipating in contact sports. When evaluating an athletic headache, it is important to rule out other forms of headache, which may be secondary to medication, intracranial mass, sinusitis, or other medical ailments. The most common sports headache is the effort headache. T here is an equal incidence in both males and females. This is felt to be secondary to increased intracranial pressure associated with athletic effort. It typically has a rapid onset and is described as a frontal or bi-frontal type of headache. Duration can be from several minutes to up to 24 hours. Another common sports-related headache is the cervicogenic headache, or headache related to cervical sprain. This is felt to be secondary to stretching of cervical ligaments and tendons, which results in a reAex muscle contraction, or spasm, of the paracervical musculature. This headache is probably more common in males, and is frequently associated with combative sports, such as foot ball, boxing, wrestling, or marcial arts. Because of the tremendous forces generated in luge and bobsled, this headache is also fre quently described in these athletes as well. Typically, patients will complain of pain in the upper cervical, occipital, and/or parietal regions, and the pain may last for several days or weeks. Acute effort migraine may also occur in athletes. This typically follows short, intense activity. Mechanism for this is unclear, but is felt to be related to decreased cerebral CO2 secondary to hy perventilation, which results in vasoconstriction. Contributing factors may also include caffeine use or discontinuance, poor nu trition, dehydration, head load, hypoglycemia, and alcohol use. I nterestingly, similar to the refractory period that can be induced

in exercise asthma, a gradual warm-up may help in prevention by inducing this "refractory period" with respect to migraine. A trauma-triggered migraine is initiated by head trauma and is found to be more common in athletes with a prior history of migraine headache. This is seen more commonly in contact or collision sports, and usually responds to the patient's typical treat ment for migraine. Posttraumatic headache may also occur in athletes and is more common in males that are involved in contact and combative sports. It is important to note that the intensity of headache may not be related to the severity of trauma, and that this is a headache that is also often associated with concussion. Duration of this headache may be from hours to weeks. One of the biggest issues facing the sporTS medicine clini cian is concussion. Sports that are at highest risk for concussion include football, gymnastics, ice hockey, and wrestling. In U.S. football alone, 250,000 head injuries are estimated per year. Un fortunately, there is no universal agreement on the definition of concussion or the various grades or severity of concussion. As a result, multiple different evaluation systems have developed (Ta ble 37. 1 ) . Some athletes may develop post-concussive syndrome, which can include on-going headache, headache with exertion, dizziness, fatigue, irritability, impaired memory, and decreased concentration. This is felt to be most likely secondary to altered neurotransmitter function posttraumatically. Decisions governing return to sports after head injury most often lies with the primary care physician (22). There are a num ber of clinical guidelines in the literature that are intended to help physicians. The guidelines (Table 37. 1 ) most widely accepted are those proposed by Cantu (23, 24), by the Colorado Medical So ciety (25) , and by the American Academy of Neurology (26) . None of these guidelines are based on prospective studies. Cur rently, there is no consensus in the sports medicine community as to which guidelines are most appropriate. Further leading to confusion, a recent study by Lovell (27) questions the validity of guidelines that use loss of consciousness as a marker of concussion severity in return-to-play decisions. The long-term health and the prevention of secondary neuro logic injury to the athlete should be the only concern that guides return-to-play timing and permission from the team physician. The restriction from play of any athlete with persistent symptoms is generally accepted (22 ) . To avoid second-impact syndrome, re turn to contact sportS should only be allowed after the athlete is asymptomatic both at rest and with exertion. Further, repeat concussions generally require a longer period of asymptomatic rest, although the exact amount is unclear. A number of stud ies have demonstrated that neuropsychiatric testing, through a battery of tests, can detect cognitive impairment after mild trau matic brain injury (28-32). Any athlete with repeat concussions ' should probably undergo multidisciplinary evaluation, including neuropsychiatric testing prior to return to play. In general, athletic headache management strategies include both an acute management component and a prophylactic com ponent. The pathophysiology is felt to be secondary to a num ber of factors, including the so-called neuroinAammatory model, with vascular involvement, as well as stimulation of nocicep tive nerve fibers. Management strategies include both non-drug

37.


547

TABLE 3 7 . 1 . G U IDELINES FOR RETURN TO PLAY AFTER CONCUSSION Concussion Grade Cantu (23, 24) 1 (mild)

Features

Management

No loss of consciousness; posttraumatic amnesia < 3 0 min.

Remove from contest; observe on sidelines.

2 (moderate)

Loss of consciousness 3 0 min.

Remove from contest and disallow return that day; athlete should be evaluated by a neurologist at a medical facility; cervical spine precautions as indicated.

3 (severe)

Loss of consciousness >5 min OR posttraumatic amnesia > 24 hrs.

Transport athlete to nearest hospital with neurosurgical facilities with head and neck immobilization; admit to hospital and check for intracranial bleeding .

Colorado Medical Society (25) No loss of consciousness; 1 (mild) confusion without amnesia.

2 (moderate)

No loss of consciousness; confusion with amnesia.

3 (severe)

Any loss of consciousness.

American Academy Neurology (26) No loss of consciousness; 1 (mild) transient confusion; concussion symptoms 15 min. Any loss of consciousness, either brief (seconds) or prolonged (minutes).

Remove from contest; examine immediately and at 5 min intervals for development of mental status changes or postconcussive symptoms at rest with exertion. Remove from contest and disallow return that day; examine on site frequently for signs of evolving intracranial pathology.

Transport athlete to nearest ER by ambulance with cervical spine precautions; CT scan or MR imaging if symptoms worsen or persist > than 1 week.

Remove from contest; examine immediately and at 5 min intervals for development of mental status changes or postconcussive symptoms at rest and with exertion. Remove from contest and disallow return that day; examine on site frequently for signs of evolving intracranial pathology. Transport athlete to nearest ER by ambulance with cervical spine precautions; CT scan or MR imaging if symptoms worsen or persist > 1 week.

Return to Play

May return if asymptomatic"; second grade- 1 : May return in 2 weeks if asymptomatic for 1 week; third grade-1: terminate season, may return next year if asymptomatic. Return after asymptomatic for 1 week; second grade-2: wait at least 1 month , may return then if asymptomatic for 1 week , consider terminating season; third grade- 2: terminate season, may return next year if asymptomatic. Wait at least 1 month, may return if asymptomatic for 1 week; second grade-3: terminate season , may return next season if asymptomatic.

May return if asymptomatic at least 20 minutes; second grade-1 in same contest: disqualify athlete for that day; third grade-1: terminate season. May return after 1 full asymptomatic week; second grade-2: return to play after 1 month symptom, consider termination of season; third grade- 2: terminate season. May return after 1 month if asymptomatic for at least 2 weeks; second grade-3 : terminate season, return to any contact sport seriously discouraged. May return if symptoms clear

0

/

Explanation

Y===

�

Fascial Pattern i n g

including elements important in the osteopathic hospital screen ing examination. Example: Screening Examination of the Musculoskeletal System of the Ambulatory C linic or Ambulatory Hospitalized Patient

A 3- to 5-m inute osteopathic strucrural screening examination is part of the standard history and physical examination per formed by osteopathic physicians on all patients. To help the

physician develop an organ ized approach to an osteopathic struc tural examination, sample screening examinations are provided for outpatients, ambulatory inpatients (Table 44.3), and hospi � talized patients unable to stand (Table 44.4). Only the positions in which the patient was examined and the presence or absence of spinal curvatures need to be added to make the recording fit AOA standards. Often an office patient comes to the osteopathic physician because they think they have a m usculoskeletal problem. They believe this because there is pain near the spine or in an extremity or the head. The physician must determine if there is a primary

TABLE 44.4. SCR E E N I N G M USCULOSKE LETAL EXAMI NATION FOR THE HOSPITALIZED PAT I E N T Tests

Test Results

Explanation

Neg.

Pos.

This screens shoulder, el bow, forearm, and wrist motion combi nations . Positive = unable to bring arms above the head with the u pper arms touch i n g ears and the backs of the hands together. If any joint tests positive, do a more focused exa m i nation of that restricted joint and check the u p per thoracic region for somatic dysfunction .

Screen for Body Fascial Patterning

Neg.

Pos.

Screens rotation preference of the fascias at specific reference areas. This was described by Gordon Zink. Regional sites = occipitoatlantal, cervicothoracic, thoraco l u m bar, and l u m bosacra l . Positive = uncompensated-motion preference does not alternate one region to next. Compensated-preference alternates from one region to the next. U ncom pensated pattern-this pattern is the g reatest h i ndrance to f l u i d motion in the body. Compensated pattern-poses less obstruction to fluid flow. Correlate with sites of congestion; next step-segmental d i agnosis and manipu lative treatment of somatic dysfunction present.

Col lateral Ganglion Palpation

Neg.

Pos.

Screens for collateral ganglion tenderness i n d icating dysfunction of orga n groups segmenta lly innervated with i n the g a n g l ion-celiac, superior mesenteric, or i nferior mesenteric. Positive = Palpable tissue texture change and tenderness of g a n g l i o n area. Correlate this with the organs that receive sympathetic innervation from prega ngl ionic fibers that synapse i n the tender gangl ion. Correlate collateral g a n g l ion tenderness with their related organs and the patient's history. Look for more specific signs; may need laboratory testi n g .

Neg.

Pos.

Screens f o r dysfunction o f organ groups and is more specific than the collateral ganglion screen. Positive = palpable asymmetry of paraspinal tissue texture and related joint motion; tenderness is usua lly present. Head and neck Heart and l u ngs U p per gastrointestinal (ga l l bladder [GBj-right [Rj, l iver-R, pa ncreas-Ra, spleen-left [L]. stomach-L, duodenum-L) Small intestines, proximal colon, adrenal, kidneys, upper half of ureter, gonads Distal colon, lower half of ureter, bladder, pelvic organs Correlate f i n d i ngs with visceral dysfunction; next step rib ra ising

Screen Joi nts of the Upper Extremities

",

,

,

.... .. . - - - - .. .

� ' + .'

..

. . _ _ . . .

-

Celiac ganglion

n.-'---ir-r- Sup. mesenteric ganglion Inf. mesenteric ganglion

Anterior view Paraspinal Segmental Palpation

�

T 1 -4

T 1 -4 T 1 -6 T5-9

T 1 0- 1 1

T 1 0-1 1

T 5-9

T 1 2-L 2

T 1 2-L1

Th is is a n AP transpare n t d i a g ra m w i t h s p i n a l l a n d m a rks superim posed. Parasp i n a l p a l pation i s performed o n the poste rior side of the body. (continued)

654

V[{ Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment

TABLE 44.4.

(continued) Test Results

Tests

Screen Joi nts of the Lower Extre m ity

Neg.

Pos.

Active Passive ... . . . .

Explanation

Screens h i p, k nee, a nd ankle combinations. Positive = restricted flexion of h i p or knee or dorsal flexion of the a n k l e . Normal = at least 90 . If a ny joint tests positive, do a more focused exa m i nation of that restricted joint and check the upper thoracic region for somatic dysfunction .

Leg Flexion 'Some bel ieve that the pancreatic reflex can be found bilateral ly, (i.e., right and left). Protocol of W.A. Kuchera.

musculoskeletal problem or if there is pain in the m usculoskele tal system being referred from the viscera, vasculature, or cen tral nervous system. The physician also has the opportuniry to find musculoskeletal dysfunctions that may hinder the patien t's recovery or abiliry to stay well after healing. The screening ex amination for ambulatory patients considers all key areas of the musculoskeletal system and i ncludes a screen for musculoskeletal clues of possible viscerosomatic dysfunction (Table 44.3, Collat eral Gangl ion; see also Table 44.4, Chapter 7 1 , Fig. 7 1 . 5). The data obtai ned from this exam ination can be used to help for mulate a plan that incl udes providing osteopathic manipulative support for the patient with primary and/or secondary somatic dysfunction.

Example: Screening Musculoskeletal Examination of a B edridden C linic or B edridden Hospitalized Patient

(See Chapter 7 1 , Fig. 7 1 . 1 .) Treatment of somatic dysfunctions in the hospital is directed toward support of the patient's own homeostatic mechan isms. I f the patient does have a primary musculoskeletal problem, it is usually obvious and the examination can be altered accordingly (Tables 44.3 and 44. 4) . I n the present health care environment, people are usually hospi tal ized for delivery, major surgery, a systemic disorder, or a disease. A musculoskeletal screening exami nation may seem to be useless unless the patient is an orthopedic patient. However, treatment of the musculoskeletal system of hospitalized patients is more often used to support the patient's autonomic, vascu lar, and immune systems. The presence of a somatic dysfunction locates spinal regions that are not functioning properly. These regions can then be examined segmentally to identifY specific so matic dysfunctions, and via the physician's physiologic and func tional neuromusculoskeletal knowledge, it can be determ ined i f they could have a bearing o n recovery o f the patient fro m their present dysfunction. These somatic dysfunctions are often associ ated with related facilitated spinal cord segments, resulting from contin uous or frequently occurring somatic or visceral dysfunc tions in localized regions (see Chapter 7 J , Fig. 7 1 . 5 ) .

Hospitalized patients are often unable t o move or change po sitions com fortably and the screening exam inations must take that i n to consideration and not be so extensive as to tire the pa tient. Primary musculoskeletal problems do not currently lead ' to a large number of admissions to the hospital. Most pa tients are not in the hospital for primary musculoskeletal dis orders; secondary involvement of the musculoskeletal system, however, is common. The osteopathic examination integrates m usculoskeletal findings, viscerosomatic reAexes, and other tis sue texture changes with a thorough history and standard phys ical examination, providing a comprehensive clinical approach and unique i nsights into the differential diagnosis of the pa tient's present health level. Detailed knowledge of functional anato my, visceral innervation, the importance of the sympa thetic and parasympathetic components of the nervous system, and awareness of factors involved in the efficiency for lymphatic drain age helps the physician decide where to focus the physical examination ( 1 1 ) . Key regions involved in the homeostatic bal ance of a patien t are evaluated to determine if musculoskeletal fi ndings could be related to the health status change in the pa tient and whether OMT might make a difference in the healing process. The screening examination for the hospitalized patient col lects data that will fulfill the current standards required by the AOA (see Chapter 7 1 , "Standard AOA Hospital Structural Ex amination," Fig. 7 l. 1 ). While not the only acceptable method of gathering data, it is comprehensive, easy to perform, and does not require much change in the patient's position (but remember the AOA still recommends three positions during this exami nation or wants documentation why it was not accomplished). Specific regions where somatic dysfunction can affect systemic dysfunction, disease, or recovery from surgical or obstetrical stress include: •

•

• • •

•

•

Occipitoatlantal (OA) region Midcervical region Thoracic inlet Abdominal diaphragm Paraspinal regions from T 1 to L2 Collateral ganglia Sacroiliac regions and ischiorectal fossa

I

O u tpatient H e a l th S u m ma ry

naIr .. �::I:::::;�II";��m: ',1 I'aliell!', ;-.lame of lIi t h

Il

®-"-

\)

\1t ) (h� !

,\

"'

tJ \0 1/

Level of GMS

0

Key to the Severity Scale

Methods Used For Examination

"t

All

0

A

R

T

0

0 0 0

0

0

0

0 0 "2

"3 ·4

"5 "6

Region

T

0

0

0

0 0 0

0

0 0 0

0 0

0 0

0

0 0

0 0

0 0

0

0

0

0 0

0

0 0 0 0

0

0

0 0

0 0 0 0

0

0 0

0 0

0

0 0

Signalure or transcriber: Pumkd by

II gmnl

0

0 0 0

0 0

0

0 0 0

Evaluated

Head and Pace Neck Thoracic

T5-9 T I O- 1 2 Ribs Lumbar Sacrum / Pelvis

Pelvis I Innom. Abd

.I Other

0

Upper

0

Lower

0

T l -4

Extremity

from the DUreal! (If Rescurth.

Extremity

R L R L

0 = No SO or background (BG) levels 1 = More than BG levels, minor TART 0 0

Severity

1 0

0 0 0 0

0 0

0 0

0 0

0

0 0 0 0

0

0

0 0 0

0

0

0

0 0 0 0

0 0 0

0 0 0

0 0 0

0

0 0

0 0

0

0

I

IV

or 6 areas OR 1 2+

0

V

2+ from each elements in 2+ areas

Perform a l l elements � 9 areas

2 = Obvious TART (esp. R and T), +/- symptoms 3 = Key lesions, symptomatic, R and T stand out

0

0

Signature of examiner:

., 2002 An'ICricil" Ac::.derny of OSICOP:Hhy. Form. Recollllnc: nd(d hy Amcncltn

Dcsignc:d to counlinale with OUlp!llic:nl OSlool':llhic SOAP Note

0

0

0

0

6+ elements

0 0 0

0 0

1 -5 elements

III

Somatic Dysfunction and Other Systems MS / SNS / PNS / LY M . / CV / RESP. / GI / FAS. / etc.

3

2 0

11

0

ALWCtaflOn of College", of OSle

, I

or::

I,

I

\i�\.

.�1 :,,-

�

a,\

Nasal bone

+�--:---

LaCrimal bone

'P' , l/�1 \. ") lj;

Cf

Inion or external occIpital protuberance -

s;rt'

'() 0

�

�� , ;

Asterion

External acoustic meatus Tympanic part

A, Lateral view

Angle of mandible Inferior border of mandible

FIGURE 45.3. Lateral view of sku l l . (From Agur AMR. Gran t's Atlas of Anatomy, 9th ed. Balti more, MD: Will iams & Wilkins; 1 991:454.)

All drainage from the head passes through the neck, cervical fasciae, and thoracic inlet to return to the general circulation. Dysfunction in any of these structures can hinder the pathways and lead to lymphatic congestion. I ncreased sympathetic sti mu lation constricts the smooth muscle ofthe larger lymphatic vessels of the head and neck (associated with upper thoracic and cervical dysfunction) , leading (0 decreased lymphatic drain age (2).

PARASYMPATHETICS Parasympathetic nerve fibers (0 the pupil are suppl ied by cra nial nerve (eN) I I I (oculomotor nerve) ( Fig. 4 5 . 1 G). They in nervate the ciliary muscle and cause constriction of the pupi l . Parasympathetic activity shortens t h e focal length oft h e lens and is associated with visual disturbance. Parasym pathetic fibers (0

the lacrimal gland and nasopharyngeal mucosa originate in eN Vl I ( facial nerve) . They synapse in the sphenopalatine ganglion (Fig. 4 5 . 1 7) . The postganglionic fibers then travel in the max illary branch of eN v (0 the lacrimal gland. Parasympathetic hyperactivity resulting from sphenoid, max illa, and palatine dys fu nction results in excessive tear production and profuse, clear, thin secretions f(Om the mucosa of the nasopharynx and sinuses. Parasympathet ic nerves to the thyroid gland arise from the su perior and inferior laryngeal nerves, a branch of the main vagus nerve (eN X) (2).

SYMPATH ETICS The structures of the head and neck obtain their sympathetic in nervation from cell bodies located at spinal cord levels Tl- 4

664

VI!. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment

Artie ular tuberc I� ____.;.,...__.,--______,. Mandibular fossa. articular part

------...!...:,.....,-"""\

....L=---T--r:::;...".....,mm---

Infratemporal crest

r-rrm"':"'7f.7T;m;.:,;;..--_ lnferior orbital fissure

�-�-7.��nn�nT��---Tympanic plate ___:......;.

m;:'Tr------

U

SPhenopalatine foramen Pterygopalatine fossa

Posterior superior alveolar foramina

off.im-r,",,'I7T��'-'7'-:rr�i:""iiii:---- Tuberosity of maxi lIa

Tegmen tympani

Spine of sphenoid

Foramen spinosum

Foramen ovale Hamulus of medial pterygoid plate

Pyramidal process of palatine bone

FIGURE 45.4. Lateral view of sku l l (close-u p of sphenoid and temporal bones). (From Agur AMR. Gran t's A tlas of Anatomy, 9th ed. Balti more, MD, Wi l l i a ms & Wilki ns; 1 99 1 : 502.)

(Fig. 4 5 .(8) . Preganglionic and postgangl ionic fibers synapse in the upper thoracic region and/or cervical sympathetic gan glia. Sympathetic fibers to the head generally form sympathetic plexi that fol low the course o f the arterial supply (2). The su perior, middle, and i n ferior cervical paraspinal ganglia lie in the fasciae of the cervical region at levels C2, C6, and C7, re spectively. Upper thoracic, upper rib, and cervical somatic dys function can i ncrease sympathetic tone to the structures of the head. Visceral afferent nerves stimulated by organ dysfunction usu ally follow the same fascial pathways as the efferent sympathetic fibers of i n nervation. Excessive afferent input from head and neck structures is a factor i n the production of facilitation in upper thoracic cord segments. Facilitation of cord segments is associated with excessive sympathetic outRow from the affected regions of the cord (TI-4 to head and neck). Hypersympathetic stimulation to associated viscera, over time, produces physio logic changes in the viscera and in the somatic tissues i n nervated by the i nvolved cord segments (2) . Relevant palpatory changes

mediated by viscerosomatic reRexes from HEENT structures can therefore be found in TI- 4 paraspinal tissues and in pre dictable anterior Chapman points on the anterior chest wall above rib 2. Palpatory changes i n the upper thoracic and cervical paraspinal tissues can therefore be a clue to structural or functional involve ment of the head and neck structures innervated by sympathetic fibers. Conditions such as Horner syndrome (constricted pupil, ptosis, and facial anhidrosis on the affected side) i ndicate sig n ificant structural involvement or blockage of the sympathetic nervous system. I ncreased sympathetic tone also leads to func tional photophobia, unsteadiness, and tinnitus. Hyperesthesia of the pharyngeal tissues causes patien ts to cough and expectorate in an attempt to rid themselves of an imaginary foreign body i n t h e throat (2) . I ncreased sympathetic activi ty alters the normal physiologic responses the tissues can provide. Vasoconstriction results in de creased nutrient supply to and reduced lymphatic and venous drainage from target organs and tissues. The body's abil i ty to

45. Head: Diagnosis and Treatment S uperior sagittal sinus A rachnoid granulations Cereb ral veins

--""-".-""'""''--- F a Ix ce re b ri Anterior clinoid process

�---;---- F rontal sinus 1.�.:"'T'fr----"-- Crista galli

:;-�'i��j;;;��";::.---

D iaphragma sellae

"',.,.,....,·"��-:;--=; ... I:T=- -�;;----- Sella turcica

Occiput bone ----'-

Straight Sinus

S uperior cerebellar arteries

Tentonum cerebelll

s

Vertebral arteries

Lateral view of i nterior of ku ll . (From Agur AMR. Grant's Atlas of Anatomy, 9th ed. Balti more, MD: W i l l i ams & Wilkins; 1 99 1 :466.)

FIGURE 45.5.

Frontal bone Cri briform plate of ethmoid bone

F rontal sinus

Nasal spine

Nasal bone

Sphenopalatine foramen

Frontal process Pterygoid tube rcle

Lacrimal bone Pterygoid spine Medial pterygoid plate

Anterior nasal spine

Maxilla

j

Lesse Greater

Pterygoid hamulus

. Palatine canals

\ Interior view of nasal cavity. (From Agur A M R . Grant's Atlas of Anatomy, 9th ed. Balti more, MD: Williams & Wi lkins; 199 1 :5 1 9.)

FIGURE 45.6.

665

666

VII Osteopathic Considerations in Palptltory Diagnosis and Manipulative Treatment

IncIsive fora men

Palatine process of maxilla Greater and les ser palatine foramina

�

Homontal plate of palatine bone posterlor nasal spine V o mer Choana

l J

Spine of spheno ld Foramen spinos u m

l J

Mandibular fossa Tympanic plate

-----

[

Lateral pterygoid plafe Fora men ovale

.,..--;;::.'---- A u ditory tube

rFora men lacerum l! haryng eal tu bercle Carotid canal WII_Hl-il!llk:--it.--- r LJ ug u lar foramen

....;

__ ,,-

---=----

l J ---�;;

Sfylold process Stylomastoid fora m en

_--- Groove for digastriC posteri or belly Groove for occIpital artery OCCIpital condyle

E xternal occIp ital crest

E xternal occIpital protu berance FIGURE 45.7. Inferior view of sku l l . (From Agur AMR. Grant's Atlas of Anatomy. 9th ed. Balti more. M D: W i l l iams & Wilki ns; 1 99 1 :582.)

TABLE 4S.1. BONES OF THE ADULT SKULL Cranial Group (8)

Facial Group (14)

Miscellaneous (7)

Occiput Sphenoid Eth moid Frontal Pa i red temporals Pa i red parietals

Vomer M a ndible Paired maxi l lae Paired palatine Pa i red zygoma Pa i red lacri mal Pa i red nasal Pa i red i n ferior conchae

Six middle ear ossicles Hyoid bone

mount an immune response and obtain effective concentrations of medications is reduced in areas of vasoconstriction and tissue congestion (2). Prolonged sympathetic stimulation changes the composition of the cel ls of the respiratory epithelium resulting in nasal and pharyngeal secretions that are thick and sticky, thereby reducing effective cleaning and clearing by the pseudostratified ciliated ep ithelium of the mucosa. Epithelial hyperplasia is present, with a relative increase in the activi ty and number of goblet cells, con striction of arterioles, decreased vascular and lymphatic drainage of the tissues, and the mechanical difficulty in moving the mu cus. Sympathetic stimulation also produces vasoconstriction and inh ibits secretion , leading to dryness of the nasopharyngeal mu cosa. Dryness and cracking of the mucosa breaks down the normal

45. Head: Diagnosis and T reatment

667

� Vertex pain ��•••< Temporal headache

headache

pain

eyebrow

eyebrow pain Cheek and jaw pain

mandibular

pain

Back-of head pain

Eye and

Ear and temporo

Eye and

Frontal headache

joint pain

Toothache

jaw pain Toothache

pain

Ear and temporomandibular joint pain Back-of-neck

Throat and

pain

pain pain Pain Guide Vertex pain

Sternocleidomastoid (sternal)

Levator scapulae


Semispinalis capitis Frontalis

Infraspinatus

Splenius capitis Back-of-Head Pain

Splenius cervicis

Zygomaticus major Throat and front-of-neck pain Ear and Temporomandibular pain

Cheek and jaw pain

Trapezius (TP1)

Lateral pterygoid



Masseter (deep)

Masseter (superficial)

Sternocleidomastoid (clavicular)

Sternocleidomastoid (clavicular) Medial pterygoid

Trapezius TP1)

Semispinalis cervicis Splenius cervicis Suboccipital group

Masseter (deep) Eye and Eyebrow Pain

Digastric Medial pterygoid

occipitalis Digastric Temporalis (TP4)

Lateral pterygoid


Platysma

Temporalis (TP1) Splenius cericis

Orbicularis oculi Zygomaticus major

Temporal Headache

Masseter (superficial) Suboccipital group

Toothache


Occipitalis


Orbicularis oculi

Temporalis (TPs1 ,2,3)

Semispinalis capitis

Trapezius (TP1)

Masseter (deep)

Frontalis Sygomaticus major Zygomaticus major Frontal Headache


Digastric (anterior) Trapezius (TP1) Trapezius (TP2)

Back-of-Neck Pain

Trapezius (TP3) Multifidi

Sternocleidomastoid (sternal) Digastric Medial pterygoid

Muscle trigger points pain guide (left) and areas of referred pain (right) in the head and nec k . (From Trave l l JG, Si m o ns DG. MyofasciaI Pain and Dysfunction: The Trigger Point Manual. The Upper Extremities. Vol 1 . Baltimore, MD: Wi l l ia m s & Wi l k i ns; 1 983 : 1 66- 1 67.) FIGURE 45.8.

mucosal defenses, thereby permitting secondary bacterial i n fec tion (2). Dilation of the pupil (mydriasis) also occurs with i ncreased sympathetic activity to the eye. This elevates intraocular pres sures in patients with narrow angle glaucoma. Prolonged upper thoracic and cervical dysfunctions have been associated with the development c10udi ness ofthe lens (2). The Barr-Lieou syndrome (vertigo, ataxia, vasodilation, and eye pain) results from hyper sympathetic activity and proprioceptive dysfunction that o ften follows wh iplash inj uries. The sympathetics i nnervate blood vessels that supply the thyroid and innervate the cells that produce thyroid secre tions. I ncreased sympathetic stimulation may alter thyroid gland secretion (2) .

CRANIAL NERVES There are 1 2 sets of cranial nerves (Fig. 4 5 . 1 9) . The actions, associated symptoms, and somatic dysfunction considerations are summarized in Appendix I . The reader is referred to T he Netter Atlas o/Human Anatomy, plate 7, published by Ciba-Geigy Corp. (Summit, NJ), which correlates the cranial nerves with associated foramina.

Olfactory Nerve (I) The nerve of smell has olfactory neurosensory cells located in the olfactory neuroepithel ium covering the superior conchae of the nasal cavity and the superior portion of the nasal septum.

668

VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment

TABLE 45.2. MYOFASCIAL TRIGGER POINTS

Falx cerebri Sutherland

Eye symptoms and/or p a i n Sternal division of t h e sternocleidomastoid muscle Splenius cervicis muscle Occipita l i s muscle Orbicularis ocu l i muscle Trapezius muscle Ear pain, t i n n itus, and/or dimin ished hearing Deep portion of the masseter muscle Clavicu lar portion of the sternocleidomastoid muscle Medial pterygoid muscle Occipita l i s muscle Eustachian tube dysfunction Medial pterygoid muscle Nose pain Orbicu laris ocu l i muscle M a x i l l a ry sinus pain and/or sinus symptoms Lateral pterygoid muscle Masseter muscle Sternal division of the sternocleidomastoid muscle T h roat pain and/or difficu lty swal lowing Medial pterygoid muscle Digastric muscle Cra n i a l nerve entrapment V: (buccal nerve branch). lateral pterygoid muscle XI: sternocleidomastoid muscle

Anterior

Lateral pole Anterior inferior pole

Sigmoid sinus

�

Tentorium cerebel l i

FIGURE 45.9.

D u r a l reflections with i n sku l l .

does n o t exist (2) . CN I may b e affected at the point where it crosses the lesser wing of the sphenoid or by dysfunction of the fron toethmoid articulation (l).

The axons o f these cells form nerve bundles that pass through the foramina of the cribriform plate of the ethmoid bone and even tually travel to the olfactory areas of the brain (anterior per forated substance and uncus) (3). Dysfunction o f CN I may lead to an altered sense of smell or an impression of an odor that

Inferior sagittal sinus

fulcrum

Optic Nerve (II) Fibers arise from the ganglion cells of the rerina and unite to form the optic nerve. The optic nerves pass through the optic canal (in

Cavernous sinus

/:

Superior . sagittal sinus Falx cerebri

T ransverse sinus _

I ntercavernous sinus

Great cerebral --Infundibulum Straight sinus

Supraorbital vein Superior ophthalmic vein

Confluence of sinuses Tentorium cerebelli/

Inferior ophthalmic vein Facial vein

Edge of tentorial notch

r Petrosal _ I n ferio r sinu s ' Superior Median section of head and relationsh i p of dural folds to intracra n i a l structures. Supero lateral view. (From Moore KL, Agur AMR. Essential Clinical Anatomy. Baltimore, MD: Wi l l iams & W i l k i ns; 1 996:359.)

FIGURE 45.10.

45. Head: Diagnosis and Treatment

669

PAD

/

I I

Sph e noid

Squama of the occiput

��ff-,''h-I'ff-+--- Atlas

1I"'*""�Tt--+--

Third cervical

Internal carotid artery

Dural sheath of spinal cord

Vertebral artery Basilar artery

0/��*=---

Firm dural attachments

4--w-:+-- Second sacral

FIGURE 45.12. Major arterial supply to bra i n . Areas above dotted line are supplied by internal carotid arteries; areas below dotted l i n e are supplied by vertebral arteries. ACA, anterior cerebral artery; MCA, m id dle cerebral artery; PCA, posterior cerebral artery; PAD, pia, arachnoid, and d u ra.

1*--- Filum terminale

Superior sagital sinus

FIGURE 45.11. Dural continuity of skull, cervical vertebrae, and sacrum. (Adapted from Magoun H. Osteopathy in the Cranial Field, 3rd ed. K i rksville, MO: The Journal Printing Co; 1 976.)

sinus

the lesser wing of the sphenoid) and unite in the middle cranial fossa to form the optic chiasma. From the optic chiasma, optic tracts continue dorsolaterally around the midbrain to the lateral geniculate bodies of the thalamus. Optic radiations from these lateral geniculate bodies of the thalamus relay i n formation to the visual cortex in the occipital lobes of the brain (3) . Lesions of the sphenoid or membranous tension may affect the optic nerve anywhere between the sphenoid and occiput ( 1 ) .

Oculomotor Nerve (III) The oculomotor nerve arises from the midbrain, passes through the lateral wall of the cavernous sinus after passing over the top of the petrosphenoidal ligament, and enters the orbit via the supe rior orbital fissure (opening between the greater and lesser wings of the sphenoid). I t supplies the levator palpebrae and all of the ex traocular muscles of the eye except the superior oblique and lateral rectus. Clinically, dysfunction of this nerve causes the ipsilateral eye to turn upward and outward. By way of the parasympathetic

sinus

Inferior petrosal sinus FIGURE 45.13.

Venous drai nage of s k u l l . (Adapted from Magoun H.

Osteopathy in the Cranial Field, 3rd ed. K i rksvil le, MO: The Journal Print

ing Co; 1 976.)

670

VII. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment

• • • • • • • •

Upper eyelid Scalp Forehead Eyeball Ethmoid sinus Nasal cavity Lacrimal gland (fibers of CN VII pass via the trigeminal nerve to innervate this structure) Adjoining conjunctiva

The dysfunctions l isted under the oculomotor nerve may also affect the ophthalmic nerve (3).

Maxilla ry Branch (V2) The maxillary nerve (V2) is a pure sensory nerve and runs an teriorly in the i n ferior portion of the cavernous sinus. It leaves the middle cranial fossa via the foramen rotundum in the greater wi ng of the sphenoid. I t courses through the pterygopalatine fossa and the i n fratemporal fossa and enters the orbit via the inferior orbital fissure, supplying portions of (3) : FIGURE 45.14. Lymph drainage from regions of the head and scapu la. (Courtesy of W i l l iam A. Kuchera, DO, FAAO .)

•

ganglion, i t suppl ies the smooth muscle in the sphincter pupillae and ciliary muscles (3). Tension o n the petrosphenoid ligamenr (anterior aspect of the tentorium cerebelli), especially from dys function affecting the temporal or sphenoid bones, can be asso ciated with dysfunction of this nerve. Symptoms would include double vision, ptosis, or dysfunction of accommodation. Conges tion of the venous sinuses of the cranium, resulting from restric tion at the j ugular foramen , may cause overdistension of the cav ernous sinus, producing dysfunction in CN I I I, I V, V, and V I ( 1 ) .

•

• • • • •

Dura M axil lary sinus Roots of the max i llary premolar and molar teeth Nasal septum Lower eyelid Nose Upper l ip

The sphenopalatine ganglion is a parasympathetic gangl ion that hangs from the maxillary nerve and is located in the ptery gopalatine fossa. Tic douloureux may be associated with dysfunc tion of the V2 division of the trigeminal nerve and may result from dysfunction of the temporals, sphenoid, maxillae, palatines, and mandible (3).

Trochlear Nerve (IV) The trochlear nerve emerges dorsally from the midbrain, en ters the lateral wall of the cavernous sinus after passing through the petrosphenoidal ligament, and enters the orbit via the su perior orbi tal fissure. This nerve has a long course and is more easily torn during head inj ury (3). The dysfunctions listed un der the oculomotor nerve may also affect this nerve ( 1 ). The most common symptom, diplopia, occurs when the patienr looks downward.

Mandibular Branch (V3) The mandibular nerve (V3) exits the middle cranial fossa via the foramen ovale of the sphenoid. It contains both motor and sensory roots. V3 supplies these areas (3): • • • •

Trigem inal Nerve (V) The trigeminal nerve, arising from the pons, consists of three large sensory nerves from the face: the ophthalmic branch (VI) , the maxillary branch (V2), and the mandibular branch (V3).

Ophthalmic Branch (V1) The ophthalmic (V 1 ) nerve passes through the lateral wall of the cavernous sinus and enters the orbit through the superior orbital fissure. It suppl ies these areas (3):

• • • •

Teeth Gingiva of the mandible Skin of the temporal region Part of the auricle Lower face Muscles of mastication Floor of the oral cavity Part of the tongue

It may be affected by sphenoid dysfunction (I). Temporomandibular joint (TMJ) dysfunction or poor-fitting dentures may precipitate trigeminal neuralgia in this division. When present, it may be triggered by shaving. The extensive i nterconnections of rhe trigemi nal nerve with other cranial nerves play an important role in a variety of reAexes. Sensory afferent i n formation from innervated structures (such as the sinuses) is often perceived as headache in the anterior


Jugular tru n k -----ffi,.I'-'R ight lymphatic duct ----.11

1+--'rI\---- Jugular trunk 1+-';--\-\r:---- T h 0 racic duct -,n�=-"'--- S u bclavian trunk

--v"lllil:ll trunk --+�'-------H'��

S u bclavian trunk Broncho mediastinal

671

'-'�.....:J... . __ . �'.H7""'----,.-\-

Superior vena cava ------1-

lH�o::--tll':Tr�---'--::-�r_:--- 8 ron c h omedi astina I tru n k /f\,\:-»==-=-....J...--- Left superior intercostal vein

llr-=;;::---- Collecting trunk Azyg 0 s vei n ----...::.:..,-'---"'-----.,..k Collecting trunk

-----�

Thoracic duct--------+�

-+H....,:----'-+'- Desce nd i ng

t h oracic a o rta

Collecting trunk

-----..."...;.,�'----.:�

Diaphragm

I n ferior vena cava

�.

_______

Esophagus

FIGURE 45.15. Lym phatic drainage through thoracic inlet. (From Moore KL. Clinically Oriented Anatomy, 3rd ed. Baltimore, MD: Wi ll iams & Wil kins;1985:78.)

or middle cranial fossae, behind the eyes, or at the vertex of the head.

Abducens Nerve (VI) The abducens nerve suppl ies the lateral rectus muscle of the eye. It arises from the pons, ascends the clivus, runs underneath the pet-

rosphenoid ligament, courses through the cavernous sinus, and enters the orbit via the superior orbital fissure (3). Dysfunction of this nerve may be secondary to petrosphenoid l igament tension resulting from severe lesions of the sphenoid or temporals (1). Of th ree nerves passing in proximity to the petrosphenoidal lig ament ( I I I , I V, VI) and innervating the extraocular muscles, the abducens nerve is most often affected and may result in medial


672

Deep petrosal nerve (sympathetic)

Supraorbital foramen

J

Superior VII salivatory

Supraorbital foramen

Maxillary division Infraorbita(

)

foramen

Sphenopalatine ganglion (pterygopalatine) Nasal

Carotid plexus

nerves

foramen Vidian nerve

Pharyngeal nerves

FIGURE 45.16. Parasympathetic nerves to orbital and nasal areas. (Modified from Kuchera M L, Kuchera WA. Osteopathic Considerations in Systemic Dysfunction, 2nd ed. rev. Co l u m bus, OH: Greyden Press; 1 994.)

strabismus (commonly associated with a lateral strain pattern maintained by a unilateral condylar compression) and diplopia.

Sphenopalatine ganglion (pterygopalatine)

II "

,, , '

• • • • • • •

"

Great superficial petrosal nerve

Vidian

��f��l�

Superior

Palatine Pharyngeal Deep petrosal nerve (sympathetic)

Sphenopalatine gangl ion. (Modified from Kuchera M L, Kuchera WA. Osteopathic Considerations in Systemic Dysfunction, 2nd ed. rev. Colum bus, OH: G reyden Press; 1 994.)

FIGURE 45.17.

Middle sympathetic ganglion

AA

, I

Pharyngeal nerves -'

'

-

Thoracic inlet (cervicothoracic junction)

Sympathetic nerves to head. OA, occip ito atla nta l; AA, atlantoaxial. (Modified from Kuchera M L, Kuchera WA. Osteopathic Considerations in Systemic Dysfunction, 2nd ed. rev. Colum bus, OH: Greyden Press; 1 994.)

FIGURE 45.18.

the external audiwry meatus. It supplies secrewry stimulus w the submandibular, sub l ingual, and in tralingual salivary glands and sensory fibers w the lacrimal glands. The facial nerve arises from the pons, enters the i n ternal acoustic meatus of the temporal bone, joins the facial canal, and exits the skull via the stylomas wid foramen (3). This nerve may be affected by dysfunction of the sphenoid, occiput (especially condylar compression), tempo rals (especially occipiwmasw id compression), cervical and upper thoracic spine, and cervical fascia ( 1 ) .

Genticulate ganglion 0,11 VII nerve -


, ,

Palatine nerves

The sensory root conveys fibers for taste buds i n the anterior two- thirds of the w ngue, soft palate, and a small area around

OA

Inferior sympathetic ganglion

II

Scalp Auricle Buccinawr Platysma Stapedius Stylohyoid Posterior belly of the digastric muscle

Superior sympathetic ganglion

Nasal nerves -,

Fac i al Nerve (VII) The mowr root supplies the muscles of facial expressIOn and muscles of the:


Auditory Nerve (VIII) This nerve has two parts: a vestibular nerve involved in the main tenance o f equilibrium and a cochlear nerve, involved with hear i ng. For this reason it is sometimes called the vestibulocochlear nerve. Both divisions arise in a groove between the pons and medulla and course through the i nternal acoustic meatus with the facial nerve (3). Lesions of the sphenoid, occiput, and temporals


673

Foramen cecum

£t�r,!A.;ffi:PiJ.��S:::---- Frontal crest Ethmoidal foramina

I Anterior LP osterior

Superior orbital fissure Anterior clinoid

Hypophyseal fossa

Foramen rotundum

Posterior clinoid Carotid groove Foramen ovale Dorsum sellae Foramen spinosum Groove for greater petrosal nerve

Foramen lacerum

Arcuate eminence

Internal acoustic meatus

Hypoglossal canal

Foramen magnum Cerebellar fossa Vermian fossa

Internal occipital crest

Internal occipital protuberance

Foramen for exit of cra n i a l nerves from sku l l . (From Agur AMR. Grant's Atlas of Anatomy. 9th ed. Balt i more. MD: Williams & W i l k i ns; 1 99 1 :477.)

FIGURE 45.19.

may affect the functioning of this nerve, producing vertigo or hearing dysfunctions ( 1 ) .

Glossopharyngeal Nerve (IX) The glossopharyngeal nerve supplies the stylopharyngeus mus cle. Ie sends secreromoror fibers ro the parotid gland and car ries sensory fibers from the pharynx, ronsils, and posterior por tion of the rongue. It arises from the medulla and leaves the skull through the j ugular foramen (3). Dysfunctions affecring the jugular foramen (temporal, occiput, occipiromasroid suture,

or cervical fascia) may i nrerfere with normal function of this nerve (1).

Vagus Nerve (X) The vagus nerve supplies srructures in the: Head (dura of posterior cranial fossa) Neck (pharynx, soft palate, carotid sinus, and larynx) • Thorax (hean and l ungs) • Abdomen (sromach, l iver, pancreas, duodenum, and smooth muscle of the gut up ro the left colic flexure) •

•

674

VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment

TPs within the sternocleidomastoid are often overlooked and can produce balance abnormalities. Torticol lis is an associated clinical condition that benefits from osteopathic manipulative treatment (OMT) .

The vagus nerve arises from the medulla and exits the skull via the j ugular foramen (3). Dysfunction anywhere along its course through the head (especially compromised in the j ugular foramen secondary to an occipitomastoid compression) , neck (especially occipitoatlantal , atlantoaxial, and C2), thorax, and abdomen may affect normal function. Extensive direct interconnections with C2 and several other cranial nerves result in a number of referred pain and parasympathetic reflexes. Common symproms i nclude: • • • • • •

Hypoglossal Nerve (XII) The hypoglossal nerve is the motor nerve of the tongue. It arises from the medulla and exits the skull via the foramen magnum. It courses through the hypoglossal canal in the occipital bone (3). Dysfunction of the condylar pans of the occipital bone (condylar compression) may affect functioni ng of this nerve ( 1 ), resulting in suckling disorders in infants (may also involve dysfunction ofCN IX and X in the j ugular foramen) and in dysphagia, dysarthria, and swallowing difficulties in adults.

Posterior headaches (often referred from throat, l ung, heart, or bowel) Bradyarrhythmias Cough Accentuated gag reflex Vomiting Shallow respiration patterns

FOURTH VENTRICLE

Accessory Nerve (XI) The accessory nerve supplies the sternocleidomastoid and trapez ius muscles; it also supplies muscles in the pharynx and palate. It arises from both the cervical spinal cord and medulla, and exits the skull through the j ugular foramen. Dysfunctions af fecting the j ugular foramen (temporal, occiput, occipitomastoid suture, or cervical fascia) may interfere with normal function of this nerve ( 1 ) . Sternocleidomastoid dysfunction andlor TPs of ten accompany somatic dysfunction affecting this cranial nerve.

The diamond-shaped fourth ventricle is an opening in the pons that acquires cerebrospinal fluid (CSF) from the third ventricle via the cerebral aqueduct and transmits it into the subarachnoid space (Fig. 4 5 . 20) (3). Nuclei of cranial nerves V th rough Xl i are a l l located in t h e floor of t h e fourth ven tricle (Fig. 4 5 .2 1 ) . Dysfunc tions affecting CSF flow through the fourth ventricle can have significant impact upon any of rhe cranial nerves. Compression of the fourth ventricle is a manipulative techn ique used to normalize

Third ventricle Superior cistern

r-tnT��o.d-.f.:lL..J.- Cerebral

--��f-+-

/ �

; ��-=,"-9'+��""'�+-+--

aqueduct

Pons Fourth ventricle

Pontine cistern Medulla

�

Spinal subarachnoid space

� . 41

Subarachnoid cisterns Lateral view of fourth ventricle. ( Modified from Moore KL, Agur AMR. Essential Clinical Anatomy, Baltimore, MD: Williams & Wil kins; 1 996:365.) FIGURE 45.20.

45. Head: Diagnosis and T reatment

/

Nucleus solitarius of facial nerve

Superior salvatory nucleus of facial

Motor nucleus of facial nerve

Transverse pontine fibers Corticospinal and corticonuclear fibers FIGURE 45.21. Floor of fourth ventricle. (Modified from Snell RS. Clin ical Neuroanatomy for Medical Students, 2nd ed. Boston, MA: Little,

Brown and Co; 1 987.)

fluctuation of the CSF. This is postulated to improve function ing of the associated nuclei ( 1 ) . The technique is performed with the occiput (or sacrum) held i n craniosacral extension, resisting flexion until a still point and release are perceived ( 1 ) .

ADJ UNCTS FOR SINUS, EYE, AND EAR DISORDERS Paranasal S i nuses The paranasal sinuses are air-fil led extensions of the nasal cavity into the fol lowing cranial bones: Frontal Ethmoid • Sphenoid • Maxillae

675

Ethmoid S i nuses The anterior and middle ethmoid cells drain into the middle meatus. The posterior ethmoid cells drain into the superior mea tus. The i nnervation is from the anterior and posterior ethmoidal nerves (sensory supply) and orbital branches of the pterygopala tine ganglion (parasympathetic secretomotor fibers) (4) .

Sphenoid S inuses These drain into the sphenoethmoidal recess i n close approx imation to the cavernous sinuses. The i nnervation arises from the posterior ethmoidal nerves (sensory) and orbital branches of the pterygopalatine ganglion (secretomotor fi bers) (4). Infections of the sphenoid sinus are especially dangerous because of close association with the pituitary, brainstem, cavernous sinus, and cranial nerves. Sphenoidal sinusitis is usually severely disabling and is associated with severe, deep head pain.

M ax i l l ary S i nuses The largest of the paranasal sinuses drain into the middle meatus. The i nnervation is derived from the infraorbital and the anterior, middle, and posterior superior alveolar nerves (4). Sinus dysfunction (acute and chronic si nusitis and chronic postnasal drip) may result from dysfunction in the cranium. The physician should focus on improving the general health of the mucous membranes by correcting ventilation and circulation, restoring autonomic balance, and e l iminating stagnant secretions by removing mechanical hindrances (1). Associated dysfunction in the upper thoracic spine, cervical spine, and sacrum should also be treated. See Osteopathy in the Cranial Field by Magoun ( 1 ) and Osteopathic Considerations in Systemic Dysfunction by the Kucheras (2) for specific techniques.

•

•

The sinuses are lined with mucous membranes and connect via orfices with the nasal cavities. All of the paranasal sinuses drain directly or indirectly into the nasal cavity. The balance of parasympathetic and sympathetic tone determines the nature of the mucosal secretions. Parasympathetic fibers from CN V11 synapse i n the sphenopalatine ganglion and promote thin, watery, saliva-like secretions. Sympathetic fibers from Tl-4 synapse i n the cervical gangl ia a n d promote thick, sticky secretions. Frontal and sphenoidal sinuses are absent at birth, although a few eth moid cells and small max illary sinuses are presenr . The ethmoid and maxillary si nuses enlarge during childhood. The frontal and sphenoidal sinuses develop during childhood and adolescence. Sinus headache referral patterns are predictable because branches of the trigemi nal nerve innervate the si n uses.

Frontal S i nuses The frontal sinuses drain into the middle meatus. The i nnervation is from the supraorbital nerves (4).

EYE Each orbit is composed of seven bones ( Fig. 4 5 . 2) ( 1 ) : • • • • • • •

Frontal Sphenoid M axilla Zygoma Palatine Ethmoid Lacrimal

Four of the eye muscles (superior, inferior, medial, and lateral rectus) originate from a common tendinous ring surrounding the optic canal i n the lesser wing of the sphenoid. The superior oblique muscle arises from the body of the sphenoid bone super omedial to the common tendinous ring and the i n ferior oblique muscle originates on the maxilla in the floor of the orbit. All are involved in eye movements (Fig. 4 5 . 22) (3). Dysfunction of the frontal, sphenoid, and maxillae may produce muscle imbal ance of the eye ( 1 ) . Restrictions of the orbital bones, through fascial connections, contribute ro venous stasis i n head structures ( 1 ) . A lateral stain pattern, maintained by a unilateral condylar

676


S u p e r i o r rectus

A

Pupi l

J

I ri s

C ut edge of conjunctiva

Seen through cornea

Lateral rectus

Medial rectus

S u p e r i o r rectus

B

I nferior rectus

Lateral rectus

Medial rectus

D u ra l sheath Inferior o b l i q u e

----;::\11

I nferior rectus

c

S u perior reclus ----,

,----- Levator paloebrae superioris S u perior oblique

Optic nerve fascicles Ophthalmic artery Lateral rectus

CN I I I

C N VI C i l iary ganglion

Medial rectus

----'�--� '-----��-- I nferior rectus

�---- Inferior oblique FIGURE 45.22. Extraocular muscles and nerves. A: Anterior view of muscles. B: Posterior view of muscles. C: Nerves of the orbit. eN, cra n i a l nerve. (From Agur AMR. Grant's Atlas of Anatomy, 9th ed. Ba ltimore, MD: Wi l l iams & W i l kins; 1 99 1 :486.)

45. Head: Diagnosis and Treatment compression, is oFten associated with strabismus. A vertical strain pattern, maintained by a bilateral condylar compression, is often associated with either myopia or hyperopia. DysFunction of the occiput can obstruct the jugular Foramen, leading to backward venous pressure in the orbit. These factors may contribute to such conditions as ( 1 ): • • • • • •

Amblyopia Astigmatism Diplopia Hyperopia Myopia Strabismus

The patient receives clinical benefit From removal of cranial somatic dysFunction. Gentle eye mobil ization using indirect tech niques may also decrease ocular tension resul ting from glaucoma.

677

associated with the perception of a roar or low-pitched noises ( 1 ) . Eustachian tube dysfunction is the most common precursor o f otitis media a n d is often responsive t o treatment o f somatic dys function affecting the cranium, cervical and thoracic spine, me dial pterygoid m uscle, cervical fasciae, and sacrum . DysFunction affecting the ganglion i m par is often associated with asth ma, chronic otitis media, and chronic sinusitis. The ganglion impar is formed by the convergence of the pelvic sympathetic trunks and l ies anterior to the coccyx. This ganglion ulti mately com muni cates with thoracic sympathetic chain (4). Sacral and/or coccygeal restrictions may irritate this gangl ion, contributing to increased tension in the upper thoracic and cervical spine. Treatmenr of sacral and/or coccyx somatic dysfunction will al low the gangl ion i mpar to optimal ly Function. Dysfunction of the ganglion i m par is especially responsive to the percussion hammer techn iques de veloped by Robert C. FulFord, DO.

EAR

TH ROAT

The ear serves two major functions: mai ntenance of equilibrium and hearing (3). Most of the structures of the ear reside within the petrous portion of the temporal bone. Hence, dysfunction of the temporal bone can be a factor i n i m paired hearing and asyn chrony of temporal bone motion can be associated with vertigo (Fig. 4 5 .23) . The eustachian tube connects the m iddle ear to the nasophar ynx (Fig. 4 5 . 24) (3). It functions to equalize m iddle ear pressure with atmospheric pressure. Fixed i nternal rotation of the temporal bone, typically secondary to an occipitomastoid o r sphenosqua mous compression, maintains partial or complete closure of the eustachian rube. This is associated with two eFFects: perception of high-pitched noises and i mpaired drain age From the m iddle ear, thereby producing a media For recurrent ear i n fections. Fixed external rotation maintains patency of the eustachian tube and is

Impaired arterial supply to and venous and lymphatic drainage From the throat predisposes this region to inFection. DysFunc tion of the sacrum, upper thoracic and cervical spine, and/or hyoid bone is oFten seen i n patienrs with pharyngitis and tonsill itis.

COMMON COLD Viral illness decreases host resistance and produces uncomFort able subjective symptoms. InAam mation From any cause can pre dispose a patient to secondary bacterial infection. Visceral af Ferent impulses fro m the upper respiratory tract Facilitate the upper thoracic spinal cord segments, resulting in excessive sym pathetic output to structures of the head, neck, and bronchial

S e m i C I rc u l a r duct and ca n a l ----...

",,+,.----

S t a p e s ------.. I n c us _--", Malleus Temporal bone

External acoustic meatus

_......

___

E n d o l y m ph a t i c sac

Nt-.--'-::T--- Aqued u c t of vesti b u le c o n t a i n i n g e n d o l y m p h a t i c d u ct

#----;,---

Perilymphatic duct ( a q u e d u c t of c o c h l e a )

_ _ _ _

I';�----

_ _ _ _

D u c t of coch l e a

T y m pa n i C m e m b ra n e -------_'+,

T y m p a n i c cavity --------' Ves t i b u l e of b o n y l a b y ri n t h

------.

'------ F e n e s t ra c o c h leae ...:.....---- A u d i t o ry t u b e

FIGURE 45.23. I nternal structures o f t h e ear. (From A g u r AMR. Grant's Atlas o f Anatomy, 9th e d . Balti more, MD: Wil l iams & W i l k i ns; 1 99 1 : 534.)

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Bony tube, opened

,----.....,..--r---iii"Mr---

]

StYlOmastoid artery Facial nerve

'bi;:--':---

Middle meningeal artery Emissary veins in foramen ovale

Cartilagino us part of auditory tube Poste r i o r s upe r i o r alveo l a r artery

rMe m b ranous part o f auditory tube LLevator veli palatini

""""if--7..

-

1IImr---

l J

[

I nternal j u g ular vein I nternal carotid artery

Lateral pteryg oid plate

Bu ccinator Tonsil ---r ;---- S uperior constrictor

L a teral view A s cending palatine vessels Tympanic

Connection of m iddle ear to nasopharynx. Lateral view. (From Agur A M R . Grant's Atlas of Ana tomy, 9th ed. Ba lti more, M D : Will iams & W i l k i ns; 1 99 1 : 54 1 .)

FIGURE 45.24.

tubes. Osteopathic treatment: 1 . I mproves the blood supply 2 . I ncreases venous and lymphatic drainage from the affected area 3. Relieves m uscle spasm, thereby improving breathing 4 . Rel i eves pain 5. Reduces reflex disturbances 6. I mproves circulation to and from the reticuloendothelial sys tem and thereby improves immune function Treatment of cranial dysfunction assists i n managing a patient with sinus congestion . Circular pressure applied to the supraor bital and i n fraorbital nerves eases sinus pain. Treatment of the up per thoracic spine (rib raising) and cervical spine reduces excessive sympathetic outflow to the nose, sinuses, and bronchial tubes and aids the body i n producing thin, saliva-like secretions. Treat ment of cervical myofascial and articular dysfunctions and fas cial torsions at the thoracic i nlet improves lymphatic and venous drainage ( 2 ) . Facial effleurage and lymphatic pump procedures augment drainage. These manipulative treatment measures assist in cleansing the structures of the head and upper a irways.

H EADACHE Headache is one of the most common conditions seen i n a pri mary care practice. Every year, 40 to 5 0 m illion Americans seek treatment for headaches ( 5 ) . This condition can be caused by a number of i ntracranial and extracranial abnormalities. The un derlyi ng cause of many headaches is o ften described as "un-

known" or " idiopathic." A thorough knowledge of anatomy and physiology and ability to diagnose structural abnormalities of the cran ium, neck, upper thoraces, and sacrum often allows a physi cian to logically explain and treat previously unknown causes of headache. The i mplementation of a rational treatment plan sig n i ficantly reduces suffering of the patien t and i mproves overall functioni ng. The head and scalp contain many pain-senSItive structures. These i nclude: • • • • • • • •

Skin and its blood supply Muscles of the head and neck G reat venous sinuses and their tributaries Portions of the dura mater at the base of the brain Dural arteries Intracranial arteries Cervical nerves Trigeminal (y), abducens (Vl), and facial (VII ) nerves

The brain parenchyma itselfis not sensitive to pain . Pain from structures above the tentorium cerebelli travel via the trigeminal nerve, so pain referred from structures above the tentorium cere belli is perceived in the frontal, temporal, and parietal regions of the head. Pain fibers from structures below the tentorium cere belli travel via the glossopharyngeal ( I X) and vagus (X) nerves and the upper cervical spinal nerve roots. Therefore, pain re ferred from structures below the tentorium cerebelli is perceived i n the occipital region ( 5 ) . Structural abnormalities, usually acting v i a the fasciae, place tension on pain-sensitive structures and cause discomfort. Exam ple: parietal bone dysfunction produces strain on the superior

45. Head: Diagnosis and T reatment sagittal sinus, producing discomfort in the parietal region. Upper cervical dysfunction leads to discomforr i n the occipital region. Gastroi nrestinal abnormalities result i n headache i n the occipital region via vagal transmission. A detailed h istory is vital to the diagnosis and treatmenr of headache, especially if they are recurrent or chronic i n nature. In formation regarding the patient's birrh history (length of mother's pregnancy, maternal complications, length of labor, method of delivery, use of forceps, pitocin or vacuum extraction, neona tal complicat ions) and childhood growth and development may shed l ight on the precipitating factors for headache. A h istory of trauma is often important. Clinical experience has revealed that a forgotten fall or head inj ury that has resulted in a sacral shear has often been overlooked and is the key to providing effective treat ment of a chronic headache. Fam ily h istory should be obtained ( 5 ) , including information about: • • • • •

Headache: onset, frequency, location, duration, and severity Associated symptoms Trigger factors Previous medical, surgical, and dental h istory Prior headache therapy

A complete physical exam i nation is performed, including a neurologic evaluation, in addition to the structural examination. Carefully document your findi ngs. Always rule out serious or ganic causes of headache, such as brain tumor, aneurysm, ar teriovenous malformation, hemorrhage, and temporal arteritis. Neuroradiologic studies such as computed tomography (CT), magnet ic resonance imaging ( M Rl), and/or magnetic resonance angiography (M RA) are needed if any of the aforementioned are suspected ( 5 ) . There are four major classifications of headache ( 5 ) : I.

Vascular (migraine and cluster)

2. Tension (muscle contraction) 3. Traction and inflam matory type (brain tumor, infection, cere brovascular disease) 4. Cranial neuralgias (trigeminal neuralgia, TMJ )

M i graine M igraine headaches are recurrent and vary widely in i ntensity, frequency, and duration . The pain is often described as a unilateral throbbing, pounding pain. It may later radiate to the opposite side. Migraine headaches can be associated with : • • • • • • • • •

Nausea Vom iting Diarrhea Verrigo Tremors Photophobia P honophobia Sweating Chills They are often preceded by:

• •

Aura Scotomas (blind Spots)

679

Photopsia (flash ing lights) Paresthesias • Visual, olfactory, and auditory halluci nations • Verrigo • Syncope •

•

The initial episode most often occurs during puberty but can occur at any age between 5 and 40 years. Migraine headaches may be triggered by ( 5 ) : • • • • • • • •

Head inj ury or other trauma Stress Hormone fluctuations Fasting Oversleeping and undersleeping Vasoactive substances in foods (wine and cheese, cold foods) Changes in weather and temperature (bright l ight, poor ven tilation) P hysical stimuli (smoki ng)

The production of m igraine symptoms involves two major events: vasoconstriction and vasodi lation. The cerebral blood ves sels can be divided into twO major systems: the in nervated adren ergic system and the noninnervated arterial system. The large innervated vascular system consists of the arteries at the base of the brain and the pial arteries. These have a rich adrenergic nerve supply and respond to catecholamines. The nonin nervated vas cular system consists of the parenchymal arteries and the terminal h igh-resistance arteries. They respond to local metabolic factors. Trigger factors ( listed above) ptoduce unilateral cerebral vaso constriction via the adrenergic nervous system. Platelets system ically aggregate and release seroton i n , which augments vasocon striction of these adrenergically i nnervated blood vessels. The overall result is vasoconstriction with a reduction in cerebral blood flow. When blood flow is sufficiently reduced, an aura develops with symptoms occurring as a consequence of which brain re gion is affected by the constriction. The vasoconstriction phase causes local anoxia and acidosis and a systemic drop i n serotonin. Seroton in sensitizes the pain receptors in the blood vessels. In response to local metabolic factors (anoxia and acidosis) , the ves sels of the noninnervated arterial system dilate, increasing cerebral blood flow and promoting local vasomotor changes resulting in a combined dilation of the i n nervated extracranial and intracra nial arreries on the same side. This vasodilation , along with the sensitization of pain fibers, produces the pain of migraine ( 5 ) . A trigeminal vascular reflex may also explain some of the events seen in the production of migraines. Afferent pain fi bers from the cortex, thalamus, hypothalamus, and cervical toots Cl-3 com municate with the spinal nucleus of the trigemi nal nerve. These impulses can then travel via the facial nerve (CN VlI ) to produce parasympathetic dilation of the internal and external carot id ar teries. Pain perception is increased when the effects of this dilation feed back i nt o the spinal nucleus of the trigeminal nerve. Stimu lation of the trigeminal ganglion, through vasodilation, can also produce edema in the dura ( 5 ) . H o w m ight somatic dysfunction play a role in t h e gene sis of migraines? Somatic dysfunction in the upper thoracic spine increases the level of sympathetic tone to the in nervated blood vessels of the head. I ncreased sympathetic tone produces

680


vasoconstriction of related vessels and results in the decrease of cerebral blood flow. This results i n a relative cerebral anoxia that can further lower the threshold for vasodilation , leading to the production of m igraine sym p tomatology. Cranial dysfunction affecting the cortex, thalamus, and hypothalamus (side-bending rotation pattern), and upper cervical dysfunction affecti ng cer vical roots C l -3 can transfer afferent pain stimuli to the spinal nucleus o f the trige m inal nerve. This would produce vasodilation and resultant symptoms via the facial nerve (CN V I I ) . T h e trigeminal nerve courses through various portions o f t h e sphenoid bone. A n elevated greater wing of t h e sphenoid (torsion) may apply dural pressure resulting i n irritation of the trige m inal nerve, thereby feeding i n to the trigeminal vascular re flex. A sphenosquamous compression can compromise the func tion of the m iddle meningeal artery. The facial nerve courses through the temporal bone. Dysfunction of the temporal bone, such as i n ternal rotation, can result in reflex vasodilation of the internal and external carotid arteries via the facial nerve. Occip itomastoid compression can result i n reduced venous drainage through the j ugular foramen, thereby producing congestion and dysfunction i n the cortex, thalam us, and hypothalamus as well as CN IX and X. These dysfunctions are l isted as generalizations. Dysfunction i n areas not directly adjacent to the head (lumbar spine, sacrum, pelvis) may produce fascial strains that are transmitted to the head and play a key role i n the genesis o f migraines. Treating the whole patient is an osteopathic approach.

Cluster Headache Cluster headaches occur in series or groups lasting several weeks to several months with pain-free i ntervals of 1 4 or more days. The average age at onset is 20 to 30 years. They are more common i n men than i n women. The pain is typically unilateral and is described as an excruciating, boring sensation behind o r around one eye that may radiate over the entire side o f the head. The opposite side may be affected in a subsequent series. Associated symptoms include: • • • • • • •

Conj unctival injection Tearing Nasal congestion Rhinorrhea Partial Horner syndrome Sweating Flushing on the same side of the head

Alcohol consumption and cigarette smoking trigger cluster headaches. Extracranial vasodilation and i ncreased cerebral blood flow are associated with cluster headache attacks, s i milar to mechanisms �een with m igraine headaches. Somatic dysfunction l isted in the preceding section on m igraine headaches can also be a factor in the genesis of cluster headaches. The associated Horner syndrome (unilateral m iosis, ptosis, sweati ng, and flushing) is due to an ab normality with the sympathetic nerve supply to the orbit. This may occur as a result of compression of the cervi co thoracic (stel late) ganglion secondary to upper thoracic or upper rib (elevated first rib) dysfunctio n . Compression of the pterygopalatine gan-

glion from dysfunction of the sphenoid, palatines, and maxilla can affect parasympathetic supply to the orbit ( 1 ) .

Tension Headache Tension ( m uscle contraction) headaches are the result of the body's response to: • • • • • • •

Stress Anx iety Depression Fatigue Emotional conflicts (work, school, fami ly, marriage) Work habits Poor posture

The etiology of tension headaches includes conn'action of the skeletal muscles of the head, neck, and face and some reflex vasodi lation of the extracranial vessels. They generally begin between the ages of 20 and 40 years and are more common in women. Tension headaches usually occur bilaterally and may be described as a full ness, tightness, or pressure in the forehead, temples, or back of the head and neck. They are occasionally described as a bandlike tightness around the head. Tension headaches are usu ally not associated with nausea and vomiti ng. Those associated with anxiety may cause difficulty fal l i ng asleep. Headaches associ ated with depression are often associated with early and frequent awakening. Depression is more co mmon with decreased levels of serotonin in the brain. Reduced levels of endorphins, seen i n depression, also make the patient susceptible t o chronic pai n ( 5 ) . Postural i m balance significantly contributes t o tension headaches and needs to be addressed. Somatic dysfunction in the upper thoracic spine, cervicothoracic junction, and cranium, such as a n i n ternally rotated temporal bone, can result in i ncreased lev els of sympathetic tone. This is associated with i ncreased muscle tone and vasoconstriction and facilitation of afferent pain signals, thereby reducing blood supply to the muscles of the upper back, neck, and head. The net effect is i ncreased muscle tenderness and sensitivity to pain. In addition to osteopathic manipulative medicine, the patient may also need stretch ing and/or strength ening exercises for the neck and upper back.

Traction and Inflam m atory Headache Headaches can be produced when pain-sensitive structures are distended, d isplaced, or in flamed. Early diagnosis is vital for effec tive treatment of these conditions and to prevent complications that can be associated with a late diagnosis.

Cerebrovascular Disease Headaches can develop when hypertension becomes moderate or severe. Headaches produced by hypertension are usually located i n the occipital region and are described as moderately severe, nagging, and throbbing. They usually begin in the morning and decrease when the patient stands up. They may become severe and persistent when the diastolic blood pressure rises above 1 1 0 m m Hg. They may be associated with episodes of blurred vision, confusion, and drowsiness. Adequate blood pressure control is

45. Head: Diagnosis and T reatment imporrant III the prevention and reduction of cerebrovascular accidents. Hypertensive encephalopathy can develop if untreated (5).

Transient Ischemic A ttacks Headaches as a result of a transischemic arrack (TIA) are usually described as a pressure sensation and can develop both during and after the attack. They generally persist for several m i n utes, rarely for hours. Similar headaches may occur between TIA episodes. Carotid TIAs usually cause uni lateral fronral headaches associated with rransienr hemiplegia, hemiparesrhesia, unilateral blindness, and speech abnormali ties. Vertebrobasi lar TIAs may cause ( 5) occipital headaches, dizzi ness, diplopia, i m paired vision, numbness, or dysarthria.

Aneurysms Headaches from aneurysms can produce extraocular muscle ab normalities. This headache is noted in the eye or fron tal area and may be associated with m iosis, ptosis, decreased vision, or carotid bruit. Extraocular muscle abnormalities occur through compression of the oculomotor nerve (CN I I I ) . The symptoms may be similar to those seen with cluster headache but are of a more prolonged duration ( 5).

Large Lobar Hemorrhages Large lobar hemorrhages are more l i kely to cause headaches than smaller hemorrhages into the thalamus or basal ganglia. The headache most commonly occurs o n the same side as the hemor rhage. Frontal hemorrhage com monly produces pain in the fore head and eyes. Occipital hemorrhage often produces headache i n the occipital region a n d neck. Subarachnoid hemorrhages (SAH ) typically have a sudden onset and i ncapacitating severity. They may be described as "the worst headache of my l i fe" and may be associated with exertion. The pain may persist for hours to days. The patienr may be completely asympromaric i mmediately prior to bleeding or may experience "a warning headache" days to weeks before the rupture. The associated headache is usually generalized and may spread to involve the neck, back, and lower extremities. Nuchal rigidity develops and associated symptoms may include: • • • • • •

Photophobia Pain with eye movement Confusion Autonomic disturbances (elevated temperature, pulse, blood pressure) Focal neurologic symptoms Visual abnormalities Funduscopic exam ination may reveal papilledema ( 5 ) .

681

the cerebral hemispheres, primarily i n the d istribution of the m iddle cerebral artery. The headaches may be accom panied by auras and may m i m i c a m igraine. A skull bruit may be auscul tated. Prior to rupture, the symptoms are local ized in the area of the malformation. Rupture may not be associated with exertion and may result in a sudden, lateralized, severe headache. Confusion and neurologic deficits may develop ( 5).

Brain Tumors The pain ftom a brain tumor is usually i ntermi ttent, deep, ach i ng, nagging, and pressure-l ike. Throbbing is not usually noted. Coughing, straining, or bending over usually make the headache worse. Other posrural changes can induce the headache. The pain worsens as the tumor grows and the i n tracranial pres sure i ncreases. The pain fro m headaches associated with brain tumors may awaken the patient from sleep ( 5 ) .

Acute Hydrocephalus An acute hydrocephalus produces a secondary ventricular ob struction or shunt malfunction. The headache may be severe and visual disturbances may occur. E mergency ventricular drainage m ust be performed ( 5 ) .

Temporal Arteritis This condition results fro m i n flammation of a scalp artery, usually the superficial temporal artery. It i s generally seen i n patients over age 5 0 . The affected artery is swollen and tender. The associated headache is severe, throbbing, or stabbing and is local ized over one temple. The artery may be palpable and tender. The pain is worse when the patient stoops or l ies flat and is decreased when pressure is applied over the common carotid artery. Other symptoms i ncl ude fever, weight loss, n ight sweats, and joint pain. Visual disturbances can develop as a result of secondary ischemic optic neuropathy. The diagnosis is confirmed by biopsy (5).

Cranial Neuralgi as Trigeminal Neuralgia Trigeminal neuralgia is associated with unilateral recurring pain over any one or combination of the three divisions of the trigemi nal nerve. I t usually affects the max i llary division but may include the ophthalm ic division late i n the disease. The pain is described as intermittent, severe, short, sharp, momentary bursts that are s i m i lar to electric shocks. Patients may cry or twitch in response to the severe pain. M ild stimulation to trigger zones can i n iti ate attacks (5). Somatic dysfunction of the temporals, sphenoid, maxillae, palatines, and mandible can lead to trigeminal nerve irritability and subsequent symptoms. Trigemi nal neuralgia may appear following dental extraction ( 1 ) .

Arterio venous Malforma tions

Bell's Palsy

Arteriovenous malformations (AVMs) are abnormal blood vessels connecting the arterial and venous systems. Most are located i n

Bell's palsy affects cranial nerve V1 I and is typically associated with a rapid onset of unilateral facial paralysis. The condition

682


may Follow exposure to cold or a recent viral ill ness (upper res p i ratory inFection ) . The exact cause is unknown, but is thought to be associated with a component of i nflammation aFFecting the Function of the Facial nerve (CN VII) i n the Facial canal. Patienrs may presenr with a Facial droop, i nabil i ty to close the eye on the afFected side, pain behind the ear or around the jaw, hyperacusis, and loss of taste. Many patienrs recover within 1 ro 3 weeks. The cornea must be protected and kept lubricated while the condition is resolving (6) . DysFunction of the sacrum, upper thoracic and cervical spine, and craniosacral mechanism can contribute to impaired lym phatic drainage From the Facial canal , leading to inflammation of the Facial nerve. Look For a com pression of the occipitomastoid maintaining an internally rotated temporal bone on the side of Facial paralysis.

Temporomandibular Joint Dysfunction Anatomy and Motion Review

The TMJ is Formed by the head of the mandible and mandibular Fossa o f the temporal bone. These structures are separated by a fibrocartilaginous articular disc. The stylomandibular l igament connects the angle of the mandible to the styloid process of the tem po ral bone and the sphenomandibular ligament connecrs the lingula (medial aspect) o f the mandible to the spine of the sphe noid ( Fig. 4 5 . 2 5 ) . When the mouth is opened, the head o f rhe mandible and arTicular disc move anteriorly on the articular sur Face of rhe remporal bone as the head of the mandible rotares about a transverse axis on the i n Ferior surFace of the articular disc ( Fig. 4 5 .26). During protracrion, the heads o f the mandible glide anteriorly and rhe articular discs slide posteriorly. The reverse occurs during retracrion. The mandible is protracted by the lareral pterygoid muscle and retracted by rhe posterior fibers of rhe temporalis muscle. G raviry normally opens the mouth bur may be assisted by the lateral pterygoid, suprahyoid, and i n Frahyoid m uscles (3). The remporalis, masseter, and medial pterygoid muscles close the mouth. The anrerior gliding motion of rhe mandible and articular disc is oFten restricted. For example, assume that rhe parienr has

Opening motion of temporomandibular joint. (After Blaschke DD, from Solberg WK, Clark GT. Temporomandibular Joint Problems: Biologic Diagnosis and Treatment. Chicago, I L: Qui ntessence Publishi ng; 1 980:73, with permission.) FIGURE 45.26.

a leFr TMJ resrr·icrion . As the mouth opens, the right side of the mandible and right articular disc glide anteriorly wh ile the left side is restricted. This results in deviation of the chin toward rhe left side, the side of restricrion. Cranial dysfuncrion can affecr TMJ morion because as the remporal bone externally rotates, the ipsilateral mandibular fossa moves posteriorly and medially. I n ternal rotation allows the ipsilateral mandibular fossa to move anteriorly and laterally. The mandible will deviate toward the side of the externally rotated temporal bone or away from the side of the internally rotated temporal bone. Sphenoid dysfunction can affecr the TMJ through its d i rect articulation with the tempo ral bone or by i ts articulation with the mandible th rough the sphenomandibular l igament. Short leg syndtome has also been associated with TMJ (2). Dysfunction Diagnosis:

'>---- Spine of

sphenoid

,."...--- Styloid process

Stylomandibular ligament

/--..... /

,

Lingula

2 . The patienr i s i nstructed to open his or her mouth slowly. Observe the chin (or midincisural l i ne) for deviation from the midline while palpating the TMJs. Note: Remember that deviation occurs to the side of the restricted TMJ . Muscle Energy Treatment for Temporomandibular Joint Dysfunction

Angle of mandible

Ligamentous attachments of sphenoid and temporal bones to mandible. M e d i a l view. (From Moore KL, Agur AMR. Essential Clinical Anatomy. Ba lti more, M D : Wi l l iams & Wilk ins; 1 996:384.) FIGURE 45.25.

I. The physician places his or her hands on either side of the patient's head with the index fingers anrerior to the external auditory meatus (area of the TMJ ) .

Diagnosis: Assume that the patient has a left TMJ restriction with chin deviation to the left as the mouth is opened. Position: Patient is supine and the physician sits at the head of the table.


683

1 . Physician uses right hand to support the right side of the pa tient's head and contacts the left side of the patient's mandible with the left hand. 2 . Patient is i nstructed to open h is or her mouth . Patient is instructed to stop when mandibular deviation to the left is palpated. 3 . Physician's left hand applies a force along the left side of the patien t's mandible to direct it toward the right. 4. The patient is i nstructed to push his or her chin to the left against the physician's hand while the physician maintains isometric resistance. 5. The patient's effort is continued for 3 to 5 seconds. The pa tient is then i nstructed to relax. When com plete relaxation is palpated (usua[[y 2 seconds) , the physician moves the patient's j aw further to the right. 6. Steps 4 and 5 are repeated until the best motion is obtained (average of 3 times) . 7. Reevaluate the motion of the jaw.

CRANIAL MOTION ASSESSMENT The vault hold is used both to assess and normalize motion of the bones of the cran ium. The patient should be in the supine position, comfortable and relaxed. G lasses, nonfixed dental ap pliances, and bulky objects in pockets should be removed. The physician should be seated at the patient's head, forearms resting comfortably on the treatment table. The fingers of both hands must be relaxed. Hand placement is specific. I ncorrect placement may give improper information and may disrupt the patient's mecha nism. The physician places the fingerpads in the fol lowing posltlons: 1 . Little fi nger on the squamous portion of the occiput 2. Ring fi nger behind the ear on the mastoid region o f the tem poral bone 3. M iddle fi nger i n front of the ear on the zygomatic process of the temporal bone 4. I ndex finger on the greater wing of the sphenoid 5 . Thumbs resting gently (crossed or uncrossed) over the top of the head (Fig. 4 5 .27) Assess amplitude, flexion, extension, and specific motion of rhe individual bones. Treat the entire cran ium. Pay special atten rion to rhe remporal bones. Dysfunctions may be treated with indirecr technique or direct techniques applied to specific artic ular resrrictions. It is i m portanr to remember thar progress can only be made as fast as the patient's body can respond. The sacrum has an involuntary motion pattern thar is closely relared to rhe morion of the head. This motion occurs about the respiratory axis located at the level of the second sacral segment. During craniosacral flexion, the sacral base moves posterosuperi orly and the apex moves anteriorly (anato m ic exrension ) . Duri ng craniosacral extension, the sacral base moves anteroinferiorly and the apex moves posteriorly (anatomic flexion) ( 1 ) . Dysfunctions in sacral morion can affect the cranium and vice versa. Sacral motion can be assessed as fo[[ows:

Fi nger position for vault hold. (Modified from Gehin A. Atlas of Manipulative Techniques for the Cranium and Face. Seattle. WA: Eastland Press; 1 98 1 : 1 2.)

FIGURE 45.27.

1 . The parient is i n the supine position. The physician sits at the level of the patient's pelvis facing toward rhe head. Palpation is performed with the domi nant hand. A right-handed physician sits o n the patient's right side. A left-handed physician sits on the patient's left side. 2 . The physician places the domi nant hand between the patient's legs and under the sacrum . The base of the sacrum should rest on the physician's terminal phalanges. 3. The hand is relaxed to palpate the i nherent morion. The sacrum is fol l owed into flexion and extension. The physi cian determines if the motion is s mooth and symmerric or if a dysfunction pattern presents. Sacral dysfunction can be treated using borh direcr (engage the barrier) or indirect (moving toward rhe direction of freer motion) technique. The physician should conti nually "l isten" with the fingers until a release occurs. Again, progress is only as fast as the patient's body allows.

CONCLUSION Symptoms i n H EENT structures are often seen and may be sources of significant functional disabil i ry. The structural and functional relationships berween the structures of rhe head should be considered to more accurately diagnose various conditions and to implement appropriate treatment.

REFERENCES I . Magoun H I . Osteopathy i n the Cranial Field, 3 r d ed . Kirksville, M O : The Journal Printing Co; 1 976.

2 . Kuchera ML, Kuchera WA. Osteopathic Considerations in Systemic Dys junction, 2nd ed. Columbus, O H : G reyden Press; 1 994.

3. Moore K L. Clinically OrientedAnatomy, 3rd ed. Balti more, M D : Will iams

& Wilkins; 1 992.

4 . W i l l iams PL. Gray's Anatomy, 38th ed . Edinburgh, Scotland: Churchill Livingstone; 1 99 5 . 5 . Diamond S. Clinical Symposia: Head Pain, Diagnosis {trid Management. Su m m i t, N J : Ciba-Geigy Corp; 1 994. 6. Taylor RB. Family Medicine Principles and Practice, 5th ed. New York, NY: Springer-Verlag, 1 998.

CERVICAL SPINE ROBERT E. KAPPLER

KEY CONCEPTS •

• • • •

Functional anatomy of the cervical spine, including skeletal, muscular, ligamentous, neural, vascular, and lymphatic aspects, and motion biomechanics Diagnosis of cervical spine, using active and passive motion testing Occipital and C2-7 motion testing of the cervical spine Clinical information on cervical spine problems Treatment of symptomatic, unstable cervical spine complaints

There are no typical transverse processes. The anterior and posterior tubercles, which serve as muscle artachments, are the true transverse processes. The bone between the facets, which we palpate and consider as a transverse process, is known as the articular pillar. The lateral portions of the arias are known as lateral masses. The lateral portions of the cervical vertebra are modified to comain a foramen through which the vertebral artery passes. Although this provides protection for the vertebral artery, it also creates the possibility of trauma to the artery from bony insult.

Muscular

The cervical spine is of great significance to those who use manip ulative treatment. The cervical region is a pathway between the head and the thorax with neural, vascular, and musculoskeletal communication. Injury, pathology, or dysfunction may interfere with these vital communications.

FUNCTIONAL ANATOMY Skeletal

The cervical spine consists of seven vertebral segments. The arias (C 1) and axis (C2) are atypical. The vertebral body of C2 is modified superiorly to form the dens (odontoid process). The arias does not have a vertebral body; instead it rotates around the dens (1). The superior surface of the arias contains bilateral joint surfaces that articulate with the occipital condyles. The transverse processes of the arias, called lateral masses, are modified and palpable. The spinous process of the axis (C2) is palpable. The articulation between C2, C3, and the remainder of the cervical joints is considered typical. The facets are in a plane that points toward the eye. Rotation motion of the typical cervical seg ments follo'ws the plane of the facets. Anterior or forward rotation is toward the eye rather than rotation in a horizontal plane. A specialized set of synovial joints is presem on the lateral surface of the vertebral bodies of the midcervical spine. They are known as uncovertebral joints (or uncinate) joints of Luschka, and provide stability to the cervical spine and decrease the likeli hood of herniated nucleus pulposus in the cervical region.

The posterior spinal muscles are continuous from the cervical spine to the sacrum. Significant modification of these muscles occurs at C2, with a group of oblique muscles traversing from arias and axis to the occiput. The anterior spinal muscles (prevertebral muscles) traverse from T3 to the occiput. The scalene muscles that go from the lateral portions of the cervical spine to the first and second rib act as lateral stabilizers, as well as accessory muscles of respiration. The levator scapula muscle goes from the posterior tubercles to the upper medial border of the scapula. The general investing fascia splits to cover the sternocleidomastoid muscle anteriorly (mastoid process to sternum and clavicle) and the trapezius muscle posteriorly. Because the trapezius muscle attaches to the scapula, it is the primary connection between the head and neck and the shoulder girdle. The process of lifting with the upper extremity distributes force to the cervical spine. Anteriorly, there are muscles that travel from the mandible to the hyoid to the sternum and clavicle.

Ligamentous

The cervical spine contains the usual spinal joint ligaments. The ribs do not attach to the cervical spine. The transverse ligament portion of the cruciate ligament supports the arias in rotating about the dens. The amerior surface of the spinal cord lies im mediately posterior to the transverse ligament. Rupture of this ligamem (or laxity, which may occur with rheumatoid arthritis) creates the possibility of the dens contacting the spinal cord and causing catastrophic neurologic damage.

46. Cervical Spine

Neural

The spinal cord extends from the medulla in the brain through the cervical and thoracic spine to the L2 level of the lumbar spine. Spinal cord injuries may occur from a number of different traumatic events, including: Automobile and motorcycle accidents Gunshots and stabbings Diving into an empty swimming pool Football and other violent contact SpOrts Damage to the cord may be ischemic as much as physical. Cervical spinal stenosis is a condition in which the spinal cord has insufficient room in the neural canal. Osteophyte formation contributes to stenosis, as does instability with excess fore-to-aft or side-to-side translation. A cervical disc may protrude posteriorly into the cord. Disturbance of the vascular supply produces neurologic symp toms and damage. The venebral anery may become occluded by thrombosis, which may be precipitated by injury to the artery as it passes through the intervertebral foramina and over the arias, then enters the cranium through the foramen magnum. In nor mal subjects, aneriographic studies have shown that extension and rotation of the occiput produce a functional occlusion of the opposite vertebral artery. The cervical spinal cord gives rise to the cervical plexus and the brachial plexus. Because the brachial plexus innervates the up per extremity, nerve root impingement at the cervical interverte bral foramen produces neck pain and upper extremity neurologic symptoms. Impingement of the nerve roots can occur from disc protrusion or osteophyte impingement. Proprioceptive reAexes from the cervical spine create a muscle response in the lower extremity. Rotation of the cervical spine in unconscious subjects causes involuntary, external rotation of the lower extremity in the direction of cervical rotation (2). Another phenomenon is cervical vertigo (3-6), in which proprioceptive input from suboccipital muscles and ligaments or the sternoclei domastoid muscle can produce vertigo. The sympathetic paraspinal trunk extends from the thoracic spine to the cranium and contains the superior, middle, and in ferior cervical ganglia. In addition to efferent fibers, the small, nociceptive afferents (C fibers) travel with the sympathetics and synapse in the upper thoracic cord; the cord contains intermedi olateral cell columns. Nociceptive input from the cervical spine produces palpable musculoskeletal changes in the upper thoracic spine and ribs, as well as increased sympathetic activity from this area (7-8). Upper thoracic and upper extremity problems may have their origin in the cervical spine. Vascular

The arterial supply to the head and neck comes from the sub clavian, carotid, and vertebral arteries. The carotid arteries lie anterior to the cervical vertebra. The carotid pulse may be pal pated for diagnostic purposes. Avoid pressure over the carotid arteries while palpating the cervical spine. Thoracic ourlet syndromes involve neurovascular compres sion. Three anatomic sites are often considered:

685

1. Compression between anterior and middle scalene 2. Compression between clavicle and first rib 3. Compression between pectoralis minor and the upper ribs Venous return from the upper extremity is not impaired by scalene tension, as the veins pass in front of the anterior scalene muscle.

lymphatic

The brain is devoid of lymphatic channels; vascular return from the cranium is venous. However, cervical lymphatic drainage is important. Superficial nodes must penetrate the general investing fascia to connect with the deep channels that return lymph to the vascular compartment in the thorax. Infections and inAammation from the head, ear, nose, and throat require effective lymphatic drainage. The use of fascial stretching/release facilitates return, as lymph channels pass through the general investing fascia. Use special lymphatic pump techniques in treating the neck. As al ways, the thoracic inlet must be free to allow lymph to return.

Motion Biomechanics

The major motions at the occipito-arlantal (O-A) joint are Aexion and extension. Side-bending and rotation are considered minor movements. The occiput rotates and side bends in opposite di rections. The occipital condyles converge anteriorly. The lateral portion of the arias articulation is higher (more cephalad) than the medial portion. Posterior movement of the occiput causes a glide to the superior lateral portion, creating side-bending to the opposite side. Anterior rotation is associated with a medial, inferior glide. This gliding motion is considered a minor move ment of the joint and is the motion involved in occipital joint restriction. The major motion of the arias-axis joint is rotation. Half of the rotation of the cervical spine occurs at the arias. Cineradio graphic studies show a significant amount of Aexion and exten sion occurring at the arias (9- 10). This motion does not seem to be involved in somatic dysfunction of the arias. Side-bending is not a significant component of arias movement. Cineradio graphic studies have shown that during rotation, anteriorly or posteriorly, the arias moves inferiorly on both sides, maintaining a horizontal orientation ( 1 1). Side-bending restriction is usually not diagnosed or treated. The arias rotates about the dens, and motion restriction of the arias involves rotation. Motion testing involves rotation testing. Motion of the typical cervical segments (C2 through C7) is similar to type I I mechanics. Cineradiography shows that the cervical spine rotates and side bends to the same side. Type I (neutral) mechanics have not been identified on cineradiogra phy ( 12-13). The vertebral bodies of typical cervical segments are saddle-shaped rather than Aat on the superior and inferior surfaces. Side-bending of the cervical spine can produce lateral translation into the convexity. Some osteopathic physicians call this motion sideslip. The motion of the cervical spine as previ ously described is echoed by Bogduk and Mercer ( 14).

686

Vlf Osteopathic Considerations in PaLpatory Diagnosis and ManipuLative Treatment

DIAGNOSIS

Occasionally, extension may produce lightheadedness. Record these motions in degrees. Measure the range with a goniometer. Osteopathic physicians may elecr ro bypass active motion testing and proceed directly ro passive motion testing. If the patient has neck complaints or has sustained trauma, first detetmine the amount the patient can move.

is tender on the right side; the lateral margin of the articular pillar is tender on the left side. The terms open facet and closed Facet are sometimes applied as positional descriprors of cervical spine somatic dysFunction. Flexion motion (in a normal spine without motion restricrion) causes the facets ro open, and extension motion closes the Facets. Side-bending motion with coupled rotation ro the same side produces a concave side and a convex side. The facets on the concave side are closed while the Facets on the convex side are open. Given a condition of C5 extended, rotated, and side-bent right (restriction of Aexion, rotation, and side-bending left), the right side is the concave side and the left side is the convex side. In motion testing, extension is Free so both Facets close. During Aexion motion testing, the facet on the right side is closed and resists opening. This produces palpable asymmetry in which the tight transverse process (technically, the articular pillar) is more posterior, and the paraspinal muscle over C5 right is tight and palpable. This concept can be applied ro C2-7 segmental motion testing. If a segment is extended (Aexion restriction), rotated, and side-benr right (restriction of rotation and side-bending left), Aexing this segment, which is engaging the barrier, intensifies the palpable postetior transverse process on the right, as well as the palpable muscle change. From this position of Aexion, motion testing reveals a dominanr testriction of left rotation and side bending. If this segment is extended, the motion restriction is significantly less. Engaging the barrier in Aexion or extension intensifies the rotation and side-bending restriction.

Palpation

Passive Motion Testing

The cervical spine may be palpated in the seated position Ot in the supine position. Tissues on the anrerior and lateral portions of the neck can be comfortably assessed with the patient seated and the physician standing behind the patient. Palpate muscle ten sion, tenderness, and tissue texture abnormality (scalenes, ster nocleidomasroid, and trapezius). Examination of the neck with the patient seated and examination of the upper thoracic spine are often integrated. Passive motion testing ro evaluate the ability of muscles ro lengthen is sometimes performed (for example, side bend the cervical spine ro evaluate scalene tension). Palpation of the cervical spine with the patienr supine allows For a detailed evaluation of tissue texture abnormality and ten derness surrounding the cervical spine. The suboccipital region contains muscles that are more lateral than the mid and lower cer vical region, so pataspinal palpation must involve a more lateral placement of the fingers. Significant suboccipital tissue texture abnormality is usually associated with changes in the ipsilateral upper thoracic and rib angle area; look For them. Palpation over the posterior portion of the articular pillars reveals local muscle hyperronicity, tenderness, and tissue texture abnormality asso ciated with segmenral dysFunction. These changes are usually apparent with rotational restriction. Palpate the lateral margins of the articular pillars (locate fin gers laterally and direct the palparory force medially) ro reveal tenderness and tissue texture abnormality over the convex (an terior component) side of segmental dysfunction. For example, given C4 rotated and side-bent right with restriction of left rota tion and side-bending, the posterior portion of the articular pillar

Regional Motion

Inspection

Observe the skin For color changes. Look For asymmetry of posi tion, including: Flexion or extension Side-bending ro the right or left Rotation ro the right or leFt Anrerior posterior curves Relationship of the head ro the lateral weight-bearing line Active Motion Testing

With the patienr seated, ask him or her ro: Rotate ro the right and ro the leFt Side-bend right and left (attempt shoulder) Flex or rouch the chin ro the chest Extend or backward bend

ro

rouch the ear

ro

the

Test the range of regional cervical rotation, side-bending, Aexion, and extension with the patient in the supine position. Evaluate these motions by contacting the head bilaterally and introducing the motions through the head. The range of extension may be difficult ro evaluate with the patient supine because the table gets in the way. Segmental Motion

A novice may test every segment. The experienced clinician tests those segments in which palpation and screening motion tests suggest a problem. The suboccipital area can be confusing. Neurologically, C 1 and C2 are considered a common neurologic segment. Hy peractivity of the C 1-2 segment potenrially involves three joints: the occipiro-arlantal (O-A) joint, the atlanto-axial (A-A) joint, and C2/C3. Therefore, positive palparory findings in the suboc cipital region demand testing of these three joints. Each joint is different in its motion, so they must be individually tested. Occipital Motion Testing of CO-1

Lateral Translation Test

The physician stands or sits at the head of the supine patient. Grasp the head with both hands, with the fingertips of the index and middle fingers over the occipital articulation (Fig. 46. 1).

46. Cervical Spine

FIGURE 46.1.

Lateral translation test for occipital motion.

FIGURE 46.2.

687

Rotation test for atlas motion.

Translate the head to the right and to the left, evaluating free dom or resistance. A more precise method is to perform the lat eral translation test in Aexion and in extension. Flex the occiput (O-A), and then translate to the right and to the left. Then extend the occiput and translate to the right and to the left. Restriction of right translation with freedom of left translation suggests an occiput rotated left and side-bent right (occiput posterior left). If translation is done in Aexion and extension, restriction is encoun tered when the barrier is engaged. Restriction of right translation in the Aexed position suggests an occiput that is extended, rotated left, and side-bent right with restriction of Aexion, rotation right, and side-bending left. There are two O-A joints, one on each side. Given a condition of occiput rotated right and side-bent left, the dominant restric tion, tenderness, and tissue texture abnormality may be on the right side or it may be on the left side. In treating this dysfunction with high-velocity technique, it may be appropriate to localize force precisely to one side or the other. The terminology that has been used by the osteopathic profession for years is positional terminology. This in no way implies that positional diagnosis is preferred; identification of motion restriction is imperative. In the above example of the occiput rotated right and side-bent left, the right side is called posterior occiput and the left side is called anterior occiput. A posterior occiput right exhibits motion re striction, tissue texture abnormality, and tenderness on the right side. An anterior occiput left exhibits motion restriction, tissue texture abnormaliry, and tenderness left. Do confirmatory mo tion tests. Focusing on one side at a time, assess freedom of Aexion and extension. The posterior occiput side exhibits restriction of extension. The anterior occiput side exhibits restriction of Aexion.

At a segmental level, C2-7 motion is difficult to assess by direcrly Aexing and extending, although this has been the method used by many osteopathic physicians in the past. The lateral translation test, which was used extensively by the muscle energy tutorial committee ( 1 5), provides a more precise method of evaluating Aexion and extension while evaluating side-bending.

Atlas Motion Test

Lateral Translation Test

The arias rotates in relation to the axis and becomes restricted in rotation. The motion test of arias function is a rotation test. It is convenient to isolate cervical rotation to the arias by Aex ing the cervical spine prior to rotation. This produces physiologic

The lateral translation test is similar to the occiput lateral transla tion test, except that the hand placement is on the cervical region with the fingertips over the lateral portion of the articular pillars. Stand or sit at the head ofthe supine patient. Support the patient's

locking of C2-7. This is an example of the third principle of phys iologic motion of the spine. Flexion of C2-7 effectively eliminates rotation in this area. Stand or sit at the head of your supine patient. Grasp the head with fingertips contacting the lateral mass of the arias. Flex the cervical spine. Rotate to the right and to the left, assessing the range of motion and freedom or resistance (Fig. 46.2). A right-rotated arias exhibits restriction of left rotation. Os teopathic positional terminology for this dysfunction is posterior atlas right. Flexion, extension, and side-bending motions are not tested. Some osteopathic physicians refer to an anterior arias. The anterior side is opposite the posterior atlas. Given an example of atlas rotated right with restriction of left rotation, the right side would be the posterior arias side. If the left side exhibited tenderness and tissue texture abnormality, it would be referred to as an anterior atlas left. These are not common, but when present, they are very symptomatic and tender. Rerro-orbital pain is often associated with an anterior arias. C2-7 Motion Testing Flexion and Extension Test

688


FIGURE 46.3.

Lateral translation test of (2-7.

head with your hands while palpating the lateral border of the articular pillars. Localizing the force to one segment, test lateral translation to the right and to the left with the segment flexed and with the segment extended. Restriction of right translation in the flexed position suggests extension. Right side-bending suggests right rotation with restriction of flexion, left side-bending, and left rotation (Fig. 46.3). Rotation Test

A rotation test can be done by applying force to one segment at a time. Rotation movement should follow the planes of the facets; therefore, the force is directed up toward the eye, rather than in a horizontal plane. Stand or sit at the head of the supine patient. Support the patient's head, with your fingertips contacting the posterior surface of the articular pillars. Rotate (following the plane of the facets) to the right and to the left, assessing restriction or freedom. Remember, any normal segment should rotate both ways with equal range and freedom. Restriction of right totation of C5 suggests a positional diagnosis of C5 left rotated, left side bent, with restriction of right rotation and right side-bending. The posterior transverse process is on the left (Fig. 46.4).

CLINICAL INFORMATION

Clinical information is available on cervical spine problems. Sub occipital symptoms of tension and tissue change are almost always associated with upper thoracic and rib problems on the same side. It is important to treat the upper thoracic area first because of sympathetic inAuence and muscle connections. Testing the sub occipital area before and after treatment of the upper thoracics reveals a significant decrease in suboccipital findings. The cervical prevertebral muscles (scalenes, longus group) are usually involved in acute neck problems. Gross cervical motion testing reveals restriction of rotation and side-bending to the same side. Sternocleidomastoid shortening causes rotation and side bending to opposite sides. Treatment of scalene and prevertebral muscles must start with treatment of the upper thoracic spine.

FIGURE 46.4.

Rotation test of (2-7.

The functional base of the neck is the upper thoracic spine and ribs. Acute extension trauma (whiplash) with actual injury to Aexor muscles takes prolonged time to treat. Counterstrain, indirect fas cial release, and cranial techniques are more appropriate for initial treatment. Look for an extended (Aexion restriction) upper or mid thoracic somatic dysfunction as part of the injury. The sequence of treatment is as follows: first, the thoracic spine; second, the suboccipital area; and third, the rest of the cervical spine. Acute torticollis with massive neck muscle spasm causes mo tion to be painful and limited. Use a muscle energy technique. Position the head at the midpoint of pain-free motion. Hold the head and ask the patient to turn the head toward the restriction. Relax. Reposition the head a few degrees toward the restriction and repeat. Sometimes a significant improvement in range of motion is achieved. This technique is not classified as direct or indirect, in that the barrier is not engaged nor is the neck posi tioned in the other direction. Instead, the neck is positioned in the middle, with the ultimate objective of reaching the barrier. Cervical root irritation or compression from osteophyte or disc produces nerve-related symptoms in the upper extremity, such as pain, numbness, or muscle weakness. Careful neurologic testing reveals the nerve root dysfunction. Remember that the thumb is innervated by the upper portion of the brachial plexus, the litrle finger by the lowest portion. Look for sensory loss and motor weakness with decreased deep tendon reAexes. The biceps reAex tests C5, and rhe rriceps reAex rests C7. Palpable flaccidity of arm muscles may be present. Somerimes rhe nerve root irriration is intermittent and insufficient to produce any neurologic deficit. Cervical roor irritarion usually produces a reAex change in rhe interscapular area, which rhen produces arm symptoms. A recal cirrant interscapular problem mighr be due to a reAex from rhe cervical spine. Many parients wirh cervical root problems expe rience shoulder pain when rhey lie supine on rhe rable. Ofren, extension of rhe neck exacerbates rhe symptoms. Oblique cer vical spine radiographs reveal osreophyres (cervical spondylosis). Electromyography confirms any neurologic findings. Magneric resonance imaging is an oursranding merhod of imaging cervical

46. Cervical Spine

discs. Computed tomography scans also reveal encroachment. Cervical myelograms are not being done as often as before, as this is an invasive test, and noninvasive tests are now available.

689

2. Asron-Jones tion and stress: basic mechanisms and clinical implications. In: Willard FH, Pa[[erson MM, eds. Nociception and the Neu.roendocrine-Immu.ne Connection, 1992 InternationalSymposium. Indianapolis, IN: American Academy of Osteopathy; 1992:107-132.

TREATMENT

3. Wing L, Hadephobes WW. Cervical vertigo. Aust N Z J Surg. 1974;44(3l:275-277. 4. Jepson O. Dizziness origination in the columna cervicalis. J Can Chiro

The following are treatment guidelines for symptomatic, unstable cervical spine problems: 1.

Avoid high-velocity manipulation of the cervical spine.

2. Decrease muscle tension. Treatment of the upper thoracic spine and ribs is essential ro accomplish this goal. 3. Counterstrain, cranial, and indirect techniques are the least traumatic co the neck. Muscle energy technique, if done with. . . out pam, IS approprtate. 4. Traction, with proper direction of force, is appropriate.

practic Assoc. 1967;11(1):78. 5. Hargrave WW. The cervical syndrome. Aust J Physiotherapy. 1972;Dec 18:144-147.

6. Greenman P. Principles ofMrlrlual Medicine. Baltimore, MD: Williams

& Wilkins; 1989:125. 7. Payan D. Peripheral neuropeptides, inAammation and nociception. In: Willard FW, Pa[[erson MM, eds. Nociception and the Neuroendocrine Immune Connection, 1992 International Symposium. Indianapolis, IN: American Academy of Osteopathy; 1992:3446. 8. deGroat W. Spinal cord processing of visceral and somatic nociceptive inpur. In: Willard FW, Pa[[erson MM, eds. Nociception and the Neuroen docrinelmmune Connection, 1992 International Symposium. Indianapo lis, IN: American Academy of Osteopathy; 1992:4773. 9. Hosono N, Yonenobu K. Cineradiographic motion analysis ofadanroax

CONCLUSION

ial instabiliry in os odonroidellm. Spine. 1991; 16(sllppl 10l0ct:S480S482. 10. Van Mameren H, Sanches H. Cervical spine motion in rhe sagi[[al plane

Manipulative treatmenr of the cervical spine can greatly assist healing of injury, pathology, or dysfunction of the cervical region. This region serves as a pathway between the head and the thorax with neural, vascular, and musculoskeletal communication.

II. Spine. 1992;MayI7(5l:467-474.

1 I. Kirksville College of Osteoparhic Medicine. CineradiographicStudies of the Atlas. Kirksville, MO: Kirksville College of Osteopathic Medicine, 1970. V ideocasse[[e. [This tape was later erased and losr.] 12. Fe/ding J. Cineroentgenography of the normal cervical spine. J Bone JointSurg. 1957;39A:1280-1288. 13. Ochs C, Romine J. Radiographic examination of the cervical spine in

REFERENCES

motion. United States Naval Med Bull. 1974;64:2129. 14. Bogduk N, Mercer S. Biomechanics of the cervical spine. I. Normal kinematics. Clin Biomech (Bristol, Avon). 2000; 15:633-648.

1. Warwick R, Williams PL, eds. Gray'sAnmomy, British 35th ed. Philadel phia, PA: WB Saunders; 1973:235.

15. MitchellJtE The Muscle Energy Manual, I. East Lansing, MI: MET Press; 1995:166-167.

UPPER EXTREMITIES ROBERT E. KAPPLER KENNETH A. RAMEY

FUNCTIONAL ANATOMY KEY CONCEPTS • • • • • •

•

• •

•

•

Skeletal and Arthrodial Structures

Functional anatomy of the upper extremities, i ncluding range of motion assessment Muscle groups and innervations of the glenohumeral, scapulothoracic, elbow, and wrist joints Arterial and venous supply to the area Lymphatic drainage of the upper extrem i ties Sympathetic in nervation and the brachial plexus Diagnosis by history and physical examination, including observation, palpation, pulses, several reflexes, motor strength, and sensation Motion testing of the shoulder, costovertebral, costosternal, sternoclavicular, acromioclavicular, and scapulothoracic joints Configuration, physiologic motion, and somatic dysfunction of the elbow and forearm Configuration, physiologic motion, and somatic dysfunction of the wrist and hand, i ncluding the intercarpal, carpometacarpal, metacarpophalangeal, and i nterphalangeal joints Special tests, including Adson, Yergason, drop arm, apprehension, bicipital tend i n it is, Apley scratch, Tinel sign, Phalen, Allen, and ten n is elbow Treatment of carpal tunnel syndrome, reflex sympathetic dystrophy, adhesive capsul itis, and thoracic outlet syndrome

B)' extemive study. / have formed in my head a perpetllaL image of evo} articuLation ill the finmework ofthe human body (/ J.

-A. T. StiLL

The upper extremities are vital to performing the activities of daily living. Even minor inj uries may produce disabilities that significantly affect overall function. Effective diagnosis and treat ment necessitates a thorough understanding of the structure and function of this i m portant region.

The bones of each upper limb i nclude the: Clavicle Scapula Humerus Radius Ulna Eight carpal bones Five metacarpal bones 1 4 phalanges Functionally, the upper extrem ity can be divided into the: (2) Scapulothoracic joint Acromioclavicular joint Sternoclavicular joint Glenohumeral joint Elbow Wrist Intercarpal, carpometacarpal, metacarpophalangeal, and terphalangeal joi nts

111-

The scapulothoracic joint is formed by the articulation of the anterior surface of the scapula with the posterior thorax. Consid erable motion is possible: Elevation Depression Protraction Retraction Rotation about a transverse axis The sternoclavicular joint is formed by the articulation of the medial end of the clavicle with the manubrium of the sternum. This joint may become sprained by clavicular displacement in relation to the sternum. The acromioclavicular joint is formed by the articulation of the lateral end of the clavicle with the acromion process of the scapula. Functionally, this joint acts as a ball and socket providing anteroposterior, superoi n ferior, and rotational motion.

47. Upper Extremities

The glenohumeral joinr is formed by rhe anicularion of rhe head of rhe humerus wirh rhe glenoid fossa of rhe scapula. The morions of rhis joim include flexion, exrension, abduC[ion, ad duction, internal rorarion, and exrernal rorarion. The elbow joint is formed by rhe arricularion of the humerus, ulna, and radius. The true elbow joint is the ul nohumeral joint. The proximal ulnohumeral joint, which allows supinarion and pronation of the forearm, is also located on the lateral side of the elbow joint. Possible motions include flexion, exrension, ab duction, and adduction of the ulna on rhe humerus; rhe pivotal motion for pronation and supination of the forearm is p rovided by the proximal radioulnar joint. The wrist is formed by the juncrion of rhe ulna, radius, and the carpal bones. The true wrist joint is the radiocarpal joim, formed by the distal end of the radius and the rhree proximal carpal bones: the scaphoid, lunate, and rhe triquetral. Possible motions include flexion, extension, abduction, and adduction , a s well a s supination a n d pronation o f the hand a n d forearm. Aniculations in rhe hand include the: Intercarpal joims Carpometacarpal joints Meracarpophalangeal joints Jmerphalangeal joinrs Osteopathic diagnosis largely involves the assessmenr of both qualiry and quamiry of motion. General ranges of motion permit effective screening of the skeletal and arth rodial componems of this region. There is a ratio of movement between abduction of the arm at the glenohumeral joint and rotarion of rhe scapulothoracic artic ulation: for every 3 degrees of abduction measured at rhe gleno humeral joinr, 2 degrees actually occurred at the glenohumeral joinr and I degree occurred at the scapulothoracic aniculation. When the arm is fully abducted to 1 80 degrees, 1 20 degrees are due to the glenohumeral joim motion alone and 60 degrees are due to rotation of the scapula and clavicle to elevate those structures 60 degrees (Tables 47. 1 rh rough 47.3). Somatic dysfunction typically involves restriction and the end of a range of motion. It is most likely to be found in the minor TABLE 47.1. MAJOR

MOTIONS

OF

THE

SHOULDER,

ELBOW, WRIST, AND METACARPOPHALANGEAL JOINTS Glenohumeral Joint Abduction

Elbow

Wrist

Metacarpophalangeal

Flexion 135

Supi nation 90

Flexion 90

Extension

Pronation 90

Extension 30--45

180 Adduction 45

Fl exion 80

Extension 45

Extension 70

Internal

U l n ar

rotation 55 rotation

Proximal Interphalangeal Joint

Distal Interphalangeal Joint

Flexion 100

Flexion 90

Extension 0

Extension 20

From Hoppenfeld

N ew York,

S. Physical Examination of the Spine and Extremities. 1976, with permission.

NY: Appleton-Century-Crofts

morion(s) of each joint. Onhopedic problems associated wirh disruption of joim stabilizers com monly involve laxiry and insra biliry at the end of a range of motion. The most time-effective, yet rho rough examination involves screening ranges of motion with careful arrention to end-morion pal patory finding. Muscles

Muscles generally act in groups to produce specific motions. De tailed assessmem of rhe upper extremiry necessitates an under standing of these groups and their innervations (2). Tables 47.4 through 47.7 presem rhe m uscles of the following joinrs: (2) Glenohumeral joint (Table 47.4) Scapulothoracic join r (Table 47.5) Elbow (Table 47.6) Wrist (Table 47.7) Arterial Supply

The left subclavian anery arises from the posterior part of the aorric arch. Ir passes posterior to the left srernoclavicular joint. The right subclavian arrery arises from rhe brachiocephalic rrunk (3). The subclavian arteries pass over the top of the fi rsr rib be tween the anterior and middle scalene muscles. The subclavian anery becomes the axillary artery at the lateral border of the fi rst rib. The axillary arrery passes posrerior to the pectoralis minor m uscle and becomes the brachial artery at rhe inferior border of the reres major m uscle. Branches from the axillary and brachial arteries supply the structures of rhe shoulder, arm, forearm, and hand. Somaric dysfuncrion of rhe following structures may affecr arterial supply: Anterior and middle scalenes Upper rhoracic vertebrae Upper ribs Clavicles Fascia of the upper extremiry

TABLE 47.3. MAJOR MOTIONS OF THE JOINTS OF THE THUMB

deviation 30 Radial Deviation 20

40--45

S. Physical Examination of the Spine and Extremities. New York, NY: Appleton-Century-Crofts 1976, wi t h permission. From Hoppenfeld

TABLE 47.2. MAJOR MOTIONS OF THE PROXIMAL AND DISTAL INTERPHALANG EAL (lP) JOINTS

0-5

Flexion 90

Exter n a l

691

Thumb

Thumb

Thumb

Metacarpophalangeal

Interphalangeal

Joint

Joint

P a l m a r a bd uction 70

Flexion 50

Flexion 90

P a l m ar adduction 0

Extension 0

Extension 90

692


TABLE 47.4. MUSCLES OF THE G LENOHUMERAL JOINT AND SHOULDER Primary flexors

Secondary flexors

Deltoid (anterior portion) muscle

Axillary nerve

C5

Coracobrach i a l i s muscle

Musculocutaneous nerve

C5-6

Deltoid (mid portion) muscle

Axillary nerve

C5-6

Supraspinatus muscle

Suprasca pular nerve

C5-6

Anterior thoracic nerve (medial. latera l)

C5-T 1

Pectoralis major muscle (clavicular head) Biceps

Primaryabductors

Secondary abductors

Deltoid muscle (anterior, posterior) Serratus anterior muscle via scapula Pectoralis major muscle

Primaryadductors

Latissi m us dorsi muscle

Secondary adductors Primaryextensors

Secondary extensors Primaryexternal rotators

Teres minor muscle Anterior deltoid muscle Latiss i m u s dorsi muscle

Thoracodorsal nerve

C6-8

Teres major muscle

Lower subscapular nerve

C5-6

Deltoid (posterior portion)

Axill ary nerve

C5-6

Infraspinatus

Suprasca p u l ar nerve

C5-6

Teres m i nor

Axil lary branch

C5

Teres minor muscle Triceps (long head) muscle

Secondary external rotators

Deltoid muscle (posterior portion)

Primaryinternal rotators

Subsca p u l aris muscle

Subsca p u lar nerves (upper a n d lower portion)

C5-6

Pectora l i s major muscle

Anterior thoracic nerves (med i a l a n d lateral)

C5-T 1

Latissimus dorsi muscle Teres m i nor m uscle

Secondary internal rotators

Deltoid muscle (anterior portion)

Venous Supply

The axillary vein lies on the medial side of the axi llary artery. The axil lary vein receives tributaries thar correspond to the branches of rhe axil lary artery and receives venae comitantes of the brachial arrery. It ends at the lateral border of the first rib, where it becomes the subclavian vei n (3). The subclavian vein passes over the first rib anterior to the anterior scalene muscle (3). The subclavian vein unites wirh the i nternal j ugular vein to become rhe brachio cephalic vein (3) . The left brach iocephalic vei n passes posterior to

the left sternoclavicular joint and crosses the midline. The right brachiocephalic vein passes posrerior to the right srernoclavicular joint. The right brachiocephalic vein joins rhe lefr brachiocephalic vein to form the superior vena cava (3). Dysfunction in rhe up per thoracic vertebrae (causing increased sympatheric tone to rhe upper extrem ities) , upper ribs, clavicles, and fascia of rhe upper extremities may i m pair venous return. Because the vein passes anterior to the scalene muscles, scalene rension does not create venous distention of the upper extrem ity. Lymphatic Drainage

TABLE 47.5. MUSCLES OF THE SCAPULOTHORACIC JOINT Primary

Trapezius m uscle

Accessory nerve

CN XI

Levator scap u l a e

Dorsal sca p u l ar

C3-4. C5

ele v ators m u scle

Secondary elevators

Primary protraction Primary retraction

Rhomboid major muscle Rhomboid minor muscle Serratus anterior muscle Rhomboid major muscle Rhomboid m i nor muscle

Secondary retraction

nerve C5 (plus)

Trapezius muscle

The major lymph nodes of the upper extremities are found i n the fibrofatty con nective tissue of the axilla. They are arranged into five groups, four of which lie inferior to the pectoralis m inor tendon and one which lies superior to it ( Fig. 47.1). These groups

TABLE 47.6. MUSCLES OF THE ELBOW JOINT Primaryflexors Long thoracic

C5-7

C5-6

Biceps muscle

Musculocutaneous

C5-6

nerve C5

nerve Dorsal sca p u lar

Musculocutaneous nerve

nerve Dorsal sca p u l ar

Brach i a l i s muscle

Secondary flexors

Brachioradialis muscle Supinator muscle

Primaryextensor

Triceps muscle

Secondary extensor

Anconeus muscle

C5

nerve

C6

R a d i a l nerve

C7

47. Upper Extrem ities

693

TABLE 47.7. MUSCLES OF THE WRIST Primaryflexors

Primaryextensors

Primarysupinators

Flexor carpi rad i a l i s m .

Median n.

Flexor carpi u l n a r i s m .

U l n a r n.

Extensor carpi rad i a l i s longus m .

Radial n.

Extensor carpi rad i a l i s brevis m .

Radial n.

Extensor carpi u l n a ris m .

Radial n .

(6(7)

Biceps m. S u p i n ator m.

R a d i a l n.

Secondary supinator

Brachioradialis

Primarypronators

Pronator teres m.

Median n.

Pronator quadratus m.

Median n. (ant. interosseous

m.

(6

branch)

Secondary pronator

Flexor carpi radialis

m.

are the: Pec[Oral Lateral Subscapular Central Apical The pec[Oral group of axillary lymph nodes lies along the medial wall of the axilla. This group receives lym ph mainly from the anterior thoracic wall and breast. The efferent vessels from these nodes pass [0 the central and apical groups of axillary lymph nodes (3). The lateral group of lymph nodes lies along the lateral wal l of the axilla. This group receives lymph from most of the upper limb.

The subscapular group of axil lary lymph nodes is located along the posterior aspect of the thoracic wall and scapular region . Efferent vessels pass from here [0 the central group o f axillary lymph nodes. The central group of axillary lymph nodes is situated deep [0 the pec[Oralis m i nor near the base of the axilla. Th is group receives lymph from the other axillary lymph nodes. Efferent vessels pass lymph [0 the apical lymph nodes. The apical group of axillary Iym ph nodes is situated in the apex of the axilla. This group receives lymph from the central lymph nodes. The efferent vessels from this group un ite [0 form the sub clavian lymphatic tru n k. The right subclavian lym phatic trunk dra i ns in[O the right lymphatic duct. The left subclavian lym phatic trunk drains i nto the thoracic duct. Somatic dysfunction affecting the venous system may also affect lymphatic drainage, thereby producing congestion in the upper extremity. Venous blood

Right subclavian vein

Jugular vein

Lateral group

Right

Lymphatic

lymphatic

vessels from

duct (RLO)

upper extremity

Brachio cephalic vein

vena cava

Pectoralis group (anterior group) Subscapularis group (posteior group)

FIGURE 47.1. Lymphatic dra i n a g e of upper extrem ity. (Il l ustration by W. A. Kuchera.)

694


Sympathetics

Observation

The sympathetic in nervation to the upper extremltles arises from the upper thoracic spinal cord. The sympathetic ganglia lie anterior to the rib head, in the fascia common to both structures. Dysfunction in the upper thoracic spine and ribs may increase sympathetic tone to the upper extremity and produce altered motion, nerve dysfunction, and lymphatic and venous conges tion. Increased sympathetic tone is accompanied by palpatory findings in the upper thoracic/rib area and increased sensitivity to painfUl stimulus. It also prevents arterial blood from getting to the structures of the arm and reduces the amou nt of lym phatic Auid returning from the arm via the lymphatic vessels. The cause of these m usculoskeletal fi ndings may be visceroso matic; they may be primary somatic in the area, or they may be reAex from the cervical spine. Nociceptive afferents from the cervical spine travel in the sympathetic chain and synapse in the intermediolateral cell col u m ns of the upper thoracic cord. This produces an irritable focus in the cord, with resulting somatic and sympathetic hyperactivity.

Observation begins the moment the patient walks into the room. Observe overall posture and motion. Is there any abnormality? Observe the patient in the standing position. Look at the height of the shoulders. A low shoulder may be the result of a short leg or a lateral curve. Look at the spine from the side. Is the thoracic kyphotic curve normal, increased, or decreased? An area of tho racic spine Aattening may indicate the presence of an extended somatic dysfunction. Dysfunction in the upper thoracic spine may alter sympathetic tone and produce dysfunction in the up per extremity. Begin at the shoulder and examine the skin of the upper extremity. Is there any asymmetry? Areas that appear red dened or have pigment changes may have somatic dysfunction. Observe the various muscle groups bilaterally. Is there evidence of hypertrophy or atrophy? Look for the presence of fasciculation (small tremors) in the muscle.

Brachial Plexus

Nerve roots C5-S and Tl form the brachial plexus. These nerve roots pass through the intervertebral foramen of the cervical vertebrae and pass berween the a nterior and middle scalene mus cles. The roots unite to form successive trunks, divisions, cords, and branches. The nerve trunks extend from the scalene triangle (formed by the a nterior and middle scalenes and the clavicle) to the clavicle. Nerve divisions extend from a position posterior to the clavicle to the axilla. Nerve cords are found in the axilla. Nerve cords divide inro branches that innervate various structures in the upper extremity. The neurovascular bundle of the arm contains the subclavian artery, subclavian vein, brachial plexus, and the sympathetic nerve plexus.

DIAGNOSIS History

When is arm pain something more? Upper extremity discomfort cannot always be attributed to dysfunction in this area. A good clinician must determine whether the discomfort is primarily caused by dysfunction in the extremity or referred from another area. If the cause lies in the upper extremity itself, there is generally restricted motion . Pain is usually localized to specific dermaromes and may be described as acute, sharp, and severe. Discomfort is usually im proved by rest, is frequently reproduced by motion , and may lead to the perception o f strength loss. If the discomfort is referred from another area (e.g., the lungs, diaphragm, stomach, intestines, heart, or cervical spine), passive motion does not appear to be restricted. Pain is diffuse, poorly localized, and may be described as nagging, achy, or dull. Discom fort is usually worse at night. Discomfort is frequently related to symptoms in other areas (difficulty breathing, chest pain, cough, gastrointestinal upset) and may not be reproduced by motion. Motion is generally good, but decreased strength or muscle atro phy is possible (e.g., disc herniation).

Palpation

Begin by palpating the superficial tissue of the shoulders. Palpate into the deeper tissues. Look for signs of acute or chronic tissue texture change. Remember to com pare the right side with the left side and areas located superiorly with areas located inferiorly. Compare muscle groups bilaterally for size and tone. Pulses

Thorough examination of the upper extremities necessitates an examination of the brachial and radial pulses. The brachial pulse is found on the medial surface of the arm just medial to the biceps tendon. The radial pulse is best palpated over the lateral and ventral side of the wrist. Examine the arterial pulses with the distal pads of the second, third, and fourth fingers. Palpate firmly but not so hard that the artery is occluded. Arterial pulses can be examined for: Heart rate and rhythm Pulse contour (wave form) Amplitude (strength) Symmetry Lack of symmetry berween the left and right extremities sug gests impaired circulation. The amplitude of the pulse can be described on the scale shown in Table 47.S (4). Reflexes

The three basic reA exes that evaluate the integrity of the nerve supply to the upper extremity are the biceps reAex, the brachiora dialis reAex, and the triceps reAex. Each of these is a deep tendon

T ABLE 47.S. STANDARD

METHOD

FOR

RECORDING

AMPLITUDE OF THE PULSE

4/4 3/4 2/4 1/4 o

Bounding

Full, Increased Expected

Diminished, barely palpable Absent, not palpable


TABLE 47.9. STANDARD

METHOD

FOR

RECORDING

AMPLITUDE OF A REflEX

o 114 2/4 314 4/4

Absent

Decreased but present Normal

Brisk with unsustained clonus Brisk with sustained clonus

reAex (lower moror neuron reAex) transmitred ro the cord as far as the anterior horn cells and returning ro the muscle via the pe ripheral nerves. ReA exes may be increased in the presence of an upper moror neuron lesion or may be decreased in the presence of a lower moror neuron lesion (bulging disc). Biceps Reflex

This primarily tests the integrity of neurologic level CS. Place the patient's arm over your opposite arm so that it rests on your forearm. With your elbow supporting the patient's arm under the elbow's medial side, place your thumb on the tendon of the biceps in the cubital fossa. I nstruct the patient ro rest the arm on your forearm and relax. Tap your thumbnail with a neurologic hammer. The biceps should jerk slightly. You should be able to see or feel its movement.

695

clinical picture. There are some simple screening procedures that are useful. Although not a test of strength, palpation for Aaccidity may reveal muscles that should be tested. For cervical root or brachial plexus problems, perform a grip strength test by asking the patient to squeeze two of your fi n gers. Another simple test is to ask the patient to squeeze the thumb and index fi n ger together while you try to pull them apart. If normal strength is present, it is difficult to pull them apart. Sensation

This can be tested by light rouch, pin prick, or two-point dis crimination. Compare both sides and areas located superiorly with areas located inferiorly. Look for areas of either decreased or increased sensation . Sensation around the upper extremity is controlled by five different nerve supplies: I. CS controls the lateral arm 2. C6 controls the lateral forearm 3. C7 controls the index fi nger 4. C8 controls the medial forearm S. TI controls the medial arm Motion Testing

Shoulder Motion

Brachioradialis Reflex

This tests neurologic level C6. Support the patient's arm in the same manner used to test the biceps reAex. Tap the brachioradialis tendon at the distal end of the radius with the neurologic hammer. Triceps Reflex

This reAex tests neurologic level C7. Use the same position as above. Tap the triceps tendon where it crosses the olecranon fossa (2) . Remember to use bilateral comparison. ReAexes may be graded as shown in Table 47.9. Motor Strength

T he strength of various muscle groups can be evaluated by apply ing force in a man ner that loads the muscle as the patient resists. Remember to test the uninj ured side first. Table 47. 1 0 shows a standard method of recording motor strength. Differences in muscle strength may be subtle. Compare the strength of various groups in different positions to get the full

TABLE 47.10. STANDARD

METHOD

FOR

RECORDING

MOTOR STRENGTH

5/5

Normal

Complete range of motion a g a i nst gravity

4/5

Good

Complete range of motion a g a i nst gravity

315 2/5

Fair

Complete range of motion against gravity

Poor

Complete range of motion with gravity

115

Trace

Evidence of slight contractility; no joint motion

0

Zero

No evidence of contract i l ity

with f u l l resistance with some resistance

e l i minated

Shoulder motions can be screened by using gross motion analysis or by the seven motions of Spencer. Gross motions can be screened by asking the patient to: Abduct the arms to put the palms together overhead Abduct the arms to put the backs of the hands together over head Reach across the chest to touch the opposite shoulder Reach behind the body to scratch the opposite shoulder (Apley scra tch test) I nternal and external rotation may be tested as follows: (S) I . With the arm at the side, the forearm is Aexed 90 degrees at the elbow and the elbow is supported. The forearm is turned medially to test internal rotation and laterally to test external rotation. 2. With the arm abducted 90 degrees at the shoulder, the forearm is Aexed 90 degrees at the elbow and the elbow is supported. An anterior arc of the forearm produces internal rotation, and a posterior arc produces external rotation . Testing o f the shoulder can b e localized t o the glenohumeral joint by stabilizing the scapula with one hand as the arm is moved with the other. A gross test of stability of the glenohumeral joint is to stabilize the scapula and translate the head of the humerus anteriorly and posteriorly. Compare both sides. An unstable joint moves too freely; with adhesive capsulitis, there is no motion. Mo tion of the entire shoulder girdle is evaluated without stabilizing the scapula to isolate glenohumeral motion. In evaluating total shoulder girdle motion, observe the amount of scapulothoracic motion as the shoulder girdle moves. Most shoulder problems involve dysfunction of muscles. Malposition of the scapula alters the working length of a shoulder girdle muscle. Treatment of

696

VlI. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment

shoulder problems necessitates and often starts with evaluation and treatment of scapulothoracic position and motion. The seven motions of Spencer systematically test all shoul der motions and can be expanded to include a treatment mode should any restrictions be identified. Du ring testing and treat ment, the scapula is fixed in position to permit movement only at the glenohumeral joint: I . Extend the upper extremity 90 degrees. 2. Flex the upper extremity 1 80 degrees. 3. Circumduct the upper extremity while compressing the gleno humeral joint (tests j oint surfaces). 4. Circumduct the upper extremity while applying traction (tests the capsule). 5. Abduct the upper extremity 90 degrees. 6. Place the patient's hand behind the small of the back and gently test internal rotation by pulling the elbow forward. 7. Extend the upper extremity and apply traction and caudal glide to the humerus while holding the proximal end of the humerus. 8. Optional: hold the patienr 's hand with the upper extremity extended and shake the upper extremity up and down while carrying it through an arch in a parasagittal plane to the limits of comfort. If the seven gross motions tested using Spencer techniques are normal, then the shoulder is considered ro have good function (5). Refer ro Chapter 55, Articulatory Treatment, for a more de tailed description of Spencer technique for the shoulder. Costovertebral Joints

•

These are the true costovertebral and costotransverse joinrs of the first rib. Both of these j oints are synovial. The first rib is an atypical rib and only articulates with the body of T l. The common somatic dysfunction of the fi rst rib is elevation: the rib moves freely in elevation and has a restriction of motion to depression. Motion is tested by placing your thumbs over the posterior aspect of the rib and instructing the patienr to take a deep breath. Assess the quality of motion in both inhalation (elevation) and exhalation (depression) . Frequently, Tl is rotated and side-bent to the side opposite the side of the elevated first rib. Costosternal Joint of the First Rib

This is a synchondrosis, not a synovial joint. It is therefore very stable. Its functional pu rpose is more for support than for motion. Because of this stability, somatic dysfunction is not often found in this area. Sternoclavicular Joint

This is a complex synovial joint that contains a cartilaginous meniscus. The subclavius muscle depresses and pulls the medial end of the first rib forward when the lateral end of the clavicle is elevated. There are th ree axes of motion in the sternoclavicular

j oinr. These are tested by having the patient shrug the shoulders up and down, forward and backward, and internally and exter nally rotating the shoulder while bridging and palpating the joint with your fingers. Acromioclavicular Joint

This joinr also has motion about th ree axes; motion about each axis is difficult to palpate. Separation of the joinr is palpated by placing your fingers over the j oinr and adducting the arm across the thorax. The most common somatic dysfunction of this j oint involves a functional glide of the clavicle upward and laterally along the acromion. Acromioclavicular (AC) separation goes beyond somatic dysfunction and is a true sprain. The extent of injury can be easily evaluated by palpating the AC joinr and applying a downward traction to the h umerus. The extenr of gaping is a measure of the inj ury. This physical examination test is also very useful in evaluating healing. Treatment ofAC separation is usually a matter of taking care of the accompanying thoracic cage problems, which are always presenr. The joint heals itself, and surgery is rarely needed. Scapulothoracic Joint

This pseudojoint allows the scapula to glide medially and later ally, superiorly and inferiorly, and rotate over the posterolateral chest cage. The position of the scapula can be evaluated in a seated or standing examination. Asymmetry of position of the scapula usually indicates asymmetry of motion. Scapular motion can be tested with the patient side-lying. Grasp the scapula with both hands and take it through the various motions. The scapula can: (5) 1 . Glide forward and separate each vertebral border 1 5 cm and glide backward to bring the vertebral borders closer. 2. Glide 1 0 to 1 2 cm su periorly and inferiorly. 3. Rotate to elevate or depress the glenoid fossa 30 degrees each way.

ELBOW AND FOREARM Configuration and Physiologic Motion

The ulnohumeral j oint is the true elbow j oint (6). The head of the radius at the proximal end of the radial bone near the elbow is not a part of the elbow joint. Primary motion of the normal elbow is 1 60 degrees of flexion and 0 degrees of extension about a transverse axis ( 1 0 degrees of hyperextension is found in some individuals). The elbow joint is stable medially and laterally but weak anreriorly and posteriorly. Its anteroposterior stability and strength depends on the muscles that pass anteriorly and posteriorly to the elbow joint and on how firmly the trochlea of the h umerus fits into the trochlear notch of the ulna. The medial side of the ulnar notch is anatomically elongated and there is a slight ridge in its joint surface. There is also a grooved spiral in the h umeral j oint surfaces. The groove-spiral anatomic characteristic causes the hand to normally move toward the mouth when the elbow is fl exed and to the lateral side of the hip when it is extended.


A

FIGURE 47.2. Carrying a n g l e a n d parallelogram effect. (Illustration by W. A. Kuchera.)

This strucrural configurarion also produces rhe normal carrying angle of rhe arm, grearer in rhe female rhan in rhe male. This carrying angle is nor very noriceable if rhe arm is hanging ar rhe side of a person because in rhis posirion, rhe forearm has a natural panial pronarion. The elbow also "wobbles" into ulnar adducrion during its normal motion. An abducrion somaric dysfuncrion of the ulna increases rhe carryi ng angle, and adducrion somaric dysfuncrion decreases rhe carrying angle (Fig. 47.2) . As rhe disral end of rhe ulna is abducted, rhe olecranon process glides more medially. This reciprocal movement of the two ends of the ulna also occurs with adduction . It is restriction in one of these glides and ease in the opposite glide that constitutes ulnar somatic dysfunction. Somaric dysfunction of the elbow joint is named according to rhe motion thar is present, that is, ulnar abduction, or ul nar adducrion (Fig. 47.3). The true wrist is the ellipsoid synovial radiocarpal joint (Fig. 47.4) formed by a concavity in the distal end of the radius, three proximal carpal bones of rhe wrist (the navicular or scaphoid bone in the snuffbox of the wrist, the lunate, and the rriquetral bones), and an articular disc. The articular disc separates rhe true wrist joinr from the disral radioulnar joint. The head of the ulna (the disral end of rhe ul na) is not a part of the true wrist joint. The true elbow and wrist joints are functionally linked wirh the radius by proximal and disral synovial radioulnar joints and a fibrous middle radioulnar joint called the interosseous membrane (Fig. 47. 5). The inrerosseous membrane maintains functional symmetry and srability of rhe forearm . The proximal and distal radioulnar joints allow pivot acrion, permitting sup in arion and pronarion of rhe hand. The fibers of rhe interosseous membrane exren d cepha-

697

B

Parallelogram mechanics:

Parallelogram mechanics:

Ulnar abduction

Ulnar adduction

FIGURE 47.3. (A) Ulnar abduction, (8) u l n ar neutral, tion. ( I l lustration by W. A. Kuchera.)

(C) u l nar adduc

lad from arrachment on rhe ulna to a more proximal attachment on rhe radius. This arrangement allows the bones of the forearm to share rhe forces of compression whether they occur fro m the hand upward or rhe shoulder downward. Note rhe reciprocal glide of rhe radial head in response to rhe direction of movement ar the dis tal end ofrhe radius i n Figure 47.8. The radius and ulna are held i n a parallelogram arrangement by the radiocarpal joints (Fig. 47.6). The ulna is parr of rhe elbow j oint, and the radius is parr of rhe wrist joint. The radius is able to move more freely than rhe ulna. With the ulna relatively fixed at rhe ulnohumeral joint and rhe radius fairly fixed at the radiocarpal joint (especially wirh rhe scaphoid), abduction or adduction of rhe ulna results i n a recipro cal posirioning of the hand ( Fig. 47.3). During abduction of the

A

�!!!"3-+- Transverse axis Articular disc

FIGURE 47.4. Right radiocarpal joint (true wrist joint) a n d d istal ra diou lnar joint. R, rad ius; U, ul na; 5, scaphoid; L, lunate; T triquetra!. ( I l lustration by W. A. Kuchera.)

698

VII. Osteopathic Considerations in PaLpatory Diagnosis and ManipuLative Treatment

Carrying angle increased

decreased

t

rn ::J

'6 � '0

rn ::J

'6 � '0

Q)

'2 0, Cii Ci) is

Carrying angle

Carrying angle normal

.

Q)

X

x+y

5' 0, Cii E

t

� x-v

.� a..

Abduction of ulna

Adduction of ulna

FIGURE 47.5. Forearm: interosseous membrane. ( I l l ustration by W. A. Kuchera.)

ul na, the radius glides distally and the wrisr is lirerally pushed inro increased adduction. During adducrion of the ulna, the radius glides proximally and the wrist is pulled into a more abducted position, compared with the position of the opposite wrisr. I f rhis reciprocal positioning principle o f rhe elbow and the wrist is incorporared in the direct and indirecr trearmenr of ulnar ab ducrion or adducrion somaric dysfu ncrions, rhese techniques will become more effective and efficienr. The parallelogram arrange ment of the forearm bones wirh the action of rhe proximal and disral radioulnar joinrs permits forearm/wrist motions. As these morions occur, rhe inrerosseous membrane (a radioulnar fibrous joint) provides srabiliry to the forearm and prevenrs srress of the ligamenrs and/or bony compression in the forearm or rhe wrisr. There is reciprocal motion of rhe radius. When rhe hand is pronated, the distal end of the radius crosses over rhe u l na as it moves anreriorly and medially ( Fig. 47.7) . Near rhe end of full pronarion, rhe head of rhe radius glides posreriorly, rhar is, there is reciprocal morion of the radial head relarive to the disral radius. Morion in an arc opposire from rhe posirion of rhe pronated hand is called supinarion ( Fig. 47.8) . When the forearm is supinated, rhe disral end of rhe radius moves posreriorly and the radial head glides anreriorly. These motions are best pal pared near rhe end offull supination or pronation of rhe hand. They are palpable if the operator's fingers are under the patient's elbow and the thumb of that hand is palpating rhe radial head while the other hand supinares or pronates the parient's hand. Motion in the symptomaric forearm is compared with motion in the opposire or normal forearm. The mechanism for strain of rhe forearm, wrist, or elbow can also very easily strain rhe inrerosseous membrane. I nterosseous membrane dysfu ncrion can perpetuare elbow or wrisr disabil iry long afrer p roper orthopedic care and apparently complere healing ofsrrains, sprains, or fractures ofrhe elbow or wrist should

A+B Increased adduction of wrist

A Normal

A-B Decreased adduction of wrist

FIGURE 47.6. Right forearm: para l l e logram effect. ( I l l ustration by W. A. Kuchera.)

FIGURE 47.7. Forearm: pronation. ( I l l ustration by W. A. Kuchera.)


699

Mechanism for posterior radial head somatic dysfunction

Supination

Distal radius rotates posterolaterally

Anterior distal end

FIGURE 47.S. Forearm: s u p i nation. ( I l l u stration by W. A. Kuchera.)

have taken p lace. In some unknown way, the collagen tissues of ten retain stress patterns of past injury. In such cases, palpation of the interosseous membrane reveals increased tension and elicits areas of subjective tenderness. Interosseous strains may be treated with direct or indirect fascial treatments. Somatic Dysfunction of the Elbow Joint Area

Several principles govern the elbow j oint area: 1 . Somatic dysfunction of the extremity is found in the minor gliding motions of the joint, not the major motions. 2. Somatic dysfunction of the ulno h umeral j oint is usually pri mary, and somatic dysfunction of the radioulnar joints is usu afl y secondary. 3. I mpaired function of any joint of the arm produces compen satory changes in all other j oints. I f total functional demand overtaxes any one of the other joints, secondary somatic dys function is also produced in those joints.

FIGURE 47.9. Forward f a l l on outstretched h a n d . ( I l l ustration by W. A. Kuchera.)

cannot be flexed completely, the problem is most likely one of the radioulnar j oints, usually the proximal one. The interosseous membrane may also be involved. Reciprocal motions of the ends of the radius are preserved, even when radial stress results in somatic dysfunction. Posterior radial head somatic dysfunction is usually produced by a fal l for ward onto the palm of an outstretched hand because the anterior motion of the distal radius, started by the pronation, is accen tuated. Though a fall forward is on the h and, the hand is in a p ronated position, and the forward vector of the hand and body pushes the distal radius into a more anterior rotation, causing the radial head to move posteriorly ( Fig. 47.9). An anterior radial head somatic dysfunction is likely to result from a fall backward, where the p atient extends the arm posteri orly to break the impact of the fal l , lands on the palm, and forces the distal end of the radius posteriorly. In this type of injuty, the forearm is in the supinated and anatomic position ( Fig. 47. 1 0) .

Somatic Dysfunction of the Forearm

Inspection by itself is usually not very helpful , although it may be helpful when the carrying angle has been affected by somatic dysfunctions of the ulnohumeral joi nt. Increased abduction ofthe ulna would increase the carrying angle and encourage adduction of the hand at the wrist. Increased adduction of the ulna at the elbow encourages some abduction of the hand at the wrist. This is noticed as less adduction of the hand at the wrist. Patient history may direct the physician to the site of the somatic dysfunction and often indicates the region in the upper extremity. Comparing minor passive gliding motions of the right and left upper extremities is the most helpful way of finding the exact somatic dysfunction. If the wrist hurts, look at the elbow. The only sign of somatic dysfunction of the elbow may be a complaint of wrist pain. If all ulnohumeral joint somatic dysfunction has been treated, there is no inflammation in the elbow joint, and the elbow still

WRIST AND HAND Configuration and Physiologic Motion

The hand j oins the forearm by way of the true wrist j oint. This is a stable j oint composed of the radius, three carpal bones, and the attached cartilage. The basic configuration of the true wrist (the radiocarpal joint) is illustrated in Figure 47.4. This j oint has two major axes of motion: the transverse axis, around which there is flexion and extension, and an anteroposterior axis, about which there is abduction and adduction. All motions are named accord ing to the anatomic position of the j oint and not according to the position in which the physician is holding the hand in relation to the body of the patient. Movement of the wrist toward the thumb side is abduction and toward the little finger is adduction. Each motion of the wrist has a normal range of motion. The wrist can flex 90 degrees and extend 70 degrees about its transverse

VI! Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment

700

Mechanism for anterior radial head somatic dysfunction

Posterior distal end

FIGURE 47.12. Wrist extension: anterior (ventral) g l ide of prox i m a l FIGURE 47.10. F a l l backward on extended a r m . ( I l l ustration by W. A.

carpa l bones. ( I l l ustration b y W . A. Kuchera.)

Kuchera.)

axis and can abduct 20 degrees and adduct 5 0 degrees about its anteroposterior axis. Combined motion about both of these axes permits a motion called circumduction . Figures 47. 1 1 and 47. 1 2 illustrate normal motion of fl exion and extension. Somatic Dysfunction of the Wrist

Somatic dysfunction is not related to the gross motions of the wrist but to dysfunction of the slight gliding motion s of the carpal bones on the radius as the wrist is moved. In Figures 46. 1 0 and 46. 1 1 , notice the direction o fglide of the carpal bone during each of these wrist motions. Somatic dysfunction of the wrist is named according to the direction of motion p reference. If a wrist extends and is re-

,.=:;---=--- --

stricted in its ful l flexion, it is an extension somatic dysfunction ( Fig. 47. 1 3) , with the wrist restricted in flexion. In this extension somatic dysfunction, the three carpal bones glide ventrally and are restricted in gliding dorsally. The opposite is true for a fle)(ion somatic dysfu nction of the wrist; similar relationships occur for the other wrist motions. Several principles describe somatic dysfunction of the wrist: 1 . Observation is not very helpful when looking for somatic dysfu nction ; swelling of the wrist is an inconsistent sign. 2. Pain ful compression means dysfunction is present, but this test does not diagnose the specific problem that is present. 3. Radial glide and limited paral lelogram motions are not ob vious until the opposite motion is attempted. If there is an adduction somatic dysfunction at the wrist with a proximal shift of the radius, the problem may not be evidem umil ab duction of the wrist is tested and the results are compared with the opposite side. 4 . Flexion extension somatic dysfunction of the wrist is usually caused by a trauma that overcomes the ligamentous restraims and opposing m uscle pull. This can often result if a strain or sprain exceeds the extent of a somatic dysfunction. Restricted extension of the wrist is its most common major motion loss caused by dysfunction. Somatic Dysfunction of the Hand

Intercarpal Joints

FIGURE 47.11. Wrist flexion: dorsa l g l ide of prox i m a l carpa l bones. ( I l l ustration by W. A. Kuchera.)

Imercarpal somatic dysfunction often occurs from a fall on an outstretched hand. For this reason, somatic dysfunction in these areas is very likely to have a compression component. If the wrist joint is swollen, the physician must rule out fracture of the navic ular bone (scaphoid). This is also true if there is pain on pressure over the snuffbox, or if there is persistent pain and dysfunction af ter proper conservative care, even if the initial post-trauma radio graphs showed no evidence of fracture. Sometimes the scaphoid does not reveal evidence of fracture until the disruption in ItS blood supply slowly produces degeneration of the bone.

47. Upper Extrem ities

701

Anteroposterior glide Mediolateral glide Il1[ernal-external rotational glide A l l of these motions are minor and cannot be initiated directly by muscle action .

Diagnosis

Extension

Comp ression is always parr of M P and IP somatic dysfunctions, as when a ring on a finger gets caught as a person jumps over a wire fence. Tl1[ermetacarpal cramps and pain may be a sign ofM P or I P somatic dysfunction. Pain in the metacarpal joints may be referred from an u lnoh umeral joil1[ somatic dysfunction.

SPECIAL TESTS FOR T HE UPPER EXTREMITY Adson Test

The Adson test is used to determine the state of the subclavian artery, which may be compressed by an extra cervical rib or by tightened al1[erior and middle scalene muscles. To perform Adson test, take the patiel1['s radial pulse at the wrist. Continue to feel the pulse while abducting, extending, and externally rotating the arm. Then instruct the patiel1[ to take a deep breath and turn the head toward the side being tested . Marked dimin ution or absence of the radial pulse indicates compression of the subclavian artery (2).

FIGURE 47.13. Wrist extension: somatic dysfunction. ( I l lustration by W. A. Kuchera.)

Carpometacarpal Joints

All of these joines, except the thumb, are classified as plane syn ovial j oines, which share a common joint cavity with the inter carpal joil1[s. Their main type of somatic dysfunction is a dorsal glide with restriction in vel1[ral glide. The carpometacarpal joint of the thumb is different; it is a separate saddle-type j oil1[, having both a concave and a convex articular surface. This configuration permits angular movemel1[s in almost any plane with the exception of limited axial rota tion. Only a ball and socket joint has more motion than the carpometacarpal joil1[ of the thumb. Because it has very good motion, it is more likely to have compression strain or sprain of the ligamel1[s than to have somatic dysfunction. Metacarpophalangeal and Interphalangeal Joints

The metacarpophalangeal ( M P) j oil1[s and all the ineerphalangeal ( I P) joints of the hand are gliding j oil1[s. The fifth MP j oint has the most motion; there is less motion in the fourth MP j oint, and the third and second MP joints have the least motion . The M P and I P joints may develop somatic dysfu nction in any one of a combination of six gliding motions:

Yergason Test

The Yergason test determines whether the biceps tendon is stable in the bicipital groove. I nstruct the patient to fully flex the el bow. Grasp the flexed elbow in one hand while holding the wrist with your other hand. To test the stability of the biceps tendon, externally totate the patiel1['s arm as he or she resists, and at the same time, pull downward on the elbow. If the biceps tendon is u nstable in the bicipital groove, it pops out of the groove and the patient experiences pain. If the tendon is stable, it remains secure and the patient experiences no discomfort. This procedure may also be performed using one hand to palpate the tendon and the other hand to introduce motion (2).

Drop Arm Test

The drop arm test detects whether or not there are any tears in the rotator cuff First, instruct the patiel1[ to ful ly abduct the arm. Then instruct the patient to slowly lower the arm to the side. I f there are a n y tears in t h e rotator cuff (especially in t h e supraspina tus muscle), the arm drops to the side from a position of about 90 degrees abduction. The patient is not able to lower the arm smoothly and slowly no matter how many times they try. If the patiel1[ is able to hold the arm in abduction, a gentle tap of the forearm causes the arm to fal l to the side (2).

702


Apprehension Test

The apprehension test detects chronic shoulder dislocation. Abduct and externally rotate the patient's arm to a position where it might easily dislocate. If the shoulder is ready to dislocate, the patient has a noticeable look of apprehension or alarm on his or her face and resists further motion (2) . Bicipital Tendonitis

The long head of the biceps muscle extends intraarticularly under the acromion through the rotator cuff to insert at the top of the glenoid. Impingement may result in inAammation of the tendon. This condition may also result from subl uxation of the tendon out of the bicipital groove. Pain is usually localized to the proximal h umerus and the shoulder. Resistive supination of the forearm aggravates pain. The distal portion of the b i ceps tendon is palpated in the cubital fossa medial to the tendon of the brachioradialis muscle. If the tendon is inAamed, the area may feel puffy and may be sensitive to touch. Also examine the coracoid process of the scapula, as the tendon of the short head of the biceps attaches there. Apley Scratch Test

The Apley scratch test is used to evaluate the range of shoulder motion. First, to test abduction and external rotation, ask the patient to reach behind his o r her head and touch the superior medial angle of the opposite scapula. To test the range of internal rotation and adduction, instruct the patient to reach in front of the head and touch the opposite acromion. To further test internal rotation and adduction, instruct the patient to reach behind the back and touch the inferior angle of the opposite scapula. Observe the patient's movement during all phases of testing for any limitation of motion or for any break of normal rhythm or symmetry. Alternatively, instruct the patient to abduct the arms to 90 degrees, keeping the elbows straight. Then instruct the pa tient to turn the palms up in supination and continue ab duction until the hands touch overhead. This tests ful l bilat eral abduction and provides instant bilateral comparison. Next, instruct the patient to place the hands behind the neck and push the elbows our posteriorly to test abduction and exter nal rotation. Finally, test adduction and internal rotation by instructing the patient to place the hands behind the back as high as they will go to scratch the inferior angle of the scapula (2) . Tinel Sign

Tinel sign is used in the diagnosis of carpal runnel syndrome. Attempt to elicit or reproduce pain or tingling in the distribution of the median nerve by tappi ng over the transverse carpal Iigament (2) . Phalen Test

The P halen test is also used in the diagnosis of carpal runnel syndrome. Attempt to elicit or reproduce symptoms by flexing

the patient's wrist to its maximum degree and holding it in that position for at least 1 minute (2) . Allen Test

The Allen test determines whether or not the radial and ulnar arteries are supplying the hand to their full capacity. Instruct the patient to open and close the fist several times and then squeeze the fist tightly so that the venous blood is forced out of the palm . Place your thumb over the radial artery and your index and middle fingers over the ulnar artery. Press both arteries against the underlying bones to occlude them. Instruct the patient to open the hand. The palm of the hand should be pale. Release one of the arteries at the wrist while maintaining pressure on the other one. Normally, the hand A ushes im mediately. If it does not react or A ushes very slowly, the released artery is partially or com pletely occluded. Test both arteries (2) . Tennis Elbow

Tennis elbow is also known as lateral epicondylitis. This condi tion is an inAammatory response to overuse of the extensor muscle group attached to the lateral epicondyle of the humerus. It is usu ally caused by repeated overload of the musculotendinous units. This condition produces pain that may be localized to the lat eral epicondyle or may radiate down the forearm extensor group or up into the brachioradialis muscle. The pain is intensified by resistive extension of the wrist and fingers, or by shaking hands. Pressure over the lateral epicondyle is painful (7,8 ) .

TREATMENT Carpal Tunnel Syndrome

This condition is most commonly described as an entrapment neuropathy of the median nerve at the wrist producing pares thesia and weakness of the hands (9). Carpal tunnel syndrome is frequently associated with repeated or sustained activity of the fingers and hands. Incidence rates are reported as high as 25.6 cases per 200,000 work hours ( 1 0) and involving 1 0% of workers. Medical cost estimates vary from $3,500 to $60,000 per case ( 1 I ). Patients experience numbness or paresthesia on the palmar surface of the thumb, index, and middle fingers, and radial half of the ring finger. Numbness and paresthesia of the whole hand may also occur. Pain may be referred to the forearm and, less commonly, to the neck and forearm regions. Pain or tingling of the fingers often occurs at night and is relieved by shaking or exercising the hand. Weakness and atrophy of the thenar mus cles usually appear late and can occur without significant sensory symptoms. On examination, symptoms may be reproduced by percussion over the volar surface of the wrist (Tinel sign) or by ful l Aexion of the wrist for one minute (Phalen maneuver) . De creased touch may be demonstrated over the fingers supplied by the median nerve. Nerve conduction studies are considered to be the gold standard for the diagnosis of this condition (9). The syndrome is traditionally described as resul ting from pres sure on the median nerve where it passes with the Aexor tendons of the fingers through the tunnel formed by the carpal bones and the transverse carpal l igament (9). Additional explanations exist.

47. Upper Extremities Si ngle compressions of dog sciatic nerves have failed to produce significan t conduction loss. Both proximal and distal compres sions have produced conduction blocks in 50% of test animals ( 1 2) . In 1 973, Upton and McComas ( 1 3) proposed the existence of the "double crush syndrome." This syndrome hypothesizes that neural function is impaired when si ngle axons that are compressed on one region become especially susceptible to damage in another area. The authors report that a slight compression may cause a reduction in axoplasmic flow that is too small to result in den ervation changes; but when coupled with the o nset of a slowed lesion, m ight further reduce axoplasmic flow below the safety margi n for prevent i o n of denervation at a distal lesion, and clini cal symptoms ensue ( 1 3). Abramson demonstrated that decreased blood supply to a nerve alters conduction ( 1 4) . Larson suggested that upper thoracic dysfunction alters upper extremity vasomo tion ( 1 5) . H urst demonstrated a relationship between cervical arthritis and bilateral carpal tunnel syndrome ( 1 6). Sunderland has suggested that lymphatic and venous congestion contribute to this disorder ( 1 7) . The treatment of carpal tunnel syndrome has tradi tionally i n volved the use of wrist splin ts, anti i nflammatory drugs, and local injection of steroids. Surgical decompression of the carpal tun nel with release of the transverse carpal tunnel l igament is used if symptoms persist or if motor abnormalities are present (9, 1 8). Evidence in the precedi ng paragraph s uggests that the hand sym p toms may be related to dysfunctions in the upper extremity, and the cervical and thoracic spine. Osteopathic treatment i ncorpo rares the modalities described above and should also i nclude: 1 . Reducing sympathetic tone to the upper extremity by correct ing upper thoracic and upper rib dysfunctions. This directly affects nerve function by i mproving blood flow and reducing congestion th rough improved lymphatic and venous drainage. An internally rotated temporal bone may be associated with increased sympathetic tone in the upper thoracic spine and, if it is diagnosed, should also be treated. 2. Removing cervical somatic dysfunction to improve brachial plexus function. 3. Removing myofascial restrictions in the upper extremity, thereby removing potential sites of addi tional compression. 4. Increasing space with i n the carpal tun nel usi ng d irect release techniques. Reflex Sympathetic Dystrophy

Reflex sympathetic dystrophy (RSD) is characrerized by pain and tenderness (usually in the distal extrem ity) that is accompanied by vasomotor instability, trophic skin changes, and rapid devel opment of bone demi neralization. A precipitating event can be identified in two-thirds of the cases. These include: Trauma Myocard ial infarction Stroke Peripheral nerve i n j uries RS D is observed most often I II individuals over the age of 50. An entire hand or foot is usually affected. The pathogenesis of RS D is poorly understood. The vasomotor manifestations are

703

thought to be caused by abnormal stimulation of the sympathetic nervous system (9). Larson ( 1 5) implicates the upper thoracic spinal segments with facilitati ng a vasomotor response i n the upper extremi ty. RSD evolves thro ugh three clinical phases. The clin ical man ifestations of the fi rst phase are pain and swel l i ng that develop weeks to months after the precipitating event. The pain has an i ntense, bur n i ng quali ty. The involved extremity is warm, edema tous, and tender, especially around the joints. I ncreased sweating and hair growth occur. In 36 months, the skin gradually becomes thin, shiny, and cool (second phase) . Clinical features of the fi rst two phases overlap. I n another 36 months, the skin and subcuta neous tissues become atrophic, and irreversible flexion contractu res of the hand or foot develop (third phase) . Motion of the shoul der on the affected side is frequen tly painful and greatly restricted, a condition referred to as the shoulder-hand syndrome (9). Early recogni tion and treatment are i mportant to prevent per manent disabi l i ty. RSD may be reversible in its early phases. Appropriate mobil ization of the patient after a myocardial in farction, stroke, or i n j ury may help prevent th is condition. Pain should be properly controlled. Exercises are helpfu l . Sympathetic nerve blocks may be i n i tially effective, but the response may not be sustai ned. H igh-dose pred nisone has benefited some patients (9). Osteopathic treatment should focus on reducing sympathetic tone to the extremity. This includes correcting cervical, upper thoracic, and upper rib dysfunctions. Apply gentle articulation and mobilization techniques. Always treat the whole patient.

Adhesive Capsulitis

Also known as "frozen shoulder," this condition is characterized by pain and restricted movement of the shoulder, usually in the absence of i ntrinsic shoulder disease. Adhesive capsulitis may fol low bursitis or tendon itis of the shoulder or may be associated with systemic disorders, such as chronic pulmonary disease, my ocardial i n farction, and d iabetes mellitus. Prolonged arm immo b i li ty con tributes to the development of this condition . Reflex sympathetic dystrophy is thought to be a pathogenic factor. The capsule of the shoulder is th ickened , and a mild, chronic, i nflam matory i n fi ltrate and fibrosis may be present. Pain and stiffness usually develop gradually over several months to a year, but may progress rapidly in some patients. Pain may int erfere with sleep. The shoulder is tender to palpation, and active and passive motions are restricted (9). Early mobil ization after an i n j ury to the arm or shoulder may help prevent the development of this condition. Local injection of corticosteroids and adm i n istration of nonsteroidal antii nflam matory drugs and physical therapy may help (9). Osteopathic manipulation should be di rected to the upper thoracics, upper ribs, and entire shoulder complex. The objective is to improve motion. Avoid taki n g the patient i n to the "crampy" pain zone. Th is only slows progress. Only progress as fast as the patient can respond. Indirect techniques may be especially effective in the i n itial treatment phases.

Myofascial Triggers

See Chapter 66, "Travell and Simons' Myofascial Trigger Poi nts."

704

VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment

Chapman Points

See Chapter 67, "Chapman Reflexes." Thoracic Outlet Syndrome

This condition results from compression of the neurovascular bundle (subclavian artery, subclavian vein, and brachial plexus) as it courses through the neck and shoulder. Several dysfunctions may compress the neurovascular bundle as it passes from the thorax to the arm, including: Cervical ribs Excessive tension in the anterior and m iddle scalene muscles Dysfunction of the clavicle, upper ribs, or upper thoracics Abnormal insertion of the pectoralis minor m uscle Patients may develop: Shoulder and arm pain Weakness Paresthesia Claudication Raynaud phenomenon Ischemic tissue loss Gangrene Exam ination is often normal unless p tovocative m aneuvers are performed. Occasionally, distal pulses are decreased or absent and digital cyanosis and ischemi a may be evident. Tenderness may be p resent in the supraclavicular fossa (9). Some forms of thoracic outlet syndrome are associated with sympathetic auto nomic dysfunction, which produces upper extremity symptoms. Sympathetic dysfunction has accompanying palpatory findings in the upper thoracic or rib area. Mosr parients can be conser vatively managed. Parients should avoid posirions thar aggravare symptoms. Osteoparhic trearment should be d i rected toward im proving mechanics in the: Cervical region Upper thoracics Upper ribs Clavicles Scalene muscles Muscles of the shoulder and pectoral girdle Surgical intervention i s a last resort.

CONCLUSION

Understanding the structure and funcrion of the upper extremi ties leads to effective diagnosis and trearment ofdisabilities in rhis area, and therefore i mproves rhe overall function of the parient.

REFERENCES 1 . Truhlar RE. Doctor A. T Still in the Living. Published by the author; 1 950 . 2 . Hoppcnfeld S. Physical Examination of the Spille and Extremilies. Nor walk, CT: Appleton & Lange; 1 97 6 : 25. 3. Moore KL.

Clinically Oriented Anatomy, 3 r d ed . Baltimore, M D :

Williams & Wilkins; 1 992:528. 4 . Seidel HM, Ball J W, Dains J E, et a l . Mosby's Guide to Physical Examina tion. Sr. Louis, M O : Mosby; 1 987:309-3 1 I . 5 . Kuchera WA, Kuchera M L. Osteopathic Principles in Practice, 2nd ed. rev. Columbus, O H : G reyden Press; 1 994:539. 6. Kuchera WA, Kuchera M L. Osteopathic Principles in Praetice. 2nd cd. rev. Columbus, OH: Greyden Press; 1 994:6 1 5-629. 7 . Roy 5, Irvin R. Throwing and tennis i n j u ries to the shoulder and elbow. I n , Sports Medicine: Prevention, Evaluation, Management, and Rehabili tation. Salt Lake City: Prentice H a l l , 1 983:22 1 -222. 8. Gun ter-Griffin, Letha Y. Atbletic Training and Sports Medicine, 2nd ed. Rosemont, I L: The American Academy of Orthopedic Surgeons; 1 99 1 :274. 9 . Wilson J 0, et a1. Harrison's Principles oflnlertlal Medicine, 1 2th ed. New York, NY: McGraw - H i l i ; 1 99 1 : 1 487. 1 0. Armstrong TJ . An Ergonomics Guide to Carpal Timnel Syndrome. Er gonomics Guide Series. Akron, O H : American I ndustrial Hygiene Asso ciation; 1 983.

I I . H il tz R. Fighting work-related i n j u ries. Nat! Underwriter. 1 985;89: 1 5. 1 2. Nemoto K. Experimental study on the vul nerability of the peripheral nerve. Nippon Sea Gakkai Zasshi. 1 983;57: 1 773- 1 786. 1 3. Upton A, McComas AJ . The double crush i n nerve entrapment syn dromes. Lancet. 1 973;2:359. 1 4. Abramson 01, Rickert B L, Alexis JT, et al. Effe cts of repeated periods of ischemia o n moror nerve conduction. J App! Physiol. 1 97 1 ;30:636642 . 1 5 . Larson NJ . Osteopathic manipulation for syndromes of the brachial plexus. J A m Osteopath Assoc. 1 972;72:94- 1 00 . 1 6. H u rst L C , et al. T he relationship of double crush syndrome

ro

carpal

tunnel syndrome (an analysis of I 000 cases of carpal tunnel syndrome).

J Hand SlIrg. 1 985; 1 0 : 202.

1 7. Sunderland S. The nerve lesion i n the carpal runnel syndrome. J Neurol Neurosurg Psychiatry. 1 976;39:6 1 5 . 1 8 . Anonymous. Carpal runnel syndrome: getting a handle on hand trauma. OCCIIP Hazards. 1 987;42:45-47.

THORACIC REGION RAYMOND J. HRUBY

KEY CONCEPTS • •

• • •

Imponance of the thoracic region for normal function Structure and fwlction of the thoracic area, including lymphatics, connective tissues, neural connections, and motion Clinical characteristics of thoracic movements History and physical examination, including observation, palpation, and motion testing Assessment, diagnosis, and treatment of structural dysfunction

Because the hean and lungs are contained in the thorax, this re gion's unique significance in life has long been recognized. The inability to draw breath or the perception of pain in the thorax often constitutes real or imagined immediate and life-threatening problems. Movement of the thorax is necessary for normal func tion in both obvious and not-so-obvious ways. Because much of the regulatory outflow of the sympathetic nervous system origi nates in the thoracic spinal cord, disturbances in the muscles and joints of the thoracic region often mimic life-threatening prob lems. Injury to thoracic venebrae can cause long-term sequelae for health and survival. The complexities of the thoracic region and the vital importance of its organ systems underscore the necessity for the osteopathic physician to understand its many functions, diagnoses, and potential treatment approaches. The thoracic region is bounded by the cervical region above and the lumbar region below. In diagnosis and treatment, it can not be considered as separate from the other body regions, because dysfunction in it or other regions is always interdependent.

ANATOMY AND PHYSIOLOGY Thoracic Region

The thoracic cage includes 1 2 thoracic spinal venebrae, 1 2 pair of ribs, and the sternum (Fig. 48. 1 ) . (See also Chapter 5 1 , Figure 5 1 .1.) Although the scapula overlies the posterior ponion of the rib cage, is connected to the sternum through the clavicle, and is otten involved in thoracic injuries and pain syndromes, this

structure is more properly considered a pan of the upper extremity (see Chapter 47) . White and Panjabi ( 1 ) divide the thoracic spine into three anatomical regions: Upper (T 1 -4) M iddle (T4-8) Lower (T8-Ll) [t is also helpful to divide the thoracic and upper lumbar spine into four functional divisions that roughly correspond to the thoracolumbar outflow of the sympathetic system: T 1 -4: Sympathetics to head and neck, with T 1 -6 to the heart and lungs. T5-9: All upper abdominal viscera: stomach, duodenum, liver, gall bladder, pancreas, and spleen. T 1 0- 1 1: Remainder of the small intestines, kidneys, ureters, gonads, and right colon. T 1 2-L2: Left colon and pelvic organs. This functional division is otten very useful to the osteopathic physician, because visceral, afferent (generally nociceptive; see Chapter 7) neurons usually follow the same pathway as the sym pathetic outflow. Visceral disturbances often cause increased mus culoskeletal tension in the somatic structures that are innervated from the corresponding spinal level through the viscerosomatic reflexes (see Chapter 9) . Manipulative treatment at that spinal level is used to reduce somatic afferent input from the associated facilitated segments, which, in turn, reduces somatosympathetic activity to the affected viscus (2). Generally, the thoracic spine has a mildly kyphotic, forward bending curve that varies from person to person. In the osteo porotic or older patients, the angle of this curve can become more acute, causing biomechanical problems and necessitating compensatory adaptation in other regions of the spine and in general posture. Individual thoracic vertebrae are parts of a con tinuum with the cervical and lumbar vertebrae; size increases from cervical to lumbar to account for increased weight bearing. The spinous processes of the thoracic vertebrae are particularly large and easily palpated, pointing increasingly caudad from T l through T9 and back to an almost anteroposterior orientation from T 1 0-12. Thoracic vertebral facet joints are plane-type synovial joints. The interarticular surfaces of these joints are smooth, shiny,


706

a functional transition to the lumbar spine. The inferior facet of each thoracic vertebra faces in the opposite direction from the superior and has a slightly concave surface. The thoracic vertebrae are separated by discs, as are the cer vical and lumbar vertebrae. The discs act as shock absorbers and permit Aexibility between the vertebrae. Each disc is composed of an outer anulus fibrosus and an inner nucleus pulposus, a gel at the cemer of the disc that acts like a semiAuid hydrophilic ball bearing that becomes less hydrated and broader under sus tained compression. The anulus fibrosus is composed of concen tric lamellae of fibrocartilage, ru nning at right angles to the fibers of adjacem layers. Its structural arrangemem is more vulnera ble to tears posteriorly, where the lamellae are thinner and less numerous. However, the restricted motion of the thoracic spine due to the attachmems of the rib cage and the fairly broad poste rior longitudinal ligamem make ruptured thoracic discs relatively uncommon. On the other hand, discopathy from trauma, aging, and degenerative disease is relatively common in the thoracic area. Muscles of the Thoracic Area

The muscles of the thoracic area are involved in: Actions of the ribs and vertebrae Posture Head and neck comrol Breathing Locomotion Stabilization of the extremities V isceral function

FIGURE

48.1. The thoracic region and its relationships.

compact bone that is covered with hyaline cartilage. The joims are surrounded by a thin, loose arricular capsule mat is lined with synovial membrane. The facet joims guide and limit gross, segmemal, and coupled movements. The superior facets of each thoracic vertebra are slightly convex and face posteriorly (back ward), somewhat superiorly (up), and laterally. Their angle of declination averages GO degrees relative to the transverse plane and 20 degrees relative to the coronal plane. A tool to remember the facet facing is the mnemonic B UL ( backward, upward, and lateral) . This is in comrast to the cervical and lumbar regions, where the superior facets face backward, upward, and medial ( B U M ) . Thus, the superior facets are B U M , BUL, B U M from cervical to thoracic to lumbar. In the lower portion of the thoracic spine, the superior facet surface begins to face more posteriorly than laterally, and at T12, it may even face medially, as part of

Table 4S. 1 lists the major muscles of the thoracic area, with the action, proximal and medial attachments, distal and lateral attachmems, and innervation of each. It is especially important to note the action of each muscle, because altered tone in these muscles can affect the function of not only the bones to which the muscles are attached but other body areas as well. In addi tion, increased or decreased tone has the capacity to alter both general and microcirculation in a myriad of ways, such as al tered homeostatic regulation and cellular immunity. As with all muscles, the thoracic muscles are fed not only by circulatory elements but also by physiologically active trophic substances delivered directly by nerves (3). In addition, there is evidence that the sympathetic nerve supply to striated and smooth muscles alters muscle tone and comractile forces. Therefore, at temion to the palpatory cues associated with altered muscle tone impl ies the presence of many differemial diagnostic factors that are discussed throughout this text. The larger muscles of the head, neck, shoulder girdle, and thorax control much of the activity of the thoracic cage and help stabilize the cervical and cranial areas, as well as the arms and shoulder girdle. For example, the splenius capitus and cervicis muscles origi nate on the lower cran ial and upper cervical areas and attach distally along the middle thoracic spine, as low as TG-S in some cases. Vertebral dysfunction in the upper thoracic areas can affect the action of these muscles, causing problems with motion outside the thoracic area in the head and neck. Lower down, the internal and external oblique muscles are generally viewed as trunk rotators, but they also attach to the lower ribs along with the diaphragm. Altered tone in these muscles can alter diaphragmatic

48. Thoracic Region

707

TABLE 48.1. REGIONAL THORACIC MUSCLES Muscle Pectoralis major

Action 1. Clavicular head: flexion,

Proximal/Medial Attachments

Distal/Lateral Attachments

1. Clavicular division:

1. Clavicular division:

adduction, horizontal flexion,

anterior surface of the

lateral lip of the

and med ia I rotation of the

medial'lz of the clavicle.

intertubercular groove of

humerus at the shoulder.

2. Sternocostal head: sternum

2. Sterncosta I head: flexion,

to 7th rib, cartilages of true

the humerus. 2. Sternal division: lateral

ribs and aponeurosis of

lip of the intertubercular

and horizontal flexion of the

external abdominal oblique

groove of the humerus.

humerus at the shoulder. Also

muscle.

adduction, medial rotation,

Innervation 1. Clavicular head: lateral pectoral, CS, C6. 2. Sternocostal head: pectoral, C7, C8, T1.

extends flexed humerus. Through its action on the humerus, it depresses, protracts, and rotates downward. Pectoralis minor

Teres major

Depresses scapula and rotates

Anterior surfaces of 3rd, 4th,

scapula inferiorly. Important

and 5th ribs near the costal

anterior shoulder stabilizer.

cartilages.

Adducts and medially rotates humerus at the shoulder.

Dorsal surface of inferior angle of the scapula.

Extends the shoulder joint.

Coracoid process of the scapula. Medial lip of intertubercular groove of humerus.

Medial pectoral, C6, C7, C8. Lower subscapular, C6,

O.

Medial to latissimus dorsi tendor.

Teres minor

Lateral rotation of humerus at the shoulder. Stabilization

Superior 2/3 of dorsal surface of lateral border of scapula.

of head or humerus.

Inferior aspect of greater

Axillary, C5, C6.

tubercle of the humerus, capsule of the shoulder joint.

Trapezius

1. Lower fibers: depress the scapula.

1. Lower fibers: spinous

Retract the scapula. Rotate the

processes of 6th-12th

scapula upward 50 the glenoid

thoracic vertebrae.

cavity faces superiorly. Give inferior stabilization of scapula. Help maintain spine in extension. 2. Middle fibers: retract and aid in elevation of scapula.

2. Middle fibers: spinous processes of 1 st-5th thoracic vertebrae. 3. Upper fiber: external occipital protuberance,

1. Lower fibers: medial % of

1. Lower division: spinal

spine of the scapula.

root of accessory and

2. Middle fibers: superior

anterior primary rami

border of spine of scapula. 3. Upper fibers: lateral % of clavicle and acromion process.

C3, C4. 2. Middle division: spinal root of accessory and anterior primary rami (3, C4. 3. Upper division: spinal

medial % of superior muchal line, ligamentum

root accessory and

in shrugging the shoulders. Rotate

nuchae, and spinous process


the scapula upward so the glenoid

of the 7th cervical vertebra.

C3, C4.

3. Upper fibers: elevate the scapula as

cavity faces superiorly. When acting with the other sections of the trapezius, it retracts the scapula. Latissimus dorsi

Extends, retracts, and medially rotates

Flat tendon that twists on

Broad aponeurosis that

the humerus at the shoulder.

itself to insert into the

originates on the spinous

Through its action on the humerus,

intertubercular groove of

processes of lower 6

it depresses, retracts, and rotates

the humerus, just anterior

thoracic and all lumbar

the scapula downward. Assists in

to and parallel with tendon

vertebrae; posterior crest

forced expiration.

of pectoralis major.

Thoracodorsal C6,

0, C8.

of ilium, posterior surface of sacrum, lower 3 or 4 ribs, and an attachment to the inferior angle of the scapula.

Levator scapulae

Elevates the scapula and rotates the scapula downward so the glenoid

Dorsal scapular C5 and

Transverse processes of first

Vertebral border of scapula

four cervical vertebrae.

between superior angle


and scapular spine.

C3, C4.

cavity faces inferiorly. Working with the upper fibers of the trapezius, it elevates and retracts the scapula. Reversed action: when the scapula is fixed, it laterally flexes and slightly rotates the cervical spine to the side. Rhomboid

1. Minor: retracts and elevates the

1. Minor: lower part of

1. Minor: medial border of

scapula. Assists in rotating the

ligamentum nuchae,

scapula at the root of the

scapula downward.

spinous processes of C7

spine of the scapula.

2. Major: retracts and elevates the scapula. Inferior fibers aid in rotating the glenoid cavity

and T1. 2. Major: spinous processes of T2-5.

2. Major: medial border of

1. Minor: dorsal scapular, C4, C5. 2. Major: dorsal scapular, C4, C5.

scapula from spine to inferior angle.

inferiorly. (continued)

TABLE 48.1.

(continued) Action

Muscle Quadratus lumborum

Lateral flexion of lumbar vertebral column; helps the


Distal/Lateral Attachments

Iliolumbar ligament, posterior

Inferior border of the 12th

part of the iliac crest.

rib and transverse

Innervation Anterior primary rami T12,

L1, L2, L3.

processes of the upper

diaphragm in inspiration.

four lumbar vertebrae. Serratus anterior

1. Accessory muscle of respiration. 2. Protraction of the scapula.

Serratus posterior

Accessory muscles of

Superior lateral surfaces of upper 8 ribs at the side of

Costal surface of the medial

Long thoracic, C5, C6, (7.

border of scapula.

the chest. 1. Superior: lower portion of

1. Superior: superior

(superior!

inspiration. Superior

ligamentum nuchae and

borders of 2nd-5th ribs

inferior)

elevates superior ribs;

spinous processes of the 7th

distal to the angles.

inferior depresses inferior

cervical and 1st, 2nd, and

ribs.

3rd thoracic vertebrae. 2. Inferior: spinous processes

2. Inferior: inferior borders

1. Superior: anterior primary rami T2-5. 2. In ferior: anterior primary rami T9-12.

of lower 4 ribs just beyond their angles.

of 11th and 12th thoracic and 1st, 2nd, and 3rd lumbar vertebrae, and the thoracolumbar fascia. Intercostals

1. Keep the intercostal spaces from bulging and retracting with respiration. 2. Elevate the ribs anteriorly with inspiration.

External intercostals Internal intercostals Innermost intercostals Subcostals

Depress the ribs.

Transversus

Depress the second to sixth

thoracis Levatores

ribs. Elevate the ribs.

costarum

Transverse processes of the 7th

The outer surface of the rib

Anterior primary rami of

cervical and upper 11

immediately below the

the corresponding

thoracic vertebrae.

vertebrae from which it

intercostal nerves.

takes origin, between the tubercle and the angle. Splenius

1. Capitis: acting bilaterally,

1. Capitis: spinous processes of

1. Capitis: posterior primary

extends the head and neck.

(7-n, inferior half of

and lateral third of the

rami of the middle

Acting unilaterally, laterally

ligamentum nuchae.

superior nuchal line.

cervical spinal nerves.

flexes and rotates the head

2. Cervicis: spinous processes of

and neck to the same side.

3rd-6th thoracic vertebrae.

2. Cervicis: laterally bends and rotates the neck. Spinalis

1. Capitis: mastoid process

1. Cervicis: laterally bends and rotates the neck. 2. Thoracis: acting unilaterally, lateral flexion of the spine. Acting bilaterally, extension of the spine.

1. Cervicis: lower portion of

2. Cervicis: transverse processes of 1st, 2nd, 3rd,

lower cervical spinal

on the posterior aspect.

nerves.

1. Cervicis: spinous process of the axis and the 3rd

spinous processes of the 7th

and 4th cervical spinous

cervical and 1st and 2nd

processes.

thoracic vertebrae. of the 1st and 2nd lumbar

primary rami of the

and 4th cervical vertebrae

ligamentum nuchae,

2. Thoracis: spinous processes

2. Cervicis: posterior

2. Thoracis: spinous processes of upper

1. Cervicis: posterior primary rami of the spinal nerves. 2. Thoracis: posterior primary rami of the spinal nerves.

thoracic, vertebrae T4-T8.

vertebrae, thoracic vertebrae 11 and 12. Semispinalis

Extends the thoracic and

1. Capitis: between superior

1. Capitis: 7th cervical and

1. Capitis: posterior

cervica I reg ion and rotates

and inferior nuchal lines of

1st-6th thoracic

primary rami of cervical

it toward the opposite side.

the occipital bone.

transverse processes, and

spinal nerves.

2. Cervicis: spinous processes of 2nd-5th cervical vertebrae. 3. Thoracis: spinous processes of the 1st-4th thoracic

articular processes of 4th, 5th, and 6th cervical vertebrae. 2. Cervicis: transverse

2. Cervicis: posterior primary rami of cervical spinal nerves. 3. Thoracis: posterior

vertebrae and 6th and 7th

processes of the 1st-6th

primary rami of thoracic

cervical vertebrae.

thoracic vertebrae.

spinal nerves, T1-6.

3. Thoracis: transverse p rocesses of 6th-10th thoracic vertebrae. (continued)

TABLE 48.1.

(continued)

Muscle longissimus

Action 1. Capitis: acting bilaterally,


Distal/lateral Attachments

1. Capitis: transverse processes

1. Capitis: the posterior

extends the head; acti ng

of the 1st-5th thoracic

margin of the mastoid

unilaterally, laterally flexes

vertebrae and the articular

process.

and rotates the head to the

processes of the 4th-7th

same side.

cervical vertebrae.

2. Cervicis: acting unilaterally,

2. Cervicis: transverse processes

2. Cervicis: transverse processes of the 2nd-6th cervical vertebrae and

Innervation 1. Capitis: posterior primary rami of spinal nerves. 2. Cervicis: posterior primary rami of spinal nerves. 3. Thoracis: posterior

laterally flexes the neck.

of the 1st-5th thoracic

transverse process of the

primary rami of spinal

Acting bilaterally, laterally

vertebrae.

atlas.

nerves.

flexes the vertebral column.

3. Thoracis: the common broad

3. Thoracis: the tips of

Acting bilaterally, extension

thick tendon with the

of vertebral column; draws

iliocostalis lumborum, fibers

all thoracic vertebrae and

ribs down.

from the transverse and

the lower 9 or 10 ribs

accessory processes of the

between the tubercles

lumbar vertebrae and

and angles.

transverse process of

thoracolumbar fascia. Iliocostalis

1. Cervicis: acting bilaterally,

1. Cervicis: the posterior

1. Cervicis: superior borders

extension of the spine;

tubercles of the transverse

of the angles of the

acting unilaterally, laterally

processes of the 4th, 5th,

3rd-6th ribs.

flexes the vertebral column.

and 6th cervical vertebrae.

2. Thoracis: acting bilaterally,

2. Thoracis: into the angles of

2. Thoracis: superior borders of the angles of lower 6

extension of the spine;

the upper 6 or 7 ribs and

ribs medial to the

acting unilaterally, laterally

into the transverse process

tendons of insertion of

flexes the spine. 3. Lumborum: acting

of the 7th cervical vertebra. 3. Lumborum: inferior borders

bilaterally, extension of the

of the angles of the lower 6

spine; acting unilaterally,

or 7 ribs.

the iliocostalis lumborum. 3. Lumborum: anterior

1. Cervicis: posterior primary rami of spinal nerves, C6,

0, C8.

2. Thoracis: posterior primary rami of spinal nerves. 3. Lumborum: posterior primary rami of spinal nerves.

surface of a broad and thick tendon, which originates from the

laterally flexes the spine.

sacrum, spinous processes of the lumbar and 11th and 12th thoracic vertebrae, and from the medial lip of the iliac crest. Rotatores

Rotate the vertebral column

1. Brevis: bases of the spinous processes (lamina) of the 1st

processes of the

vertebra above.

vertebrae.

2. Longus: bases of the spinous

Multifidus

1. Rotate the vertebral column toward the

1. Brevis: transverse

2. Longus: transverse

processes (lamina) of the

processes of the

2nd vertebra above.

vertebrae.

Spinous processes of all the vertebrae except the atlas.

opposite side.

Posterior surface of the sacrum, the dorsal end of

1. Brevis: posterior primary rami of spinal nerves. 2. Longus: posterior primary rami of spinal nerves. Posterior primary rami of spinal nerves.

the iliac crest, the

2. Stabilize the vertebral

mammary and transverse

column.

processes of lumbar and thoracic vertebrae, and the articular processes of the 4th-7th cervical vertebrae.

Interspina les

1. Unite the spinous processes.

Pairs of small muscles joining

2. Produce slight extension of

the spinous processes of

the vertebral column.

See proximal/medial attachment.

Posterior primary rami of spinal nerves.

adjacent vertebrae, one on each side of the interspinous ligament. Continuous in the cervical region extending from the axis to the 2nd thoracic vertebra and in the lumbar region from the 1st lumbar vertebra to the sacrum.

Intertransversarii

1. Unite the transverse processes. 2. Produce lateral bending of the vertebral column.

Unite transverse processes of consecutive vertebrae. Well developed in the cervical

See proximal/medial attachment.

Anterior and posterior primary rami of spinal nerves.

region. (continued)

710

V II. Osteopathic Considerations i n Palpatory Diagnosis and Manipulative Treatment

TABLE 48.1.

(continued)

Muscle Diaphragm

Action Contracts into the


Distal/lateral Attachments

The central tendon, which is

An approximately circular

abdomen with

an oblong sheet forming

inhalation and relaxes

the summit of the dome.

into the thorax with

Innervation Phrenic nerve, C3, C4, C5.

line passing entirely around the inner surface of the body wall:

exhalation.

1. Sternal portion: two slips from the back of the xiphoid process.

2. Costal portion: the inner surfaces of the cartilages and adjacent portions of the lower 6 ribs on either side, interdigitating with the transversus abdominis. 3. Lumbar portion: medial and lateral arcuate ligaments and right and left crura from the anterolateral surfaces of the bodies and discs of the upper three lumbar vertebrae. Obliquus capitis inferior

Rotates the atlas, turning the face toward the

Apex of the spinous process of the axis.

part of the transverse

same side. Subclavius

Depresses clavicle, draws it medially.

The inferior and dorsal

Posterior primary rami of C1.

process of the atlas. 1st rib at junction with costal cartilage.

Groove on the inferior

Subclavius, C5, C6.

surface of the clavicle, between the costoclavicular and conoid ligaments.

and respiratory function and vice versa. Experienced palpation readily identifies these relationships. Ofspecial note are the erector spinae groups (Fig. 48.2), which extend and side-bend the vertebral column, and allow smooth Aexion by gradually decreasing resistance to forward bending. These muscles are often involved in group or m ulriple move ment dysfunction (i.e., altered coupling or non-neutral vertebral unit dysfunction) , and are vulnerable to insult with unplanned movements or trauma. The deep back muscles, especially the ro tatores and multifidus, are also implicated in this type of problem. These small muscles are richly innervated with m uscle spindles, which provide proprioception. In fact, one of their primary tasks is to signal position and speed of motion of the vertebral column. (This task makes them important in the maintenance of posture and in directing movement.) They are also very vulnerable to sudden stretch and unplanned movement, which appears ro alter the sensory input ro the spinal cord and brain, with resultant de velopment of altered motion and pain typical of vertebral somatic dysfunction (4-6).

Lymphatics

As blood moves through the capillaries, Auid filters into the in terstitial tissues. The rerurn of interstitial Auid through the lym phatic system is necessary for health and proper function, and

is even more important when the patient has disease. Lymphatic drainage from the lower half of the body is supplied by the tho racic duct (or left lymphatic duct) . Smaller lymphatic vessels drain inro the cisterna chyli in the abdomen. Trunks from the left side of the head, the left arm, and the thoracic viscera also empty into rhe thoracic duct before it drains into the juncrion of the lefr internal jugular and lefr subclavian veins (Fig. 48.3). In approxi mately 20% of the population, three trunks, the right jugular, the right subclavian, and the right transverse cervical join ro form the right Iympharic duct. The remainder of the population varies in the way the three trunks empty inro the jugulosubclavian junc tion in the anterior neck. The right lymphatic duct enters the juncrion of the right internal jugular and right subclavian veins (7) . Connective Tissue and Fascia

Connective tissue unites and surrounds all other tissues. It is found between the cells of organs, as tendons of muscles, and as ligaments joining skeletal parts. Of special importance to the osteopathic physician are the fasciae of the body. These con nective tissues surround virtually all organs, muscles, and vessels (8) . Fascial elements called the pericardium and pleura even sur round the heart and lungs, respectively. Fascia is a fibrous tissue that is effectively wound around the invested organs at various angles.

48. Thoracic Region

711

Interspinalis muscle Multifidus muscle Longissimus muscle

Psoas fascia

-�'--'""�

Anterior·IOngitudinal ligament

Intervertebral disk FIGURE

48.2. The erector spinae muscle groups of the thoracic region.

Trauma, chemical alterations of the bathing Ruids (immune changes), and other pathologic agents alter the angles of the fas cial bands and change cross-linkages between the bands, causing altered tensions of the fasciae throughout the body. An i ncrease in tension in the fascial sheets leads to altered interstitial fluid (lymph) Rows, decreased blood Row, and decreased efficiency of organ function. Normalization of the fascial tensions returns the body to more efficient funcrion, rhereby using less energy.

FIGURE

48.3. The lymphatic system of the body.

Osteopathic manipulative techniques, including direct and in direct myofascial release, have been developed to address these problems in ways not generally found to be effective with most other manipulative techniques. The thoracic fasciae are often in volved in dysfunction due to thoracic trauma. Neural Connections of the Thoracic Area

The neural connections of the thoracic area are of vital impor tance to all body functions. Not only do the usual connections to the m usculoskeletal system exit the spinal cord in the thoracic region, but a large part of the sympathetic nervous system also originates in the thoracic region (Fig. 48.4). The composite au tonomic innervation of the body is shown in Chapter 73. An understanding of the relationships between the thoracic nerves, as well as their relationships to the bony landmarks is vital to understanding neurologic problems associated with the thoracic regIOn. The spinal cord, which runs from the brainstem to about the level of L3, is a continuous structure with no segmentation. During embryologic development, the spinal nerve bundles are gathered into spinal nerve roots that course between the encir cling bones through the intervertebral foramina. This imposes what appears to be a dermatomal segmentation effect. Inherently, however, the function of the spinal cord is not segmented. The spinal nerves exit through the intervertebral foramina, which identifY their vertebral level. Each spinal nerve is num bered at the level at which it exits, except in the cervical region, because there are eight cervical nerve roots and seven cervical ver tebra. Spinal nerve C 1 exits above the atlas, and the eighth root exits below C7. All other roots exit below their corresponding vertebrae. Because the intervertebral foramen is a bounded space and the nerve roots share that space wi th other tissues, the roots are especially vulnerable to pressure from herniated nucleus pul posus and even edema. Somatic dysfunction in a thoracic area

VI! Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment

712

Head

Arms

� Legs

a. Upper GI tract

\ b. Small intestines and

�

right half of colon

\

Rectum and

- Umbilic uS

-

Left half of colon

}

FIGURE 48.4. The sympathetic innervation of the body.

may cause local edema and tissue tightening, which can exerr pressure on the nerve root and, importanrly, can alter blood and fluid flows to and from the nerve sheaths. Such pressure can al ter neural conductivity in the affected roots, although the lack of proper blood and fluid flow to the sheaths can cause irritability in the nociceptors of the sheath, causing pain along the nerve distri bution (9). Local disturbances can often be relieved with proper manipulative treatment that is designed to restore proper motion and fluid flow to the region . As stated previously, radiculopathy is somewhat rare in the thoracic region, although discopathy is less rare. These problems in the thoracic area are not easy to diagnose because of overlapping dermatomes and a lack of readily testable deep tendon reflexes (see Chapter 30). The abdominal diaphragm receives its motor innervation through the phrenic nerves coming from C3-5. Perhaps more importanrly, sensory nerves of the diaphragm innervate the me diastinal pleura, the fibrous pericardium, and the parietal layer of the serous pericardium (10). This relationship helps explain the very common palpatory findings of cervical tension and so matic dysfunction associated with pericardial or diaphragmatic irritation that are mediated via the viscerosomatic reflexes (see Chapter 9). Manipulative treatment of the involved cervical seg ments is designed to ameliorate thoracic and diaphragmatic dys function through somatovisceral reflex pathways. Parasympathetic innervation to the thoracic viscera and many of the abdominal viscera comes through the vagus nerve (cranial nerve X). These relationships are shown in Chapter 73 and are also discussed in Chapter 6. Treatment of problems encountered

in the function of the thoracic viscera must include assessment and treatment of cranial and cervical areas to normalize vagal function. The majority of the outflow of the sympathetic system orig inates in the thoracic region (see Chapters 6 and 73). The distribution of the sympathetic system to almost every tissue and area of the body makes this system a very important one for all body functions. It is even becoming evident that the sympathetic system is vitally imporrant in regulating immune function ( 1 1) (see Chapter 8). The importance of the sympathetic nervous sys tem for all body functions suggests that disturbances within the thoracic verrebra and their associated musculature that affect the function of the sympathetic system can have widespread conse quences. Identification and treatment of somatic dysfunction in the thoracic region is especially important in treating problems ranging from infectious processes to functional abnormalities. V isceral dysfunction that alters input to the spinal cord not only increases the sympathetic outflow back to the visceral ar eas through viscerovisceral reflex pathways but also alters somatic outflow in often unexpected patterns. Understanding this phe nomenon provides insight on how to treat many painful and/or functional problems. Due to the overlap of visceral afferents onto spinal pathways that also receive somatic afferents, the sensory experience of visceral irri tation is often one of referred pain to a somatic structure, with concomitant increased somatic muscle tone. One of the most common of these patterns is the shoulder pain and m uscle tension associated with acute myocardial infarc tion. The nociceptive inpur from the compromised myocardium is experienced as shoulder or chest pain. Often, a vicious circle of increased somatic involvement results, as increased somatic activ ity also increases sympathetic outflow to the heart, further exac erbating the pathologic process. Although obviously not the only course of treatment, treating the somatic component of the pro cess can be beneficial. Recognition of the visceral origin of referred pain patterns can save the osteopathic physician much time and m issed diagnoses. Likewise, recognizing that osteopathic treat ment of the involved somatic structures can also help the course of the problem. Understanding the somatic areas likely to show effects of underlying visceral pathologic conditions through vis cerosomatic reflexes (2) provides the osteopathic physician with another important diagnostic and treatment tool.

VA RIATION AND DYSFUNCTION Vertebral and Costal Cage Motion

Thoracic spinal movement is an integral part of total body move ment and includes intimately detailed, interdependent fu nctions with both the craniocervical and lumbopelvic systems. Both bony and general configuration anomalies are common; Wolff's law is always at work. Wolff 's law states that bones and soft tissues de form (are strained) according to the stresses (forces applied over an area) that are placed on them . Examples of general config uration alterations affecting both shape and movement charac teristics are seen with scoliosis, kyphosis, the arthritides, and leg length inequalities. General body shapes and movement characteristics are also affected by gtowth, aging, and lifestyle factors. For example,

48. Thoracic Region

experienced tennis players tend to develop thoracic alterations in association with repetitive rwisting and stressing from the dominant hand side. So do automobile assembly line workers as they bend, rwist, and turn in the same direction hundreds of times a day. On the other hand, age-induced osteoporosis and arthritic changes also affect these same characteristics. Interde pendent spinal movements are always changing as life processes unfold. Thoracic Spinal Motion

Available thoracic spinal motion is generally less than in the cer vical or lumbar areas. This is because all planes of motion are affected by costal cage mechanics and their complicated relation ships with head, neck, shoulder girdle, and lumbopelvic anatomy. Thoracic spinal motion is further complicated by a number of other factors that go beyond basic costovertebral configuration and mechanics. A few of the elements include configuration characteristics of the anteroposterior curves in the sagittal plane, such as: Kyphosis Costal cage asymmetries, such as pectus excavatum and pectus cannatum Osteoporosis/osteoarthritis effects Increased chest wall diameter associated with a variery of car diopulmonary problems 'Cervical, shoulder girdle, rotator cuff influences (i.e., ante rior muscles are generally tighter than posterior groups); under these circumstances, anteroposterior curves tend to become more kyphotic Effects of lifesryle and affective states, such as slumping with depression Characteristics of primary and secondary lateral deviations include: Scoliosis with and withour kyphosis Effects of upper and lower motor neuron lesions Effects of repetitive motion activities General thoracic spinal motion characteristics Because of configuration changes in size and shape, thoracic spinal motion characteristics vary markedly from the cervicotho racic to thoracolumbar junctions. The upper and middle portions demonstrate greater rotation than elsewhere in the spine, with the exception of the adanto-axial (A-A) joint. Generally, flexion ca pabiliry is greater than extension. Side-bending capabiliry is even less, because of rib cage constraints. In the lower portions, flex ion and extension capacities are greatest, although side-bending abilities exceed those of rotation (i.e., they are more like lumbar spine mechanics) . In general, thoracic spinal motion occurs according to the mechanical principles formulated by Fryette. Thus, both neutral (rype I) and non-neutral (rype I I) vertebral unit dysfunction is common in the thoracic spine. Neutral/rype I asymmetries ryp ically involve three or more segments that are neither flexed nor extended; they are mildly scoliotic. Non-neutral/rype II vertebral unit dysfunction generally involves a single vertebral unit with both proximal and distal neutral/rype I responses.

713

However, there are times when variations from Fryerre princi ples occur in thoracic vertebral motion. Upper thoracic vertebrae may exhibit neutral/rype II motion, which may occur as low as T4, and movements are similar to normal cervical spine behavior. Some suggest that these motions are associated with the interde pendent combination of asymmetrical vertebral and upper rib shapes and attachments and their interactions with cervical mus cle extensors and side-benders that attach as low as T5 and T6 (splenius mechanics). Middle thoracic vertebral motion is commonly a mix of neu tral/rype I and non-neutral/rype II movements, which may pro duce rotation to either the formed convexiry or to the formed concaviry. Lower thoracic vertebral motion is more apt to be similar to lumbar neutral/rype I mechanics. Clinical Characteristics of Thoracic Movement

Cli nically, there is a constant tendency for spinal flexion because of the effects of graviry and the tendency for the back extensors to become inhibited while flexors tend toward contraction . Clin ically, it seems that the rotatores, intertransversarii, and multifidi are often involved in postural stress, somato-somatic, and viscero somatic reflexes (see Chapters 7 and 30). When these muscles are reflexively affected by facilitation, they are often responsible for maintaining non-neutral somatic dysfunction of the vertebral units that are innervated by the involved m uscle, neural nerwork, or viscera. Some refer to this phenomenon as the somatic com ponent of impairment, ill ness, or disease (see also Chapter 73). Neurologic pathologic conditions, trauma, visceral disease, and intrinsic mechanical asymmetries are common sources of spinal dysfunction. Trauma, for example, often flexes, extends, and/or rwists the spine simultaneously in such a way that the accumulated forces localize around a vertebral unit, thereby dis turbing the mechanics of both the single vertebral segment and the vertebral units. Deforming inj uries of this rype often alter physical shapes; that is, they cause plastic deformations with per manent stretching of ligaments and distortions in facet joints and osseous-ligamentous relationships. Not surprisingly, recur ring non-neutral/rype II vertebral unit dysfunction is common under these circumstances. This rype of vertebral unit change is sometimes associated with altered visceral functions; for example, somatic dysfunction is superimposed on vertebral segment and vertebral unit changes with resulting facilitated peripheral, au tonomic, and centrally mediated reflex activities (see Chapters 7 and 30). Patients report many clinical symptoms when these pro cesses occur.

HISTORY AND PHYSICAL EXAMINATION

The evaluation of the thoracic region includes: Elements of history taking Observation Auscultation Percussion

714

VII Osteopathic Considerations i n PaLpatory Diagnosis and Manipulative Treatment

Palpation Motion testing The following sections focus on aspects of the history and physical examination that are uniquely osteopathic in nature. History

Ask standard questions of the patient as part of the total evalu ation of the thoracic region. Do a history of the systems most closely associated with this region, including the cardiac, pul monary, and gastrointestinal systems. Ask if there has been any history of rrauma. This information is particularly important to the osteopathic physician, as trauma to the thoracic region may have produced disturbances in structural relationships that have resulted in disturbances in visceral function. Historic information should also include when the complaint first appeared, wherher a similar complaint has occurred in the past, and whether there are any underlying predisposing conditions. If there is pain, ask: About its location About its duration Whether it is constant or intermittent Whether anything has ameliorated or exacerbated it The q uality (srabbing, aching, burning, or like an electrical shock) Whether it radiates to any other location How much stress the patient has recently been experiencing Information gathered during history taking helps in formulating hypotheses as to the nature of the problem. Combined with the physical examination findings, the history allows devel opment of a working diagnosis and an appropriate comprehen sive treatment approach that includes osteopathic manipulative treatment. Observation

Observe certain aspects of the thoracic region with the pa tient standing, seated, supine, and prone. These observations help determine whether more detailed examination is warranted. Observations include: I . The skin, noting such characteristics as color, skin rashes or eruptions, and hair distribution. 2 . The relationship of the neck to midline. This gives informa tion about rotation and side-bending abilities of both the neck and upper thoracic regions. 3. The sternum, observing for pectus excavatum (hollow chest, depressed sternum) or pectus carinatum (pigeon chest, pro truding sternum). 4. The levelness of the clavicular heads. 5. The shoulders for excessive rounding. 6. The ni pple heights. In the standing position, observe the patient from the front, noting shoulder heights and the general shape and contour of the thoracic region. Also observe the patient from the back, tak ing note of shoulder heights, scapulae position, the contour and

shape of the thoracic region, and any observable evidence of lat eral spinal curvature, such as scoliosis. Observing the patient from each side, note the shape and contour of the thoracic re gion, including observable evidence of changes in the sagittal spinal curves, such as lordosis and/or kyphosis. Make the same observations with the patient seated. Evaluate the patient for trunk side-bending abilities. With the patient standing, observe right and left side-bending from the back without forward bending. Observe for symmetry of motion of the induced spinal curve. A normal curve should be a smooth C-shaped curve with paravertebral muscle fullness on the side of the convexity. Lack of a C-shape to the induced spinal curve suggests the presence of vertebral motion segment dysfunction in the region. Also from the back, observe forward bending as the patient attempts to touch the Aoor. Follow the formed contour of the spine and thoracic cage. Asymmetrical changes anywhere along the spine and rib cage raise the suspicion of vertebral motion restriction and possible somatic dysfunction in the area. Observe lateral posture using an imaginary vertical line that lies along a path drawn from the external auditory meatus to the tip of the acromion, through the middle of the femoral trochanter, ending just anterior to the lateral malleolus (see postural line in Glossary) . Thoracic kyphosis and lordosis suggest the need for more detailed evaluation. Prone and supine observations assess general thoracic shape, symmetry, and contour. Examination

When the history and screening examination i ndicate thoracic region dysfunction, look for more specific signs of vertebral mo tion segment or soft tissue myofascial dysfunction. The following points are helpful in learning to identify and describe pertil�ent thoracic anatomic landmarks. Thoracic vertebral motion segments are identified by the letter T followed by a number from 1 to 1 2, for example, T I , T2, and so on. It is important to distinguish C7 from TI when evaluating the thoracic region. This can easily be done using the following method. Ask the patient to try to touch his or her chest with the chin. With the head in this position, the seventh cervical vertebra (C7) usually has the most prominent spinous process in the cervicothoracic region. Place a finger on the tip of this spinous ptocess and ask the patient to look up toward the ceiling. In this position, the spinous process of C7 translates anteriorly. The spinous process of the vertebra just below this one is then identified as T l . The sternal notch is located at the superior border of the manubrium between the two sternoclavicular joints. This struc ture is anterior to and at the same horizontal level as the second thoracic vertebra. The sternal angle is the point at which the body of the sternum and manubrium unite. It is located anterior to and in the same horizontal plane as the fourth thoracic vertebral segment. The costal cartilage of the second rib inserts at the sternal angle. This is a clinical guide to the numbering of the ribs. The sternal angle lies anterior and in the same horizontal plane as the fourth thoracic vertebra. The xiphisternal angle is located at the inferior end of

48. Thoracic Region

the sternum and is also anrerior ro and in the same horizonral plane as the ninrh thoracic vertebra. The spine of each scapula is usually at the level of the spinous process ofT3. The inferior angle of each scapula is usually at the level of the spinous process ofT7. A useful way of idenrifYing the thoracic vertebrae involves the rule of threes. This rule is a generalization that is only approxi mate but positions the palpating fingers in a position for locating individual thoracic vertebrae: I . The spinous processes of T I , T2, and T3 project directly posteriorly so that the tip ofeach spinous process is in the same plane as the transverse processes of its associated vertebra. 2. The spinous processes ofT4, T5, and T6 project in a slightly caudal direction so that the tip of each spinous process is in a plane that is approximately half way between the transverse processes of its associated vertebra and those of the vertebra immediately below. 3. The spinous processes of T7, T8, and T9 project caudally at a sharper angle so that the tip of each spinous process is in the same plane as the transverse processes of the vertebra immediately below it. 4. For the T I D, T I l , and T I 2 vertebrae, the spinous processes are placed as follows. The spinous process ofTI 0 is similar ro those ofT7-9. The spinous process of T I l is similar ro those ..ofT4-6. T1 2 is similar ro those of T I -3. Palpation

Observation and the screening examination provide information about body regions that may have significant somatic dysfunc tion. Palpation is used ro further investigate these areas and ro further localize and idenrifY the somatic dysfunction that may be present. Somatic dysfunction may be represenrative of musculoskeletal dysfunction, viscerosomatic reRex changes, or both. Palpation of the thoracic spine can find tissue texture abnor malities and restricted motion. When either is found, more pal pation may be used ro idenrifY somatic dysfunction in specific vertebral segments. Palpate for tissue texture changes by lightly stroking the par avertebral soft tissues in a cephalocaudal direction, either bilat erally or unilaterally. The search is for changes in tissue texture defined as: Increased rone or tension (hypertonicity) Spasm Fasciculation Ropiness Bogginess (indicative of edema) I ncreased or decreased temperature Moisture Warm, moist, and boggy tissue usually suggests acute somatic dysfunction, although cold, dry, ropy tissue suggests chronic so matic dysfunction. If an area has abnormal tissue texture, asym metry, restricted motion, or tenderness, perform a more detailed assessmen t.

715

Perform the red reflex test b y firmly (but with slight pressure) stroking two fingers on the skin over the paraspinal tissues in a cephalad ro a caudad direction. The stroked areas brieRy become erythemarous and then almost immediately return ro their usual color. If the skin remains erythemarous longer than a few seconds, it may indicate acute somatic dysfunction in the area. As the dysfunction acquires chronic tissue changes, the tissues blanch rapidly after stroking and are dry and cool ro palpation. In addition ro palpating the paravertebral tissues, assess the tips of the spinous processes and the inrerspinous ligaments for evidence of gross asymmetry, edema, or tenderness. Palpation also extends laterally ro the transverse processes, the cosrotransverse articulations, and the rib angles; look for tissue texture changes and tenderness. MOTION TESTING

Thoracic region motion testing further idenrifies areas of altered movemenr of the vertebrae, ribs, and soft tissues. Use more de tailed palpation of vertebral motion segmenrs and soft tissues ro assess areas where gross motion restrictions are located. Motion restriction evaluation involves both active and passive motion testing. Active motion testing assesses voluntary motions produced by the patient. Passive motion testing is induced while the patienr remains as passive and relaxed as possible . Active Motion Testing of the Thoracic Spine

Flexion/Extension: Sagittal Plane Bending

The patienr sits on the examination table or on a srool with the feet on the Roor. The physician palpates for asymmetries and vertebral motion segment restrictions while the patienr bends forward and backward. Side-Bending

The patienr side bends right and left as the physician palpates for restriction in spinal curves and for neutral and non-neutral dysfunction in vertebral motion segments. IdenrifY the level of the apex of any curve where limitation is found. Ro tation

The patienr rotates right and left as the physician notes restriction in spinal and vertebral unit motion segmenrs, both unilaterally and bilaterally, ro identifY the spinal segmenral level where limi tation occurs. Active Motion Testing of the Vertebral Motion Segment

The physician places his/her thumbs on the posterior surfaces of the left and right thoracic transverse processes at the level ro be evaluated. Then the patienr is asked ro slightly Rex, extend, side bend right, side bend left, rotate right, and rotate left as the physician palpates ro determine the site(s) of greatest restriction in comparison with vertebral segmenrs above and below.

716


Passive Motion Testing

Regional Examination of the Upper Thoracic Spine Flexion and Extension

1 . Place one hand posteriorly on the patient's upper thorax and the other on top of the patient's head. 2. Bend the head and neck forward until flexion creates move ment in the upper thorax (T l -4). Note flexion restrictions as the process proceeds. 3. Bend the head backward until extension creates movement in the upper thorax, again noting any movement restrictions. Side-Bending

I . With a hand on the patient's upper thorax, bend the head and neck to one side and then the other side. 2 . Note any side-bend ing restrictions. Rotation

1 . With one hand on the patient's upper thorax, use the other hand to rotate the head and neck right and left. 2. Palpate for upper thoracic rotation restrictions. Regional Examina tion of the Lower Thoracic Spine Flexion/Extension

I . Place the pal mar surface of one hand on the patient's lower thorax. 2. Place the other hand on the opposite shoulder. 3. Bend the torso forward and backward, noting any flexion and extension restrictions with the hand palpating the lower thorax. Rotation

I . Place the palmar surface of one hand on the patient's lower thorax. 2. Place the other hand on the opposite shoulder. 3. Rotate the torso to the left and to the right, noting any rotation restrictions with the hand palpating the lower thorax. Side-Bending

1 . Place the palmar surface of one hand on the patient's lower thorax. 2. Place the other hand on the opposite shoulder. 3. Side bend the torso to the left and to the right, noting any side-bending restrictions with the hand palpating the lower thorax. Segmental Examination of the Upper Thoracic Spine

Segmental motion tests are most commonly done with the patient seated. Flexion/Extension

1 . Place the fingertips of one hand between the spinous processes of the fi rst four thoracic vertebrae.

2. Use the other hand to move the head and neck passively into flexion and extension. 3. Assess each vertebral motion segment as the process unfolds. 4. Typically, the spinous process of the superior vertebra moves anteriorly and superiorly before those that are more distal. I f a vertebral motion segment does not move freely into flexion, it is defined as being in an extended position, such as an extended-rotated-side-bent vertebral unir dysfunction that is restricted during flexion movements. 5. Examine extension in a similar manner, using passively in duced backward bending. 6. If a vertebral motion segment does nor extend wel l, it is in a flexed position, such as a flexed-side-benr-rotated verte bral unit dysfunction that is restricted during extension move ments. Side-Bending

1 . Place the fi ngertips of one hand between the transverse pro cesses of the firsr four thoracic vertebrae. 2. Use the other hand to move the head and neck passively into left and right side-bending. 3. Assess each vertebral motion segment as the process unfolds. 4. If the transverse process of one segment does not approximate the transverse process of the segment below, it is restricted in side-bending right or left in accordance with the restriction. Rotation

1 . Place the index and long fingers over the transverse processes of the upper thoracic segment to be examined. 2. Rotate the head and neck passively right or left until the seg ment begins to rotate in the same direction. 3 . Restricted right rotation restriction suggests that the segment is positionally rotated left. Segmental Examina tion of the Lower Thoracic Spine

Motion testing is performed with the same maneuvers used on the upper thoracic segments. However, instead of using the head and neck as a lever, do the following: 1 . For example, to examine the patienr from the patient's right side, the physician stands on the patient's right side. 2. The physician places the index and long fingers of his/her left hand on the transverse processes of the lower thoracic segmen t to be examined, in the same manner as described for the upper thoracic segments. 3. The physician places his/her right axilla over the rop of the patient's right shoulder, then reaches across the patient's chest and places his/her right hand on the patient's left shoulder. 4. The physician then uses the patient's upper trunk as a lever to move T5- 1 2. Diagnosis

Use active and passive motion testing to formulate a specific positional diagnosis for a given spinal segment. For example, if

48. Thoracic Region

T2 moves more easily into flexion than i nto extension, it is in a flexed position. I f it totates more easily to the right than to the left, it is rotated right. If it side bends more easily to the right than to the left, it is side-bent right. Examine all the lower thoracic segments for flexion/extension, right and left side-bending, and right and left rotation move ments. The principles of physiologic motion of the spine are used to identify any specific segmental motion restrictions. For example, if the examination reveals that a vertebral segment moves more easily into extension, left rotation, and left side-bending, this indicates that the vertebra is positionally extended, and rotated and side-bent to the left (ERLSL) . If the motion restriction is most noticeable with the patient in the neutral position (that is, motion improves in flexion and extension), then the motion restriction is described as a neu tral vertebral motion segment dysfunction. For example, if the vertebrae are rotated to the left and side-bent to the right in the neutral position, the segmental dysfunction is recorded as NRLSR·

717

understand the proper function, diagnosis, and treatment o f the thoracic area. REFERENCES 1 . WhiteAA, Panjabi M M . Clinical Biomechanics ofthe Spine. Philadelphia, PA: ) B Lippincott Co; 1 978:44-56. 2 . Patterson M M , Howell )N, eds. The Central Connection: somatovis

cerallViscerosomatic Interaction. I ndianapolis, I N : American Academy of Osteopathy; 1 992. 3. Korr 1 M . The spinal cord as organizer of disease processes. I V. Axonal transport and neurotrophic function i n relation to somatic dysfunction.

JAm Osteopath Assoc. 1 98 1 ;80(7):4 5 1 -4 5 9 . 4. Korr 1 M . Proprioceprors a n d somatic dysfunction. J Am Osteopath Assoc. 1 97 5 ;74(7);638-650. 5. Patterson MM, Steinmetz )E. Long-lasting alterations of spinal reAexes: A basis for somatic dysfunction. Man Med. 1 986;2: 38-42. 6. Van Buskirk RL. Nociceptive reAexes and the somatic dysfunction: a model. J Am Osteopath Assoc. 1 990;90(9):792-804. 7 . Gallaudet BB. A Description of the Planes of Fascia of the Human Body. New York, NY: Columbia Press; 1 93 1 . 8 . Budgell B , Saro A . Somaroauronomic reAex regulation o f sciatic nerve blood Aow. J Neuromusculoskeletal sys. 1 994;2: 1 70- 1 77. 9 . Moore KL. Clinically Oriented Anatomy, 2nd ed. Balti more, MD: Williams & Wilkins; 1 98 5 .

CONCLUSION

The thoracic cage is a complex region of the body, containing and ' protecting many vital organs. Osteopathic physicians must

1 0. Warwick R, Williams P, eds. Gray's Anatomy, 3 5t h e d . Edinburgh, SCOt land: Churchill Livingsrone; 1 973. 1 1 . Willard F H , Patterson M M , cds. Nociception and the Neuroendocrine

Immune Connection. Indianapolis, I N : American Academy of Osteopa thy; 1 994.

THE RIB CAGE RAYMOND J. HRUBY

.

KEY CONCEPTS

Importance of the rib cage for normal function Structure and function of the rib cage, including lymphatics, connective tissues, neural connections, and motion • Clinical characteristics of rib movements • History and physical examination, including observation, palpation, and motion testing • Assessment, diagnosis, and treatment of structural dysfunction •

•

Respiration is a process involving the participation of several sys tems of the body, none the least of which is the musculoskele tal system. As Cathie (1) noted, "RespiratOry activity requires motion in a greater number of articulations and with a greater frequency than any other musculoskeletal function." This not only includes the intervertebral joints of the thoracic spine but also the costOvertebral and costotransverse joints at the posterior aspects of the ribs. In addition to the articular motion, optimal respiration also requires a degree of elasticity of the ribs and costal cartilages. The biomechanical architecture among the vertebrae and ribs may be thought of as a complex system of levers; any thing that alters the normal movement of this system of levers may impair respiration.

ANATOMY AND PHYSIOLOGY The Costal Skeleton

The 12 sets of ribs correspond with the 12 thoracic verrebrae. All ribs are composed of a bony segment and a costal cartilage. Each rib has a cup-shaped depression in its bony segment where the costal cartilage fits into the costOchondral joint and where the periosteum of the rib joins the perichondrium of the rib cartilage. The rib heads join with the thoracic vertebrae at the costOverte bral articulations. The heads of ribs 2 through 9 articulate with a demifacet on the vertebra above and below. For example, rib 2 articulates by demifacets withTl andT2. The heads of ribs 1 and 10-12 articulate with unifacets on their corresponding ver-

tebrae.The transverse processes of vertebraeTI-10 also have syn ovial costOtransverse joints with the tubercle of the corresponding rib. Ribs 1, 2, 11, and 12 are called atypical ribs. Rib 1 is the flattest, shortest, broadest, strongest, and most curved. The sub clavian artery and the cervical plexus are vulnerable to muscular compression where they pass over the first rib between the tu bercles and attachments of the anterior and the middle scalene muscles (the so-called scalenus anticus syndrome). The latter is one of several conditions clinically labeled as thoracic outlet syn drome (see Chapter 30). The subclavian vein may also be com pressed between the first rib and the clavicle. Rib 2 is considered anatOmically atypical because of its tuberosity that attaches to the proximal portion of the serratus anterior muscle. Ribs II and 12 are anatOmically atypical because they do not have tubercles, do not attach to the sternum or other costal cartilages, and have tapered ends. These twO ribs are also called floating or vertebral ribs. Rib 10 is sometimes considered atypical because of its single articulation between the rib head andT 1O. The anatomy of the rib cage is shown in Figure 49.I. AnatOmi cally typical ribs (3-9, and in most respects 10) have heads, necks, tubercles, angles, and shafts that connect directly or via chondral masses to the sternum. Rib 1 and ribs 2-7 connect directly with the sternum by their own individual cartilaginous synovial joints (rib 1 with a stable synchondrosis); therefore, they are often called the true ribs. Ribs 8-10 merge intO a single cartilaginous mass that attaches to the sternum; therefore, these are called vertebral chondral ribs. Ribs 11 and 12 do not connect with the sternum and are hence called floating ribs. Because ribs 8-12 do not con nect direcdy to the sternum, they are often called the false ribs. The costOvertebral joints between the heads of the ribs and the vertebral bodies allow gliding or sliding costal motions. The costOtransverse joints at the tubercle of the typical ribs, with the facets at the tip of the transverse processes of their own vertebra, a synovial membrane, and a thin articular capsule, allow gliding and slight rotational motions. When these motions are restricted, respiratOry movements are commonly impeded. The sternum has three parts: Head or manubrium Body or gladiolus Tail or xiphoid process The superior portion of the manubrium cradles the clavi cles at the sternoclavicular joints, forming the sternal notch or

719

49. The Rib Cage

2

2 Vertebro sternal ribs

Ribs by

True ribs

number

12

...

�7",. 8

_ _

______

Vertebro-

ribs

ribs Vertebral (floating)

ribs False

chondral

12

Typical

1 8

___

J.o

12

FIGURE 49.1. The bony anatomy of the rib cage and the naming of rib types.

ribs

jugular notch, which is a landmark For several amerior thoracic srrain/counrersrrain tender points.The sternal notch lies almost directly anrerior to theT2 vertebral body.The manubrium joins the sternal body via a fibrocartilaginous symphysis, or secondary canilaginous joinr, called the sternal angle or angle of Louis. This joint lies anrerior to the Fourth thoracic vertebra. Because the second rib attaches to the manubrium and sternal body with a synovial joinr, the sternal angle is an anterior landmark for counring the ribs.The xiphisternal joinr is located anterior to the ninth thoracic vertebra. It is also a hyaline cartilage symphysis that Fuses into a synostosis in the fifth decade.

Muscles of the Costal Area

exhalation, it moves upward imo the thorax.This up and down movemenr produces pressure gradienrs between the thoracic and abdominal cavities, and is imporranr for both eFficient respira tion and circulation. Because there are one-way valves in the larger lymphatic vessels, the pressure gradiems also enhance the move menr of lymph and venous blood toward the heart. When the dome of the diaphragm is Aattened because of asymmetric load and/or tonus, respiration and lymphatic drainage From anywhere in the body becomes less efficient. Three apertures occur in the diaphragm: one For the vena cava at about the level of TS, another For the esophageal hiatus at TI0, and the third for the aorta at the level ofT12 (Fig. 49.2). Diaphragmatic muscle fibers are arranged so that when it con tracts in inspiration, the vena caval opening dilates, permitting

The muscles of the thoracic area are involved in: Actions of the ribs and vertebrae Head and neck control Breathing For specific inFormation regarding individual muscles of the rib cage, seeTable 50.1 in Chapter 50. As with all muscles, the rib cage muscles are Fed not only by circulatory elemems but by physiologically active trophic substances delivered directly by nerves themselves (3). In addition, there is evidence that the sympathetic nerve supply to striated and smooth muscles alters muscle tone and contractile Forces. Attenrion to the palpatory cues associated with altered muscle tone thereFore implies the presence of many diFFeremial diagnostic factors that are discussed throughout this text. The abdominal diaphragm is the primary muscle of respira tion. It forms the Aoor of the thorax and attaches to the xiphoid process, the imernal surface of the inferior six ribs, the upper two (left) or three (right) lumbar vertebrae, and their inrervertebral discs. Irs fibers converge into a common cemral tendon that has no bony attachment. When the diaphragm contracts with in halation, it descends into the abdomen; when it relaxes during

Vertebral levels

Xiphoid process

Openings for:

at the hiatus:

V ena cava

T8 T10 T12

Quadratus

lumborum

Lateral

muscle

arcuate

Gap for psoas

arcuate

ligament

muscle

ligament

lumborum muscle

FIGURE 49.2. Apertures of the abdominal diaphragm.

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V/J. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment

more venous blood to pass from the abdomen to the thorax; at the same time, the esophageal hiatus constricts to prevent gastric contents from rising in the esophagus. Its contraction has no in Auence on the aortic hiatus, which lies posterior to the diaphragm and does not truly pierce the diaphragm. The diaphragm does most of the work of breathing under nor mal conditions and during moderately forced inspiration. With increased respiratory demands, accessory muscles of respiration become involved to move the ribs even more.The scalene mus cles, attached to the upper two ribs, assist inhalation. Hyper tonicity or hypotonicity of segmental intercostal muscles alters rib behavior, making breathing less efficient. Actual spasm in these muscles can result in pain at rest or especially with each deep breath or cough. Quiet exhalation creates passive recoil of the lung as the diaphragm relaxes. Forced exhalation also in volves the inferior internal intercostal and abdominal muscles, including the trunk rotators and erector spinae. Osteopathic manipulative treatments can often resrore or par tially rehabilitate altered diaphragmatic function. These treat ments are designed to increase motion of the lower costal cage by freeing the diaphragm for better excursion. This, in turn, helps improve breathing mechanics and assists in venous blood return and lymphatic Aow. This approach can be especially helpful for individuals with asthma, respiratory infections, loss of general lung compliance, and associated disorders.

Lymphatics

In general, the superficial lymph vessels of the thoracic wall ram ify subcutaneously and converge on the axillary nodes (2). The lymph nodes from the deeper tissues of the thoracic wall drain into three groups of nodes: ].

The parasternal (internal thoracic) lymph nodes. These are four or five pairs of nodes located at the anterior ends of the intercostal spaces.

2. The intercostal lymph nodes, located in the posterior parts of the intercostal spaces in relation to the heads and necks of the ribs. 3. The diaphragmatic (phrenic) lymph nodes, located on the thoracic surface of the diaphragm.

Connective Tissue and Fascia

Like all other muscles of the body, the muscles of the thoracic cage are invested with fascia. The internal thoracic wall is cov ered by a parietal layer of fascia called the endothoracic fascia. This deep fascia invests the internal intercostal, subcostal, and transversus thoracis muscles (3). This fascia blends with the pe riosteum of the ribs and sternum and with the perichondrial tissue of the costal cartilages. The endothoracic fascia also covers the superior surface of the diaphragm, thus becoming the superior diaphragmatic fascia. The endothoracic fascia is also continu ous with the prevertebral layer of the cervical fascia and with the scalene fascia (also called Sibson fascia), where it attaches along the inner border of the first rib. Behind the sternum, it is also continuous with the fascia of the infrahyoid muscles. This

parietal thoracic fascia proceeds through the openings of the di aphragm to become continuous with the transversalis fascia of the abdomen. In addition, there are specialized fascial elements that comprise the pericardium, pleura, and mediastinum. Neural Connections of the Thoracic Cage

A detailed description of the nerve supply ro the thoracic area is given in Chapter 50. The ventral rami of the first 11 thoracic nerves are called intercostal nerves (4). They are located between the ribs, although the 12th thoracic nerve lies below the last rib and is thus called the subcostal nerve. Each of these nerves is connected to the sympathetic chain ganglia via the white and gray rami communicantes. The intercostal nerves provide. inner vation chieAy to the thoracic and abdominal walls. The first six nerves provide innervation to the thoracic wall, with the first two nerves also providing fibers to the upper extremity. The lower five nerves are distributed to the thoracic and abdominal walls, and the subcostal nerve innervates the abdominal wall and the skin of the gluteal area. The abdominal diaphragm receives its motor innervation through the phrenic nerves coming from C3-5. Perhaps more importantly, sensory nerves of the diaphragm innervate the me diastinal pleura, the fibrous pericardium, and the parietal layer of the serous pericardium (2). This relationship helps explain the very common palpatory findings of cervical tension and somatic dysfunction associated with pericardial or diaphragmatic irrita tion that are mediated via viscerosomatic reAexes (see Chapter 9). Manipulative treatment of the involved cervical segments is de signed to ameliorate thoracic and diaphragmatic dysfunction through somatovisceral reAex pathways.

RIB MECHANICS

During inhalation, the thoracic cage widens its vertical, trans verse, and anteroposterior dimensions as the diaphragm con tracts. With deep inhalation, the anterior ends of the superior ribs move more anteriorly and superiorly along with the sternum (Fig. 49.3). Typical ribs are attached to the sternum by the costal cartilage, and their pump-handle movements displace the anterior compo nent of the costosternal system upward and anteriorly. (See Glos sary for more detailed definition.)The rib shaft is the handle of the bucket and the vertebral column is the pivot point (Figs. 49.3 and 49.4). Even though the first ribs are described as being elevated or depressed when they have somatic dysfunction, the vertebroster nal ribs (1 and 2) and vertebrochondral ribs (8-10) move in a bucket-handle manner (Figs. 49.5 and 49.6). They are described as moving about functional pivots posteriorly and anteriorly. Functionally, their shafts move laterally and superiorly during inhalation, increasing the transverse diameter of the costal cage. The anterior/posterior (AP) diameter of the chest is increased as the anterior ends of ribs 8-10 are elevated by the contraction of the diaphragm. Ribs 11 and 12 are called vertebral ribs, because they do not attach to the sternum or the chondral mass.

49. The Rib Cage

721

I I

'-

-

-..,.--. - ... . ' ....

- - _ .

B

_.

FIGURE 49.3. Functional transverse rib axis. (From Gray's Anatomy, 35th ed. Edinburgh, Scotland: Churchill Livingstone; 1973:421, with permission.)

These two atypical ribs have a pincer-type motion. The types of rib motion described clinically are depicced in Figure 49.7.

HISTORY AND PHYSICAL EXAMINATION

The evaluation of the rib cage includes: Elemems of hiswry taking Observation Auscultation Percussion Palpation Motion testing The following sections focus on the aspects of the hiswry and physical examination that are uniquely osteopathic in nature.

FIGURE 49.5. Functional anteroposterior rib axis. (From Gray's Anatomy, 35th ed. Edinburgh, Scotland: Churchill Livingstone; 1973:421, with permission.)

History

Ask standard questions of the patient as parr of the wtal evalu ation of the rib cage. Do a hiswry of the systems most closely associated with the rib cage.This includes the cardiac, pulmonary, and gastrointestinal systems. Ask if there has been any hiswry of trauma. This information is particularly importam w the os teopathic physician, as trauma w the ribs may have produced disturbances in structural relationships that have resulted in the preseming sympwms. Hiswric information should also include when the complaim first appeared, whether a similar complaim has occurred in the past, and whether there are any underlying predisposing conditions. If there is pain, ask: About its location About its duration Whether it is constant or intermittem Whether anything has ameliorated or exacerbated it

Anteroposterior Axes

FIGURE 49.4. Pump-handle rib motion.

FIGURE 49.6. Bucket-handle rib motion.

122


Pump handle (predominates)

Wirh rhe patient standing, observe for symmetry of rib cage morion as the patient side bends righr and left without bend ing forward. Observe forward bending as the patient attemprs to touch the floor. Follow the formed contour of the rib cage. Asym metrical changes anywhere along the rib cage raise the suspicion of motion restriction and possible somaric dysfunction in the area. Prone and supine observations assess general costal shape, sym metry, and contour. Respiration is best observed wirh the parient supine. Is respiratory effort mostly thoracic or abdominal, or a combinarion of each? Altered parterns ofren indicate somatic, visceral, or neurosensory problems reflected partially as somatic dysfunction in the ribcage.

Bucket handle (predominates)

Pincer or caliper FIGURE 49.7. Cl inical rib movement.

Examination

When the history and screening examination indicare rib cage dysfunction, look for more specific signs of somaric dysfunction of the ribs. Morion dysfuncrion of the ribs is designated as either structural or respiratory. Specific structural dysfuncrion includes: Superior subluxation of the first rib Anterior or posterior subl uxations External rib torsions Anreroposterior compression Lateral compressions Larerally flexed ribs

The quality (stabbing, aching, burning, or like an electrical shock) Whether ir radiates to any other locarion How much stress rhe parient has recently been experiencing Informarion gathered during history taking helps formulare hyporheses as to rhe narure of rhe problem. Combined wirh rhe physical examinarion findings, the history allows development of a working diagnosis and an appropriare comprehensive trearment approach rhat includes osteopathic manipulative treatment.

Respiratory dysfunction is classified as either inhalation or ex halarion dysfunction, and may involve either single ribs or groups of ribs. Evaluation for Structural Rib Dysfunction

Observation

Observe certain aspects of the rib cage with rhe parient sranding, seared, supine, and prone. These observations help derermine whether a more detailed examination is warranted. Observarions include:

Evaluation of First Rib for Superior Subluxation The first rib is evaluated for superior subluxation as follows: 1.

The parient is seated on the examination rable.

2. The physician srands behind the parient.

The skin, noting such characteristics as color, skin rashes or eruprions, and hair distribution.

The physician grasps the anterior and superior aspecr of rhe trapezius muscle on both sides and retracts the tissues poste riorly.

2. The tissue rexrures of the muscles, fasciae, and ligaments as sociared wirh the rib cage.

4. The physician then directs rhe long fingers caudally to make bilateral contact with the posterior shafrs of the first ribs.

3. l.

3.

The sternum, observing for pectus excavatum (hollow chest, depressed sternum) or pectus carinatum (pigeon chest, pro truding sternum).

4. Any asymmetry of the bony components of the rib cage. 5. Tenderness or pain of the ribs and associated srructures. In the standing position, observe the parient from the front, noting shoulder heights and the general shape and contour of the thoracic cage. Also observe the patient from rhe back, taking note of shoulder heights, position of rhe scapulae, the contour and shape of the thoracic cage, and any observable evidence of lateral spinal curvature, such as scoliosis. Observing the patient from each side, nore rhe shape and contour of the rhoracic cage, including observable evidence of changes in the sagittal spinal curves, such as lordosis and/or kyphosis. Make the same obser vations with the patient seated.

5. A positive finding is unleveling of the first ribs. 6. The patient is instructed to inhale and exhale deeply. 7. The inability of one or the other first rib to descend into the exhalation position confirms the diagnosis of superior sublux ation of rhar rib. Evaluation of Ribs 2-10 for Structural Rib Restrictions Evaluate for structural rib restrictions in this regi0'1 as follows: l.

The patient is seated on rhe examination table.

2. The physician first stands behind rhe patient and assesses the posterior contour of the rib cage by palpating over the area of the rib angles.The physician assesses whether one rib angle is more or less prominent than anorher.

49. The Rib Cage 3.

The physician then assesses whether there is a normal posterior convexity with the inferior border of each rib being more easily palpated than the superior border.

4. The posterior rib cage is also assessed for muscle hypertonicity and tenderness. 5. The width of the intercostal spaces is assessed for symme try, intercostal muscle hypertonicity, and tenderness. Each intercostal space should be symmetrical with the one on the opposite side and with the one immediately above and below. 6. The physician next stands in front of the patient and examines the anterior contour of the rib cage. Palpation is done at the costochondral junctions, assessing the rib contours and inter costal spaces in a manner similar to that described in step 5 above. 7. The physician then similarly evaluates the lateral rib cage, palpating in the mid-axillary line. The diagnostic criteria for structural rib dysfunction are de scribed as follows: 1. Anterior subluxation. A. Posteriorly, the rib angle is less prominent. B. Anteriorly, the rib shaft is more prominent. e. There is associated tenderness and muscle hypertonicity. 2. Posterior subluxation. A. Posteriorly, the rib angle is more prominent. B. Anteriorly, the rib angle is less prominent. e. There is associated tenderness and muscle hypertonicity. 3.

External rib torsion. A. The superior border of the involved rib is more prominent. B. The inferior border of the involved rib is less prominent. e. There is a wider intercostal space above and a more narrow intercostal space below the involved rib, with associated muscle hypertonicity and tenderness.

4. Anteroposterior rib compression. A. There is less prominence of the involved rib both anteriorly and posteriorly. B. There is increased prominence of the involved rib in the midaxillary line. e. The intercostal space above and below the involved rib reveals tenderness and increased muscle tension. 5. Lateral rib compression. A. There is more prominence of the involved rib in the an terior and posterior rib cage. B. There is less prominence of the involved rib in the midax illary line. e. The intercostal space above and below the involved rib reveals tenderness and increased muscle tension. 6. Laterally flexed tib. A. There is prominence of the involved rib in the midaxillary line. B. There is a narrow intercostal space above and a wider intercostal space below the involved rib. e. There is marked tenderness, usually in the intercostal space above the involved rib. D. This restriction is most commonly seen in the second rib.

723

Evaluation of the First Rib for Respiratory Rib Restriction The first rib is evaluated for respirarory restriction as follows: 1. The patient is seated or supine on the examination table. 2. The physician stands behind the seated patient or sits at the head of the examination table if the patient is supine. 3.

The physician grasps the anterior and superior aspect of the trapezius muscle on each side and retracts the tissues post eriorly.

4. The physician then directs the long fingers caudally ro make bilateral contact with the posterior shafts of the first ribs. 5. The patient is instructed to inhale and exhale deeply. 6. The inability of one or the other first rib to descend into the exhalation position indicates inhalation restriction of that rib. The inability of one or the other first rib to ascend into the inhalation position indicates exhalation restriction of that rib. Evaluation of Ribs 2-10 for Respiratory Rib Restrictions This can be done in the following manner: 1. The patient lies supine on the examination table. 2. The physician stands at the side of the table so that his or her dominant eye is over the patient's midline. 3.

The physician places his or her hands over the patient's upper anterior thoracic cage so that the tips of the middle fingers contact the inferior borders of the clavicles.

4. The patient is asked to inhale deeply and then exhale Fully; assess pump-handle motion of the upper ribs, looking For asymmetry of motion berween the left and right sides of the upper rib cage (see Glossary). 5. Evaluate the upper rib cage in the same manner, but along the midaxillary line. This maneuver assesses bucket-handle motion of the upper rib cage (see Glossary). 6. This process is repeated For the middle and lower rib cage regIOns. Asymmetry of motion in any of the rib cage areas indicates the presence of respiratory rib dysFunction in that region. Respiratory rib dysfunction has either inhalation or exhalation restriction. There is usually one rib within a group of ribs that is responsible for maintaining the inhalation or exhalation restriction. This rib is referred ro as the key rib and is the rib that must be identified and treated to remove the group restriction. To identify the key rib within a group of ribs, examine each rib in the group individually.This is done by doing the Following: 1. Place a finger on each pair of ribs in the group, first at the parasternal area (for pump-handle restriction) and then in the midaxillary line (for bucket-handle restriction). 2. For each placement, ask the patient to inhale and exhale. Pal pate successive pairs of ribs within the group until symmetry of motion on respiration is noted. 3.

With inhalation restriction, the key rib is found at the top of the group, but it is located at the bottom of the rib group with exhalation restrictions.

724


[n summary, inhalation restrictions involve a rib or group of ribs that first stops moving during inhalation. The key rib is the top rib in the group. Exhalation restrictions involve a rib or group of ribs that stops moving first during exhalation. The key rib is the bottom rib in the group.

Evaluation of Ribs 11 and 12 Ribs 11 and 12 have no anterior cartilaginous attachment and therefore do not exhibit pump-handle or bucket-handle move ment. Instead, they move posteriorly and laterally with inhala tion, and anteriorly and medially during exhalation.This motion is sometimes described as caliper motion. Assessment for respiratory dysfunction of ribs 11 and 12 is as follows: 1. The patient lies prone on the examination table. 2. The physician stands at the side of the patient, with his or her dominant eye over the patient's midline. 3.

The physician places his or her hands over the 11th and 12th ribs, contacting the rib shafts with the thumbs and thenar emll1ences.

4. Ask the patient to inhale and exhale fully; note any asymmetry of motion in the ribs. 5. If either of the ribs does not move posteriorly with inhala tion, it has an inhalation restriction. Conversely, if the ribs do not move anteriorly with exhalation, exhalation restriction is present.

Diaphragm Evaluation

One method of examining the diaphragm for motion restriction is as follows: l.

The patient is seated on the examination table.

2. The physician stands behind the patient. 3.

The physician passes his or her hands around the thoracic cage under the arms of the patient.

4. Assess diaphragmatic motions by gently but firmly introduc ing the finger pads upward and medially under the costal margll1s. 5. Testing is easier when the patient leans slightly backward against the physician's chest in a slightly slumped position. This position lessens tension of the muscular attachments on and around the costal margins, making palpation easier. 6. Assess motion restriction and asymmetry by passively rotating the diaphragm gently right and left. Sternum Evaluation

Compression and decompression of the sternum can be a valu able diagnostic test, for many reasons.Two common examples are sternocostal problems associated with seat belt injuries in car acci dents and mechanical chest wall problems secondary to coronary artery bypass surgery. Sternal Compression Testing the sternum involves gentle compression and release with particular attention to respiratory, mechanical, and pain-related responses arising both locally and from points distant. Functional and myofascial approaches are particularly useful (see Chapters 61 and 62). To test the motion of the sternum: 1. Place one hand longitudinally on the manubrium and the body of the sternum, and place the fingers of the other hand on top of the first hand (Fig. 49.8). 2. Compress slightly, noting any indication that the tissue moves more easily in one or more directions as the patient goes through the respiratory cycle.

B

FIGURE 49.8. Evaluation of the sternum. A: By Compression. B: By superior and inferior gliding motion.

49. The Rib Cage

B

� ----

c

FIGURE 49.9. Segmental evaluation of the manubrium of the sternum.

A

FIGURE 49.10. Segmental evaluation of the body of the sternum (gladiolus).

725

726 3.

VII. Osteopathic Considerations in Falpatory Diagnosis and Manipulative Treatment

Place one hand longitudinally on the manubrium and body of the sternum and apply a superior and inferior gliding motion, noting whether motion is restricted in one direction or the other (Fig. 49.8).

and connective tissue in the absence of trauma is more indica tive of musculoskeletal dysfunction or connective tissue disor der. Palpating for tender spots and trigger points is often helpful (Chapters 66 and 67).

The sternum may also be examined segmentally as follows: I.

The manubrium may be tested by placing the thumbs first on the upper and lower portions of the manubrium in the midline (Fig. 49.9), then on the anterolateral aspects of the middle portion of the manubrium, and finally on the upper and lower opposite corners of the manubrium. Motion of the manubrium can be tested around transverse, longitudinal, and oblique axes, respectively.

2. A similar approach may be used ro test the motion of the body of the sternum (Fig. 49.10). 3.

Perform a motion test at the xiphisternal joint using one thenar eminence on the sternum and a single finger (or the thumb and a finger) on the inferior border of the xiphoid. Main tain slight pressure on the sternum while depressing and then lifting the xiphoid with slight anterosuperior pressure, and note any tendency for the tissues to move toward a position of ease.

OTHER DIAGNOSTIC INDICATORS

CONCLUSION

The rib cage is a complex region of the body, containing and protecting many vital organs. Osteopathic physicians must un derstand the ptoper function, diagnosis, and treatment of the tho racic area. Osteopathic manipulation is used to imptove sympa thetic and parasympathetic factors, diaphragm excursion, spinal and rib mechanics, and vascular and lymphatic flow (which im ptoves breathing). The goal is to decrease sympathicotonia and energy wasted on inefficient breathing by decreasing abnormal mechanoreceptor and nociceptive input to the central nervous system (decreasing pain) and assisting the body in mobilizing the immune system. REFERENCES I. Cathie AG. Physiological motions of the spine as related ro respira rory activiry. AAO Yearbook. Colorado Springs: American Academy of Osteopathy 1974:59. 2. Warwick R, W illiams P, eds.

Palpation that elicits tenderness, complaints of pain, wincing, grunting, or grimacing provides valuable assessment information. For example, point tenderness over a bone may be an indication of a fracture, sprain, infection, or even cancer. Pain in muscle

Grays Anatomy,

36th ed. Edinburgh,

Scotland: Churchill Livingstone; 1985. 3. Moore KL.

Clinically Oriented Anatomy,

Williams & Wilkins; 1985. 4. Gardner E, Gray OJ, O'Rahilly R. WE Saunders; 1975.

2nd ed. Baltimore, MO:

Anatomy,

4th ed. Philadelphia, PA:

LUMBAR REGION WILLIAM A. KUCHERA

KEY CONCEPTS

Functional anatomy of the lumbar region, including skeleton, ligaments, muscles, fascia, vasculature, lymphatics, and nerves • Normal motion and somatic dysfunction of the lumbar regIOn • Aids to diagnosis, including patient history, physical examination, observation, palpation, reflexes, muscle strength, and motion testing • Treatment examples, including abdominal aneurysm, cauda equina syndrome, psoas syndrome, radiculopathy, iliolumbar ligament syndrome, meralgia paresthetica, "the dirty half-dozen," hypermobility, and radiculopathy

•

The lumbar spine normally consists of five verrebrae and f� rms a smooth lordotic curve just above the pelvis. Lumbosacral anoma lies are fairly common (see Radiologic Aspects of the Postural Study, Fig. 42.9) Sometimes during embryologic development, a sixth vertebra forms. Although this alters muscular attachments, it usually does not hinder stability during activity. The lumbar region normally has a lumbo-Iumbar lordotic angle extending from L2-5 that averages 43 degrees (see Radiologic Aspects of the Postural S tudy, Fig. 42. 14) . The normal lordotic curve of the lumbar spine functionally permits more extension than flexion before the sagittal plane reaches a position where non-neutral multiple plane mechanics occur with motion . The lumbar spine occupies half to two-thirds of the posterior skeletal and myofascial wall of the true abdomen ( Fig. 50. 1 ) . It is directly linked to the thoracic and pelvic regions. Because of its functional anatomic connections, it can influence the head and neck, the upper extremi ties, the lower extremities, and even the viscera (Fig. 50. 1) . This means that the location of symptoms does not necessarily indicate the region of their etiology. Problems in the pelvis, abdomen, leg, arm, head and thoracic regions, as well as the lumbar region, need to be considered. Although the lumbar facets are relatively aligned in the sagitral plane, analysis reveals that the lumbar and thoracolumbar regions provide most of the motion of the trunk. The facets of the thoracic region, oriented i n a coronal plane, would seem to allow more

motion around all three axes. However, the rib cage hinders the ability of the thoracic region to rotate, side-bend, flex, or extend. The lumbar region is a frequent site for strain, pain , and dis ability. Back pain afflicts up to 85% of all people at some time in life (l ,2). It is the most common reason for limited activity in people younger than 45 years, the second most frequent reason for visits to the physician, the fifth-ranking cause of admission to the hospital, and the third most common site for surgical proce dures (3,4) . Low back dysfunction constitutes a large percentage of compensation claims and is often the reason for a worker's absence from work, an employer's need to complete an i nsurance claim, and for insurance companies sending out disability pay ments. Successful and long-lasting rreatment must be directed toward the primary cause and not only toward the symptom of "a backache" or "a back problem." To do this effectively and effi ciently, the physician must have functional anatomic knowledge of the lumbar region and its neurophysiologic connections with the rest ohhe body (Fig. 50. 1).

FUNCT IONAL ANATOMY The Anterior Element Vertebral Body

A lumbar vertebra is larger than other spinal vertebrae. It is dis tinguished by the absence of costal facets (like the thoracic ver tebrae) and transverse foramina (l ike the cervical vertebrae). The vertebral body is wider rransversely and deeper anteroposteriorly than any other vertebrae (5). This large, cross-sectional area and its longitudinal and verrical trabecular arrangement (Fig. 50.2) increase i ts strength and stabil i ty. Lumbar vertebrae are capable of sustaining the heavy, functional, longitudinal loads that will surely be acting on them. The vertebral bodies also act as accessory organs for hematopoiesis. Despite their apparent strength, the lumbar spine is the most common site for compression fracture. This is because there is a weak spot located in the anterior portion, where the trabec ular arrangement and density is reduced (Fig. 50.2). Sufficient flexion with anterior stress can result in a compression fracture of the vertebral body. This anterior area fractu res at 75% of the force needed to fracture the posterior portion of the verrebral body. With or without lifting, compression fractures occur most frequently in persons who have reduced calcium and/or frank

728

VII

Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment

Anterior rarification of trabeculae

FIGURE 50.2. Trabecu lae of a l u mbar vertebra, i l l ustrating the weak anterior reg ion of the vertebral body.

FIGURE 50.1. The l u mbar region and its functional anatomic relation s h i ps with the rest of the body.

osteoporosis. Risk factors include: poor diet, ptolonged inactiv ity, o r hypoparathyroid disease. I t may also be a consequence of a malignancy. Even i n the absence of risk factors, a compression fracture may be produced in anyone by forceful flexion, for exam ple, in automobile accidents, pratfalls, and j umping off or falling from a considerable height. Sometimes the precipitating event is unknown to the person ; they only know that they began to have a deep nagging back discomfort that did not go away. Early clues to a vertebral compression fracture are provided by the history and physical examination-not radiographs. The history will most likely reveal activities or risk factors like the ones described. If a compression fracture is suspected, do not ask the patient to perform flexion or side-bending. Instead, place the person in a lateral recumbent position for an examination.

The physical examination will reveal discomfort, even with light palpation, percussion, or vibration over the spinous process of the involved vertebra. Palpatory discomfort and a history of dis comfort with certain spinal motions will be out of proportion to the physical signs of injury. Pain is usually increased by leaning on the patient's shoulders, causing compression of the spinal col umn, and is eased by pulling cephalad from under the patient's arms, or by holding a gentle extension to the patient's spine. The physician who mistakenly believes the problem is a strain and begins manipulative treatment or who only prescribes medica tions with physical therapy soon finds out that this management is ineffective and not pleasing to the patient. Although pain i n the low back is usually immediate, it will be several days after the accident before a routine lateral lumbar radiograph will show a compression deformity of the vertebral body. Apparen tly, initial compression of the bone is followed by a rebound of its tissue matrix. Decalcification and anterior verte bral compression then occur, finally revealing the tell-tail sign: a wedged vertebral body. The spine then angulates at the site of the compression fracture, and the spinous process at that vertebral unit becomes more prominent than normal. Ifboth the anterosu perior and anteroinferior aspects of a vertebra are clearly wedged on an early radiograph, and especially if there is eburnation of the bone, the defect is old and due to osteochondritis rather than fracture. For treatment, the patient is given instructions and exercises that encourage gradual extension of the lumbar region, and/or a brace that is specifically o rdered for the patient and is applied to prevent active flexion and maintain slight extension. Adequate pain relief medication is provided, taking care not to induce de pendency or habituation. The use of codeine in lumbar fractures may be counter productive, as both the pharmacologic proper ties of the medication and the nociceptive thoracolumbar reflex facilitation from the inj ury tend to constipate the patient. Most types of direct osteopathic manipulative treatment over the site of a compression are contraindicated, although classic direct and indirect myofascial treatment may be used to improve lymphatic flow, to reduce segmental facilitation, and to comfort the patient. Pain and nociception are also reduced by myofascial treatment directed toward relief of sympathicotonia and general improve ment of lymphatic drainage. Secondary sites of somatic dysfunc tion that develop as a result of the inj ury are treated to reduce their secondary facilitation of related cord segments. Only meth ods and activations that are comfortable for the patient and that do not stimulate the site of injury are used to reduce discomfort and promote normal healing.

50. Lumbar Region

Intervertebral Disc

An intervertebral disc is located between each lumbar vertebra. Though gross anarom ists do not consider the intervertebral disc a part of the anterior vertebral element, it is certainly associated with it when functional anatomy is considered. If all the interver tebral discs were stacked up one on another, they would normally account for one-fourth of the length of the spine. Lumbar discs are large and built to rolerate and dissipate heavy loads. They are composed of:

Etc.

Herniated L4 disk

Normal 5th lumbar

Glycosaminoglycans Mucopolysaccharides Proteoglycans Collagen Intervertebral discs are named according to their region (lum bar in this case) and numbered according to the vertebral unit of which they are a part (i.e., the number corresponds to the first vertebra of the vertebral unit). Example: The intervertebral disc for the L2 vertebral unit would be the second l umbar disc. Each disc is j oined ro the inferior plate of the vertebra above it and the superior plate of the vertebra below it. There is a compressible nucleus pulposus located at its cen ter, and this is surrounded by layers of the anulus consisting of concentric lamellae of collagenous fibers. These anular fibers are oriented 65 degrees fro m vertical, and the layers alternate in a right/left direction as they encircle and contain the nucleus pul posus. Clinically, i t is i mportanr to note that the anulus of a lumbar disc is fairly thick anreriorly but is noticeably thinner posteriorly. Hisrorically, L4 and L5 inrervertebral discs are at the greatest risk for rupture. The nucleus pulposus is composed of 70% ro 90% water, and is semifluid and hydrophilic. I t is deformable but not compress ible. With postural weight bearing, the nucleus expands laterally against the anulus, and these two parts work together mechani cally to act as a shock absorber between each vertebral body of the spine. When load is applied and the nucleus is compressed, it loses water. This results in a 1 . 5 mm creep in the first 2 to 10 minutes of compressive stress. Resting supine with the lower extremities flexed and raised is the optimal position for rehydrat� ing the discs. With this rest, discs normally return to their full o r optimal height. With aging, however, the hydroph ilic properties of a disc are reduced, just as is i ts ability to reform after being stressed by prolonged pressure or a sudden and severe stress.

729

disk

FIGURE 50.3. Pedicles located on the superior t h i rd of the posterior side of a l u mbar vertebra protect the nerve from being injured by a herniated disc at its own level. It is more likely that a l u m bar nerve wou l d b e affected b y a herniated disc o f the previous vertebral u n it. That i s w h y a n 5 1 nerve root is usua lly affected by a herniated L S intervertebral disc.

cles of that vertebra are first idenrified. On an anteroposterior (AP) radiograph, the pedicles appear as two longitudinal rows of opaque ovals on the lateral, superior third of the vertebral bodies (Fig. 50.4) . These are used as landmarks for finding the other posterior elements. Transverse Processes

A transverse process projects laterally fro m the region of each pedicle. In the lumbar region, these p rocesses are anatomically lo cated directly lateral (in the same horizontal plane) to the spinous p rocess of the vertebra of their origin. This fact helps in locating and palpating the pair of associated lumbar transverse processes after palpating and idenrifying a specific lumbar spinous p rocess. This also permits accurate testing of the proper vertebra for rota tional motion of a specific lumbar vertebral unit. However, when looking at an AP radiograph of the lumbar region, the transverse processes will not be located directly lateral to the spinous pro cess of their parent vertebra. In the exposure required to obtain a standard A P lumbar radiograph, the central x-ray beam is not placed directly over the lumbar vertebral bodies. With this po sitioning of the central ray, the surrounding angled, paracentral x-ray beams project, distort, and magnify the i m ages of the bony structures they pass through.

The Posterior Elements Pedicles

Superior and Inferior Articular Processes

Pedicles connect the posterior elements to the vertebral body and mark the site where the posterior vertebral elements begin. In the lumbar region, pedicles are located on the superior third of the posterior surface of the vertebral body. This protects the nerve root of a vertebral unit from being injured by a significancly her niated intervertebral disc of that same unit ( Fig. 50.3). The nerve winds around the pedicle and exits its inrervertebral foramen before it crosses the intervertebral disc. Anatomically and radiographically, all of the posterior ele ments of a vertebra can be accurately identified if the pedi-

An inferior articular p rocess p rojects in a caudad direction from the region of the pedicle, and its articular facet faces laterally. A superior articular process projects cephalad fro m the same pedicle, and its facet faces medially. The joint space of an intervertebral synovial j o int is formed by the facet of an inferior articular process of one vertebra and the facet of a superior articular process of the next vertebra. A lumbar joint space generally has a sagittal plane orienration, so i t is best viewed o n a n AP radiograph of the l umbar region, where it appears as a gray or dark line between two articular processes.

730

VII.


o Vertebral body c

D

C

E

Superior articular process Pedicle Transverse process Lamina Spinous process

F F

Inferior

superior

half

half

l�

I nferior articular process

� y �__ �

__

I ntervertebral foramen FIGURE 50.4. I l l ustration of an x-ray view of a l u mbar vertebra. The pedicle acts as a landmark for identification of the other parts of the posterior elements of a vertebra.

Zygapophyseal tropism is the most common l umbar congenital abnormality, and is found in 30% of patients (see Radiologic Aspects of the Postural Study, Fig. 42.90). This term describes a composi te arrangement where the articular pillars on one side of a vertebral unit are twisted so that the plane of the resulting synovial intervertebral joint on that side does not match the orientation of the synovial joint o n the other side. Asymmetry of lumbar facets (j ust as finding six lumbar vertebrae) should not keep an employer from h i ri ng that person for a job. However, asymmetric joints at the same level may be associated with asymmetric muscle tensions and altered spinal motions.

Lamina

A lamina projects medially and caudad from each pedicle, and normally meets its partner in the posterior midline to form a typical rectangular lumbar spinous process. I n some instances, the laminae will not completely meet in the m i dline, and a spina bifida is produced (Fig. 50. 5). The most common congenital anomaly of this type is the "hidden" spina bifida, called spina bi fida occulta. Spina bifida occulta is frequently found at the L5-S 1 level of the spine (see also Fig. 4 2. 9F). The only physical clue to its presence may be a midline patch of coarse hair on a patient's skin over its site. In this type of spina bifida, the skin is i n tact and

there are n o meningeal components. An employer should not use this type of spinal b ifida as a reason to refuse hiri ng a person. I t m a y modify muscle attachments, however, a n d can b e associated with a higher i ncidence of other posterior vertebral anomalies, in cluding congenital or acquired spondylolisthesis (see Chapter 43, Postural Consid� rations i n the Sagittal, Coronal, and Horizontal Planes). In the more serious forms of spina bifida, meningocele and meningomyelocele, the spinal membranes protrude, with or without cord tissue. These are disabling. Spinous Processes

Clinically, the spinous p rocess of a lumbar vertebra is located in the same horizontal plane as i ts associated transverse processes. Lumbar spinous processes are distinguished by their palpable, thick, quadrangular, "spade-l i ke" distal ends. This is in contrast to the fingertip-shaped palpatory characteristic of the thoracic spinous processes. Their distinguishing shape provides palpatory evidence of where the lumbar region begins and where the tho racic spine ends. This also aids in counting lumbar or thoracic vertebrae. There is one exception; the spi nous process of the fifth lumbar vertebra is smaller, lies i n a hollow j ust above the sacral base, and its distal end is about one-third smaller than the rest of the l umbar spines. It feels more like a thoracic than a lumbar spinous p rocess (Fig. 50.4). This L5 spinous process character istic helps to identify it as the last l umbar vertebra and not the first spinous p rocess of the sacrum. Another, less accura"re way of counting lumbar vertebrae is to find the most superior portion of the iliac crests and then follow a horizontal plane from there to the m i dline. This should cross the spinous process of L4, and counting can begin from there. Spinal Canal

FIGURE 50.5. A spina bifida deform ity. The laminae do not co mpletely meet to form a spinous process. Spina bifida occulta is relatively benign, but a spina bifida that contains meningeal or neura l elements is very serious and disabli ng.

The spinal canal is actually an anatomic space between the poste rior margin of a vertebral body and parts of i ts posterior elemen ts (i.e., its two pedicles, and the laminae). It contains the dural tube, spinal cord, and origins of the spinal nerves down to ap proximately the L2-3 level, where the spinal cord ends. From that

50. Lumbar Region

level on, the dural rube contains the cauda equina and the filum terminalis interna (Fig. 50. 12) . The entire spinal canal is wider transversely than it is anteroposteriorly. In the l umbar spine, it is also triangular. The spinal cord usually terminates at the L2 level as the conus medullaris. Each of the remaining dorsal and ventral roots of the lumbar, sacral, and coccygeal nerves hang in the du ral tube and spinal canal, forming the cauda equina (horse's tail); they exit the conus medullaris or the dural tube as they approach their appropriate intervertebral foramen.

M

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The Intervertebral Foramen Intervertebral foramen (one on the right and one on the left) are formed by rwo adjacent vertebrae of a vertebral unit. They are defined by: Two adjacent vertebral bodies and the intervertebral disc be rween them Two adjacent pedicles The inferior articular process of one vertebra and the superior articular process of the next, including the synovial joint berween them A spinal nerve and a recurrent meningeal nerve, each carry ing the same identification number as the vertebral unit, pass through a lumbar foramen. The recurrent meningeal nerve then re-enters the foramina (Fig. 50.6L) . These nerves only occupy 35% to 40% of the foramina area. A lumbar intervertebral fora men is normally rwo to three times larger than the area taken up by the l umbar nerves, so it seems that compression of the nerve would be difficult. With Aexion, the facets and pedicles glide away fro m one another, and the size of the intervertebral ' foramen increases. With extension, the pedicles glide toward one another, and the foramen is reduced in size. Reduction of the foramen size also results fro m arthritis or spurs, hypertrophy of the posterior longirudinal ligament, extrusion of the nucleus pul posus, tissue congestion or edema, inflammation, and perineural edema. Removal or reduction of the effect produced by any of these factors may be enough to allow a symptomatic patient to become asymptomatic-pain free and able to work. This is im portant to remember when considering management of patients with back pain etiologies, paresthesias, or radiculopathies.

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R

s

FIGURE 50.6. Diagra m m atic representation of the L2, i ntervertebral fora men. (A) su perior a rticular process, (B) pedicle, (C) transverse pro cess, (0) l a m i na, (E) spinous process, (F) i nferior articular process, (G) L2 synovial joint and capsule, (H) L2 ventral root, (I) L2 dorsa l root, (J) ventral ramus of L2 nerve, (K) dorsal ramus of L2 nerve, (L) recurrent meningeal nerve, (M) posterior longitudinal l i g a ment, (N) spinal cord, (0) dural tube conta i n i n g spinal cord and approaching conus medul laris at L2 region, (P) posterior longitu d i n a l l iga ment, (Q) d ural tube con taining cauda equina, (R) ventral and dorsal roots of the cauda equi na, (5) filum term i n a l is i nternus, (T) gray and white rami, (U) anterior lon g itud i n a l l igament, (V) i ntervertebral d isc, and (W) L2 chain gangl ion.

Ligaments {Table 50.1} The Posterior Longitudinal Ligament

The posterior longirudinal ligament is broad in the cervical re gion, and begins to narrow when it reaches the first lumbar ver tebra. It takes on a scalloped appearance, and is only one-half

TABLE 50.1. LUMBAR LIGAMENTS

Ligament

Of the Posterior Elements: Supraspinous l igament Interspinous l iga ment Ligamentum flava Capsular l iga ment

Of the Anterior Element: Anterior longitudinal l igament Posterior longitudinal l igament Other Ligaments: I l iolumbar ligament

Comment

Degenerated i n the adult l u mbar spine and possibly ruptured. Between the l u m ba r spinous processes (weak and often absent). Between one lamina and the next. They are p u nctured when the patient is given an epidural or spinal anesthetic. Supplied by nociceptive fi bers that report somatic dysfunction. Wide and strong. ' Na rrowed and scolloped i n the l u m bar spine prod ucing a posterolateral deficiency over the i ntervertebral d i sk. Joins the l u m bar spine to the i l i u m of the pelvic region. Can produce symptoms that m i mic an i n g u i nal hernia.

VII.

732


Right iliolumbar ligament

Posterior longitudinal ligament

Tender point

Pedicle

Ruptured L4 disk

PS I S

PSIS

Normal 5th lumbar disk

FIGURE 50.7. A left-sided L4 intervertebral disc herniation. The poste rior long itud i n a l l iga ment is normally narrowed, t h i n ned, and scalloped i n the l u m bar reg ion. This leaves the lateral marg ins of a l u m bar inter vertebral disc vul nerable to herniation. Bones

its original width when it reaches L5. The scallops produce a deficiency in the posterior longitudinal ligament that is located over the posterolateral ponions of each lumbar intervenebral disc (Fig. 50.7). The posterior portion of the intervenebral disc is also the thinnest portion of the anulus. Therefore, this is the region of a lumbar disc that is most likely to rupture; if it does, it is most li kely to be associated with nerve root pressure. The Iliolumbar Ligament

This ligament is located in the lumbosacral region. It is attached to the transverse processes of L4 and L5, and extends to the iliac crest and the anterior and posterior regions of the sacroiliac joint ( Fig. 5 0 . 8 ) . It has been reponed that this "ligament" may consist of muscle fibers in neonates and children and gradually becomes ligamentous over the next thirty years, but this has recently been disputed by some anatomists. Remember that the iliolumbar ligament is typically the first ligament to become tender to palpation when there is lumbosacral postural stress and decom position. A tender point on the iliac crest, located 1 inch superior and lateral fro m the inferior mar gin of the PSIS and in the iliolumbar ligament, becomes acutely tender to palpation (Fig. 50.8). Patients with early postural de compensation may not realize that the i liac attachment of this lig-

ligament

FIGURE 50.S. T h e i l iol u m bar ligaments and t h e location o f t h e right i l iolumbar l igament tender point. The i l iolu mbar ligament is the first to become tender to palpation when there is postural decompensa tion. Radiation of pain into the groi n/testicle may incorrectly suggest an i n g u i n a l hernia on that side.

ament is tender until it is palpated. Its tenderness is a physical clue that should p rompt the physician to ask questions about posture and to carefully examine the spine, lower lumbar, and sacroiliac joints for somatic dysfunction, scoliosis, and/or evidence of sacral base unleveling. An example would be an adultwho has, for years, been successfully compensating for continuous low back strain secondary to a congenital sacral base unleveling or an acquired short leg. As a result of decompensation in the lumbosacral re gion, this patient finally becomes symptomatic with back pain. The first complaint of a patient with irritation of the iliolumbar ligament may be, "I think I have a hernia." (See I liolumbar Liga ment Syndtome in the Treatment of Non-Medical/Non-Surgical Etiologies section below.)

Muscles and Fascia (Tables 50.2 and 50.3) The first few lumbar vertebrae provide posterior attachments for the abdominal diaphragm. The left crura of the diaphragm at taches to the first two, and the right crura attaches to the first three

TABLE 50.2. EXTRINSIC LUMBAR MUSCLES FOR MOVEMENT OF RESPIRATION, THE SPINE, AND THE LIMBS

Muscle

Origin

Insertion

Abdom i n a l diaphra g m Quadratus l u m borum

Bodies of L 1-3 Iliolumbar l igament and i l iac crest

Serratus posterior inferior

Last two thoracic and fi rst two l u m bar spi nous processes Thoraco l u m ba r fascia, i l iac crest and spinous processes of l ower 6 thoracic vertebrae I l iac crest and sacrum

Lower 6 ribs and xiphoid process Tips of the L 1-4 transverse processes and the anterior surface of the 12th rib Inferior border of the lower 3 or 4 ribs Intertubercular groove of the h u merus

Latissimus dorsi

Erector spinae mass (spi nal is, longissimus, and i l iocosta l is)

Lum bars, thoracic, ribs, cervicals, and occiput

Comments (See Cha pter 51, Abdom i n a l Region.) Functiona l ly considered a posterior inferior extension of the abdom inal d i a phragm. Function a l ly con nects the thoracolumbar region with the lower ribs. Functiona l ly con nects the l u m bar, thoracic, and pelvic regions to the upper extremity. Connects to the entire spine and to the lower extremity through the l u m bo-thoracic fasci a.

50. Lumbar Region

733

TABLE 50.3. INTRINSIC LUMBAR MUSCLES FOR MOVEMENT OF THE VERTEBRAL COLUMN

Muscle Erector spinae mass (ESM) Spina lis dorsi Intersp inalis portion of the medial spinalis group (part of the ESM) Longissimus dorsi (pa rt of the ESM) I l iocosta lis l u mborum (part of the ESM) Intertransversari i Multifid us"

Comments

Origin and Insertion I l iac crest and sacrum to l u m bars, thoracics, ribs, cervicals and occiput. Spi nous p rocesses of L 1 and L2 to upper 8 thoracic spi nes. One spinous process to the next. Transverse processes and l u m bo-dorsal fascia to lower 10 thoracic transverse processes and their ri bs, medial to the rib ang les. I l iac crest and sacrum.

One transverse process to the next. One mammary process to the next.

Connect to entire spine and through the l u m bo-thoracic fascia, to the lower extremity.

From l u m ba r region to second cervical vertebra.

These attach to the posterior a n g les of the lower 6 to 7 r i bs and mark the most lateral extent of the ESM muscle group. M ost developed i n l u m b a r and cervical regions. Only i n l u mbar region.

"Multi fid i muscles in the L 1 and L2 region are usually the first to become involved by viscerosomatic reflexes f rom irritation of the left colon and/or pelvic organs. Their involvement usually results in non-neutral (type II) somatic dysfunctions of those vertebral units that are usually rotated toward the side of the involved organ. (See lumbar motion and Chapter 51, Abdominal Region.) ESM, erector spinae mass.

lumbar vertebral bodies. The diaphragm then arches cephalad past these and the lower thoracic vertebrae, with its apex some times as high as the fifth intercostal space. It then curves caudad to attach to the xiphoid process (Figure 50. 1 and Chapter 5 1, Abdominal Region). For this reason, somatic dysfunction of the fi rst three l umbar vertebrae can be associated with a flattened, ineffective, dysfunctional, resting abdominal diaphragm. A flat tened diaph ragm is often associated with a lumbar lordosis and/or psoas and quadratus muscle spasms. In this flattened resting con dition, the diaphragmatic dome is unable to develop efficient, appropriate p ressure gradients between the thorax and abdomen during contraction and relaxation, and this results in decreased lymphatic flow and venous return fro m anywhere in the body. The physician should also remember that the innervation to the diaphragm is the phrenic nerve, which originates from nerve roots C3-5 of the spinal cord. Therefore, cervical somatic dysfunction can be involved in diaphragmatic dysfunction. The lumbar spine also supplies partial origin for the erector spinae mass of muscles that extend from the pelvis all the way to the occiput. Unilateral contraction of extrinsic or intrinsic muscles of the back will side bend or rotate the spine. When working together, these muscles extend the spine. Through the lumbosacral aponeurosis and fascial divisions, the lumbar region is functionally attached to the gluteal muscles, the hamstrings, and via the iliotibial band, to the lower extremity. Through the lumbodorsal fasciae, with i ts continuity surrounding the external and internal oblique muscles and the rectus abdominus muscle, the posterior lumbar region is functionally related to the lateral and anterior abdominal wall (Fig. 50. 1). Thoracolumbar Aponeurosis

The thoracolumbar deep fascia surrounds, compartmentalizes, and protects all of the lumbar muscles and bones (Fig. 50.9). This fascia gives attachment ro the latissimus dorsi muscle, which extends ro the proximal end of the humerus. Next to the spine, it compartmentalizes the interspinalis, multifidi, and rotatores muscles. More laterally, but still near the midline, it encloses the

longissimus muscle. Even more laterally, it encloses the i liocostalis muscle group that inserts on and provides a landmark for locating the angles of the ribs. The angle of the ribs marks the most lateral extent of the erector spinae mass. Deeper layers of the deep fascia form compartments for the intertransversarii. Anterior to the transverse processes, the deep fascia surrounds the psoas and quadratus lumborum muscles. The quadratus lumborum muscle can din ically and functionally be thought ofas the posteroinferior extension of the abdominal diaphragm. Mesenteries

Approximately 30 feet of small intestines and portions of the ascending and descending colon are located anterior to the lum bar region. The abdominal mesenteries are formed by reflections of the parietal peritoneum fro m the posterior abdominal wall (Fig. 5 0 . 10). These mesenteries carry arteries and efferent auto nomic nerve fibers to the viscera. They also carry veins, lymphatic vessels, and visceral afferent nerves away fro m the viscera. In this way, somatic dysfunction of the myofascial tissues of the l um bar region can functionally influence the local environment of the abdominal viscera. Myofascial trigger points in the gluteus medius, rotatores, multifidi, i liopsoas, quadratus l umborum, and the piriformis mu scles produce pain patterns in the lumbar region and sometimes into the sacral region and lower extrem i ties (6,7) (Fig. 50. 1 1) .

Spinal Cord and Lumbar Nerves Spinal Cord

In an adult, the spinal cord usually terminates at the L2 1evel as the conus medullaris (terminal range T 12-L2, and some say to T3) . The dural sac and a string of fibrous tissue and pia, known as the filum terminalis internus, continue on. The dural sac terminates by attaching to the spinal canal at the 52 level. Fibrous tissue and cells fro m the dura continue on as the filum terminalis ex terna, which attaches to the fi rst coccygeal segment (Fig. 50. 12) . Remember that the posterior longitudinal ligament is anterior

734

VII.


Interspinalis muscle

Quadratus lumborum fascia I ntertransversarius Psoas fascia

Sympathetic ganglion I ntervertebral disK

mu scle

Psoas muscle

Anterior longitudinal l igament

FIGURE 50.9. The deep fascia and thoracol u m bar aponeurosis of the low back. It compartmental izes, protects, and gives attachments for the erector spinae mass and l u m bar muscles.

to the spinal cord and has lateral deficiencies in the areas of the lumbar discs ( Fig. 50.7) . The dural sac of the spinal canal, below the conus medullaris, contains the filum terminalis internus and lower lumbar, sacral, and coccygeal dorsal and ventral rootlets of the cauda equina (see Posterior Elements: Spinal Canal, above). The lumbar spinal canal takes on a triangular configuration and normally decreases in its anteroposterior dimension as it pro gresses fro m L l to L 5 . As a person ages, the diameter of the lumbar spinal canal or intervertebral canal may be further comprom ised by factors that include:

Hypertrophy of the posterior longitudinal ligament Thickening of the ligamentum flava on its anterior wall Osteoarthritis Exostoses Osteophytes Tumors Ruptured l umbar intervertebral discs Tissue congestion, frank edema, and perineural edema can also compromise the nerves in the spinal canal or an intervertebral foramen, especially if the region already has somatic dysfunction and/or an anatomic/pathologic deformity. If there is enough pres sure on the spinal cord or the nerves in the cauda equina, there will be loss of reflexes, weakness of m uscles, and paralysis of the lower extremities and sphincters of the bladder and rectum. This symptom complex describes a severe form of spinal stenosis called cauda equina syndrome (see Treatment of Non-Medical/Non Surgical Etiologies: Cauda Equina Syndrome below). Lumbar Plexus

The lumbar plexus (Table 50.4) is composed of nerve roots L l -4 and a branch fro m T 12 . Lumbar nerve roots enter directly into the psoas muscle, where the lumbar plexus is formed. Lumbar nerves emerge fro m the borders and surfaces of the psoas muscle (5). Dermatomes, Myotomes, and Sclerotomes

FIGURE 50.10. The location of the posterior abdom i n a l roots of the abdom i n a l visceral mesenteries.

Lumbar dermatomes are located on the posterior lumbar para spinal region and the anterior part of the thigh, leg, and foot ( Fig. 50. 13) . Pain or paresthesi a in these areas of skin provides clues to the level of nerve root involvement and nerve dysfunc tion and/or irritation. Hoppenfeld (8) has provided the easiest pattern to remember (Fig. 50. 13) . He advises that the physi cian mentally construct three oblique lines, from superolateral to inferomedial, on the anterior thigh, dividing it into three equal sections. The inferior of these three oblique lines must go through the patella. From superior to inferior, these lines delineate

50. Lumbar Region

Quadratus lumborum M. Piriformis muscle referred pain pattern referred pain pattern

Iliopsoas muscle referred pain pattern

735

Rotatores and multifidi muscles referred pain patterns

FIGURE 50.11. Pa i n patterns produced by myofasc ial trigger points in the quadratus l u m borum, piriformis, i l iopsoas, rotatores, and mu ltifidi muscles of the back.

dermatomes Ll, L2, and L3. A line visual ized fro m the patella to the big roe delineates the medial L4 dermarome fro m the lat eral L5 dermatome. A small section on the lateral side of the foot is the first sacral dermarome. This schematic approximates the location of lumbar dermaromes of any patient. Note that different books illustrate dermatomal patterns of various com plexities. However, remembering that these divisions will vary slightly from person to person, the Hoppenfeld diagram pro vides an easy ro recall , good general clinical pattern fro m which to work. Myotomal pain is associated with cramps, weakness, and my ofascia I trigger points in the muscles that share i n nervation fro m the same irritated nerve roots.

f1C".�-- Spinal cord Pia mater Dura

#'111--1'1-- Conus medularis

Filum terminalis internus Plane of the umbilicus

cauda equina

Sacral

"\'�II-\--'-..\-- Termination of the dural tube

Sacrum---�

\\\-\,--+1-- Filum terminalis externa

Coccyx -----fi::;'f'--j'--- Attachment of the filum terminalis

FIGURE 50.12. The relationships of the spinal cord, dural tube, conus medul la ris, filum terminal is internus, cauda equi na, and f i l u m term inalis externa to the l u mbar and sacral regions.

Sclerotomal pain is described as vague, deep, toothache-like pain (see Chapter 53, Lower Extremity, Fig. 53.30). It arises from ligaments, bones, or joints that share innervation from the same irritated nerve root. Knee pai n, for example, can be the result of irritation of the L3 vertebra, ligaments in the L3 region , the pubic symphysis, the hip, or the knee. All of these sites have the same L3 sclerotomal origin.

Vasculature and Lymphatics Blood Vessels

The lumbar spinal cord receives its arterial blood supply from segmental radicular arteries. In the lumbosacral region, one of these radicular arteries, the arteria radicularis magna, is larger than the rest, and is the source of blood for the inferior twO thirds of the spinal cord (9) . The rest of the cord receives blood fro m associated segmental arteries. Arteries supplying a lumbar vertebra enter around the circumference of the vertebral body, especially near its transverse processes. Venous blood drains the spinal cord via a profuse plexus of thin-walled veins that com municate with the profuse, valveless venous plexus in the vertebrae and the anterior and posterior longitudinal veins of the dura. Venous blood fro m the profuse vertebral plexus of valveless veins drains into a large basiverte bral vein ( 10), which exits from a foramen located in the poste rior surface of each vertebral body. All ofthese veins are valveless. Venous blood fro m the spinal cord can drain into radicular veins or can drain cephalad into the large, valveless venous sinuses of the dura. The profuse, valveless venous plexus of the spinal cord, ver tebrae, communicating veins, and large, intracranial venous si n uses are of great clinical importance. An i ncrease in i ntraab dominal or intrathoracic pressures, as occurs with coughing, Valsalva maneuvers, o r fascial tensions, can reverse the flow of venous blood and become a factor in the metastasis of primary abdominal and pelvic malignancies to the spine and brain ( 1 1) (Fig. 50. 14) . This mechanism also explains headaches and other central nervous system symproms from increased ve nous pressure associated with visceral, spinal cord, or vertebral dysfunction. The blood fro m the muscles of the lumbar region drains i nto the inferior vena cava. It does not drain i n to mesenteric veins or pass through the portal system of the liver, as the venous blood from the abdominal and pelvic viscera does.

736

VII.

Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment

TABLE 50.4. NERVES OF THE LUMBAR PLEXUS

Nerve

Roots

Comments

Femoral

L2, 3, 4

Exits femoral canal to i n nervate the quadriceps muscles of thigh and provides sensory fi bers to s k i n of anterior thigh.

Obturator

L2,3, 4

Exits obturator fora men to i n nervate the add uctor muscles of thigh and provide sensory fi bers from medial portion of the thigh. Innervate the psoas major, psoas m i nor, i l iacus,and quadratus l u m borum muscles.

Lumbar muscular branches I liohypogastric I l io i n g u i n a l Gen itofemoral

L1 L1 L 1, 2

The i l iohypogastric, i lioi nguinal, and gen itofemoral nerves carry sensory fi bers from lateral skin of the g l uteal region, root of the penis or mons, and upper part of scrotum and labia, inguinal and femoral triangle,and cremasteric muscle, respectively.

Lateral femoral cutaneous

L2, 3

Emerges from psoas j ust superior to i l iac crest, runs over i l iacus muscle, passes through or under the inguinal l igament just med ial to ASIS. Provides sensory fi bers for a large oval area on the anterolateral thigh.

ASIS, anterior superior i l iac spine.

Lymphatics

Lymphatic fluid from all abdominal and pelvic viscera drains into the thoracic duct, which is also called the left lymphatic duct (LLD). All somatic lymphatic vessels at and inferior to a hori zontal plane through the umbilicus drain into the inguinal nodes, the deep pelvic external and common iliac nodes, the preaortic and lateral aortic nodes, and then into the LLD (Fig. 5 0 . 1 5) . Note that lymphatic vessels from the gonads or the viscera do not drain into the inguinal region, but drain into the deep lymphatic vessels of the pelvis and then into the cisterna chyli. Therefore, gonadal and prostate i nflammation or malignancy is not associated with enlarged, palpable i nguinal nodes. (See Chapter 7 1 ). The LLD

From upper limb Superior Valveless segmental veins I n ferior vena cava Diaphragm Sinusoids of liver

1

Valveless vertebral veins

Portal vein Capillaries of alimentary tract From lower limb

FIGURE 50.13. Dermatomes of the l u m bar nerves.

FIGURE 50.14. The profuse valveless venous system of the spinal cord, spinal vertebrae, and the bra i n . (Modified from M i l lard FP.)

737

50. Lumbar Region

vertebrae of the l umbar spinal regio n move together as a group. The major motions are: Flexion Extension Side-bending Rotation

FIGURE 50.15. Lymphatic drai nage from somatic tissues below the level of the umbil icus will d ra i n into the ingui nal lymph nodes, into the deep lymphatic vessels of the pelvis, and then i nto the cisterna chyli and thoracic duct (the left lymphatic duct).

passes through the fasciae of the left side of the thoracic inlet twice before emptying into the left brachiocephalic vei n . All lymphatic fluid (from anywhere i n the body) must pass through the fasciae of the thoracic inlet on its way to the venous circulation and the heart.

Note that side-bending and rotation are coupled motions. Their direction of motion may be opposite (type I motion) or i n the same direction (type II motion), but side-bending and rotation occur together in the lumbar spine; one cannot occur without the other. There are also minor translatory motions occurring in oppo site directions on each of the three planes of motion. A vertebral unit normally has 1 2 possible movements available to it and, therefore, 1 2 movements that can be restricted in a somatic dys function of a joint . Somatic dysfunction usually involves these minor motions, and that dysfunction then affects the major mo tions that are possible for that j oint. The pattern for multiple plane motion of a vertebral unit depends o n the position of the sagittal plane of the spine when a vector of rotation or side bending is i ntroduced. When the spine is in its neutral positional range (Fig. 50. 1 6), side-bending and rotation normally occur to opposite sides i n multiple units, and this i s called type I motion o r type I mechan ics. Type I motion occurs when it is predominately the vertebral bodies and discs that influence spinal actio n .

Motion The Vertebral Unit

From a functional anatomic or osteopathic perspective, a vertebral unit "is composed of two adjacent vertebrae with their associated disc, arthrodial, ligamentous, muscular, vascular, lymphatic, and neural elements" ( 12) . I n "Clinical Biomechanics of the Spine," White and Panjabi label a vertebral unit as a functional spinal unit (FSU) ( 1 3) . They define FSU as "two adjacent vertebrae and the connecting ligamentous tissues." Therefore, the verte bral unit is different and more comprehensive than the F S U of the orthopedic specialist; the two should not be confused when communicating or when reading the literature. With stress, a ver tebral unit behaves according to its structure, strength, flexibility, and the functional ability of its ligaments, muscular, neural, vas cular, and lymphatic connections. Both the vertebral unit and the FSU are given the same number as the cephalad vertebra of the unit. For example, the third lumbar unit is named L3. According to the vertebral unit definition, however, it not only indicates L3 moving on L4, but also includes their associated disc, arthrodial, ligamentous, muscular, vascular, lymphatic, and neural elements. Normal Motion

Moore (9) sites that the cervical and lumbar regions of the ver tebral column are the most mobile and the most common sites of aches and pains. Lumbar motion is especially visible when the

c

FIGURE 50.16. The position of the body in neutral or non-neutral sagit tal plane ranges determines m u ltiple-plane spinal motion mecha n ics. Flexion and extension within ranges A-B or A-D are within the sagittal plane range where multi ple-plane motion results in neutral mechan ics. Flexion or extension within ranges B-C + or D-E are within the sagittal plane ranges where m u lt i p le-plane motion typica lly results in non-neutral (type II) mechan ics.

738

VII


When the lumbar spine is flexed far enough or extended far enough that it is out of the neutral sagittal plane range and into the non-neutral sagittal plane range (Fig. 50. 16) , rotation and side bending normally occur [0 the same side, usually in the verrebral unit where the forces are localized. This is called type I I motion or type I I mechanics. Type I I motion occurs when the facets exert the major influence on spinal motion. There is anorher way of stating these two normal motion principles. In the neutral mechanical range for the sagittal plane (where multiple plane motion is predominately directed by the vertebral bodies and discs), side-bending and then roration oc cur [0 opposite sides in a group of vertebrae, o r rotation occurs [Oward the convexity of the curve. This is type I motion and is expected [0 occur in a group of vertebral units because of the j oint facings, as well as the construction and ligamen[Ous attach ments of the lumbar vertebrae. In the lumbar region, this type of multiple plane motion occurs through a greater arc of extension than flexion. If the lumbar sagittal plane is in a mechanical range where flexion or extension is suffi cient [0 engage the facets as the prime movers of the spine, multiple plane motion will result in rotation and then side-bending occurring [0 the same side. This can also be stated as rotation in[O the concavity of the intended side-bending, and is type I I motion or type I I mechanics. Positioning in the sagittal plane that is sufficient ro induce type I I mechanics with m ultiple plane motion is usually localized in a single vertebral unit. After type II motion occurs in that one vertebral unit, the other vertebral units involved in the group side-bending curve normally move according [0 type I mechanics. Neutral, type I, and non-neutral, type I I , motions are a usual and normal biomechanical occurrence during the performance of daily activities. When an activity is over, the spinal units that are free of somatic dysfunction will return [0 their neutral, resting positions. I f motion is tested, they will exhibit ease of motion in all of their usual planes of motion. AJthough the l umbar spine can normally flex about 40 de grees and extend about 30 degrees, non-neutral, type I I motion is more likely [0 occur in the lumbar and thoracic spine when the spine is in a straightened configuration. Therefore, non-neutral mechanics with type II motion for the lumbar spinal region are more likely [0 occur when the l u mbar spine is flexed. However, it is possible [0 produce type I I morion with extreme lumbar hy perextension, as might occur when a high diver enters the water, when a gymnast does a back walkover, or when a painter stands on a ladder and reaches up [0 paint a high ceiling. Somatic Dysfunction

Somatic dysfunction occurs when, for some reason, the spine does not rerurn to its usual resting, neutral position after an ac tivity is completed. This restriction is found ro be within the joint's normal range of motion. Most somatic dysfunction in volves restrictions of the minor gliding motions of a j oint, which then restricrs the major range of motion in one direction around an axis. The restriction usually occurs during the routine activi ties of daily living when, for some reason, the biomechanical or physiologic spinal motions do not return [0 their normal resting position. It is especially likely when m uscles have been p reviously fatigued or stressed by thermal, biophysiologic, or biomechani-

cal stress, such as overuse, chilling, postural strain, psychological stress, or excessive load. Therefore, neutral or non-neutral somatic dysfunction of the lumbar spine can develop depending on the position of the sagit tal plane when the j oint motion became restricted. Somatic dys function is found by identifying tenderness, asymmetry, range of motion differences, and tissue texture changes (TART char acteristics) ( 1 2) during motion testing of a spinal region or its verrebral units. When the patient is tested, the lumbar units with somatic dysfunction will exhibit the motion preference that was maintained when the dysfunction occurred (even if the patient is prone, sitting, or supine and in a "neutral" position). The patient will also simultaneously exhibit motion restriction in the oppo site direction of the motion permitted. For this reason, when a physician finds a somatic dysfunction, he or she can reasonably conclude what motion the person was performing at the time the somatic dysfunction was initiated. Ana[Omic variations, physiologic conditions, trauma, and so on may alter the "usual" motion patterns described above. There fore, the specific diagnosis for indicated treatment depends on testing the site of the dysfunction, as it may not always follow the expected patterns of motion. Nore that the typical vertebral units of the spine can also have a somatic dysfunction that only involves a single plane (flex ion or extension). AJso, if motion is found [0 be restricted in both directions and in multiple planes, the patient's joint may be demonstrating a "capsular pattern" of barriers. Capsular patterns are seen in pathologic conditions, such as arrhritis, and warrant further diagnosis and treatment beyond the manipulative treat ment of simple somatic dysfunction (see also Chapter 53, Lower Extremity). In capsular patterns, the restrictive barriers of joint motion have less resilience and a definite, firm end-feel. For the initial musculoskeletal examination on a hospitalized patient, the physician need only look for and document regional tissue texture change, and/or asymmetry of tissues, and/or re striction of motion, and/or tenderness (TART), and the name of the spinal region in which any of these were palpated. (See Chapter 7 1, Treatment of the Acutely III Hospital Patient, Fig. 7 1. 1. ) Specific segmental diagnosis is not necessary in this initial hospital patient encounter unless a specific manipulative treatment is [0 be given right at that time. However, segmental di agnosis of a spinal region or other regions of somatic dysfunction m ust be performed, each time, before a manipulative treatment for the somatic dysfunction is administered. Writing a somatic dysfunction formula without an additional qualifier assumes that the formula is a statement of the preference for motion of the vertebral unit(s). To indicate that the formula describes the restrictions of motion, the physician must precede the written formula using the word, "restricted." Examples:

Ll -4 SL RR (also L l -4 N SL RR) or L l -4 restricted SR RL (motion p resent and then motion restricted) L5 F RR SR or L5 restricted E RL SL (motion present and then m otion restricted) I

1

When the somatic dysfunction is type I, rhe sagittal plane does nor have ro

be determined, bur if rhe somatic dysfunction is type I I , the sagittal plane

preference for Aexion or exrension must be derermined and indicared.

50. Lumbar Region

These formulae are not appropriate for recording capsular patterns. The above formulas should be reserved for describing somatic dysfunction.

EXAMINATION History Consideration of the onset, duration, and p rogression of a com plaint is essential. An inventory by systems is taken, especially those systems that could be related to the lumbar complaints. Al though the history is discussed as an entity that precedes the phys ical examination, further questioning (history) may take place as positive clues obtained from the history are combined with func tional anatomic knowledge and considerations. This approach to history will prompt the physician to ask questions about areas that the patient does not consider important enough to mention initially, and it yields an organized, total etiologic list of condi tions to be considered by the physician in his or her differential diagnosis of the complaints. For example, if a patient complains of lumbar dysfunction, questions about bowel and bladder func tion, whether the urinary stream is ful l and forceful, and whether there is any pain or burning on urination are all functionally rel evant questions to ask. During the physical examination, if the patient complains of acute tenderness when the iliotibial bands are palpated, questions about bowel habits and function are rel evant. In women, these findings should also initiate questions about menses and pelvic discomfort; in men, questions about prostate or penile discomfort, or deep, unc-omfortable pressure in the perineal region are indicated. Asking if chilling or muscle stressing activities increase the symptom might alert the physician to consider and examine for select myofascial trigger points re lated to the symptomatology. When planning total management of patients with lumbar complaints, it is also important to ask the patient about past "prat falls" or accidents that could have produced a unilateral sacral Aexion or an up-slipped innominate (shears), upset spinal me chanics, or affected the craniosacral mechanism. Most patients forget about these types of accidents because they think, " I d idn't break anything when I fell, I recovered, and therefore, it is not i mportant and could not be related to my problems." Or they think, "I almost fell but I caught myself, so that couldn't have stressed my body-it was not an accident." Ask the patient about choking feelings (thyroid) and breast changes or masses (breast tumors). These questions explore the possibility of cancer of the organs that usually metastasize to bone and can produce pain in the back. Other positive answers during a history provide clues requiring a differential diagnosis: chilling (myofascial triggers?), frequency and burning (infection of the genitourinary tract?), blood in the stool and/or changes in bowel habit or function (colon dysfunction or cancer?), prat falls (non-physiologic shear somatic dysfunction and/or somatic dysfunction in the cranial field?), and so on.

739

ter, only the more common points related to a patient with lumbar complaints are described. Ifthe patient has leg pain or paresthesia, ask the patien t to show exactly where it is located, and then decide if this could represent a dermatomal, myotomal, sclerotomal or radicular pain pattern. Sclerotomes and myotomes have been documented and mapped. They are i mportant and are often overlooked pain patterns (see Dermatomes, Myotomes, and Sclerotomes in this chapter and Chapter 53, Lower Extremity, Fig. 53.30). A radicular pattern would indicate that there may be nerve root pressure, perhaps related to a herniated intervertebral disc or a tumor in the cauda equina. In this particular case, traditional orthopedic and neu rologic testing, which includes deep tendon reflex assessment, assessment of muscle strength/weakness, and testing key der matomes for sensation and/or pain are important. The physical examination is extremely i mportant in formulating a differential diagnosis. Observation

What is the patient's appearance? Observation of posture and activity often provide the first clue to dysfunction. Posture mimics a patient's inner self more than their complaints or responses to direct questioning. An example would be the slumped posture of a depressed patient. Is there asymmetry of a region of the body when the whole body is observed? Clues to lumbar dysfunction may be indi cated by observing the spacing difference between the arms and the hip/waist on each side of the body ( Fig. 50. 1 7) . This sign may indicate the presence of scoliosis, strain fro m sacral base

Space here Little space here Hand and arm close to the body

Physical Examination A complete physical examination is performed, with special em phasis on regions that are spotlighted by the history or that have functional association with the symptomatic region. In this chap-

FIGURE 50. 1 7. The space around the patient provides clues to postural i m balances, such as scoliosis, u n level sacral base, and so on.

740

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unleveling, or a unilateral m uscle spasm. Could there be sacral base unleveling? If the patient likes to stand in a forward-bent position, consider bilateral psoas muscle spasm of mechanical or visceral etiology, or a condition that is putting pressure on lumbar nerves in the intervertebral foramen. If the patient is leaning forward, to one side, and has the ipsilateral foot everted when standing or walking, consider a unilateral psoas spasm. I f this develops into a full psoas syndrome o n one side, the pa tient may also complain of pain in the contralateral hip and leg, rarely past the knee (see Clinical Examples: Psoas Syndrome and Fig. 50.25). When a patient stands very erect and dislikes bend ing forward, he or she may be protecting a herniated disc or be suffering the effects of spinal stenosis, especially if there are other symptoms, such as muscular weakness, reflex changes, or m uscle atrophy.

over o�er

R

11 " 2" up Adrenal � from umbilicus)

R

K i d ney

\

U reth ra

R

�

ureter

ll "

�

1 " up)

U ri nary blad der (umbi l i c us )

Ovary

Intestinal

( + urethra a nd a bd . )

R Colon

Auscultation

Auscultate the four quadrants of the abdomen to determine the presence, location, frequency, and pitch of peristaltic waves. An interm ittent, low, occasional slow gurgle is normal. Conversely, high-pitched tinkling sounds may denote a developing bowel ob struction. Absence of bowel sounds may indicate a paralytic ileus. A bruit in the midline of the abdomen between the xiphoid pro cess and the umbilicus could indicate renal stenosis or abdominal aortic aneurysm (especially when associated with a pulsating ab dominal mass). A bruit at the j unction between the m iddle and oLlter two-thirds of the inguinal region could indicate a signifi cant atherosclerosis of the common iliac or femoral artery. A bruit over the umbilical region could indicate a saddle thrombosis or severe atherosclerosis at the bifurcation of the abdominal aorta. Other physical examination tests for the abdomen of a patient are covered in other chapters (see Chapter 5 1 and Chapter 7 1 ) .

R

Broad l i g .

or Prost ate

FIGURE 50.18. These Chapman poi nts i n the anterior abdom inal wa l l around the u m b i l icus, around the pelvis, andlor i n t h e i l i otibial bands may provide non-i nvasive clues to visceral irritation or dysfu nction that can produce symptoms i n the l u mbar region of the body.

pulse of the popliteal, posterior tibial, and dorsal pedis arteries in that leg and compare them with the pulses of the opposite leg.

Palpation and Motion Testing

Anterior Chapman points related to organs associated with symp toms in the lumbar region ( F ig. 50. I S) are located around the umbi licus, the pelvis, and in the iliotibial bands. Tender points in these locations may be associated with hypersympathetic activ i ty resulting from viscerosomatic reflexes initiated in an irritated colon or pelvic organ, and the physician should question the patient regarding dysfunction of the organ most likely ro be as sociated with that particular tender point (see Chapters 5 1 , 66, and 67) . A positive response to specific questioning helps posi tion a somatic clue according to its significance and rank when considering a differential diagnosis. The abdomen is also palpated for masses. Palpation is aided by mental visualization of the liver, kidneys, stomach, small in testines, bifurcation of the aorta at the level of the umbil icus, and the colon (Fig. 50. 1 9) . The midline region between the xiphoid and umbilicus should be palpated for any pulsating tumor (abdominal aneurysm). An teriorly occurring pulsations are normal, but lateral pulsations of the aorta suggest an aneurysm , especially ifit is widened greater than 1 inch (a normal adult abdominal aorta should not be wider than 1 inch) . Palpate the inguinal area, evaluating and comparing the right and left femoral pulses. If a decreased pulse is found on one or both sides, ask the patient about claudication. Palpate the

Neurologic Testing and Muscle Strength

For an excellent summary on neurologic testing and muscle strength, see Table 50.5 and Table 50.6. For the standard method of recording reflexes, see Chapter 47, Table 47.9. For the stan dard method of recording muscular strength, see Chapter 47, Table 47. 1 0.

Specific Tests Testing the Abdominal Diaphragm

For additional information on testing the abdominal diaphragm, see Chapter 6S, The Lymphatic System: Lymphatic Manipulative Techniques. This test is for the diagnosis of abdominal diaphrag matic dysfunction, or testing for evidence of flattening of the dome of the diaphragm. Position: The patient is supine, and the physician stands beside the patient's hips with his or her dominant hand nearest the patient's feet. 1 . The physician grasps the lateral sides of the patient's lower rib cage and tests for right and left rotational preference of the deep fasciae. Freedom of rotation in both directions is a negative test (i.e., no somatic dysfunction is present).

50. Lumbar Region

741

TABLE 50.6. T ESTS FOR EVALUATING LUMBAR INNERVA TION USING MUSCULAR STRENGTH

Muscle Innervations and Strength Quadriceps and anterior tibialis Extensor d i gitorum longus, brevis, and h a l l ucis longus "Wa l k on your heels." Gastrocnemi us/so leus and intrinsic foot muscles "Wa l k on you r toes."

Right lumbar region

Left lumbar region

Right iliac region

Left iliac region

ASIS Pubes

Comments I n nervation predominately L4 I n n e rvation predomi nately LS Tests strength of LS I n nervation predominately 51 Tests strength of 5 1

2 . The patient is i nstructed ro, "Take a deep breath in and out." At this point, i f the patient has a Aarrened diaphragm, move ment can be detected on only one side of the thoracoabdom i nal region. The physician adds thoracolumbar side-bending roward h imself or herself, carrying it ro its restrictive barrier by pulling his or her caudad hand contact roward, and his or her cephalad contact away. At the same time, the physician continues ro adjust rotation ro its restrictive barrier. At that point, it will be sensed that both sides of the thoracolumbar region begin ro move with inhalation.

3. The physician holds the thoracolumbar region i n that position FIGURE 50. 1 9. The approximate location of major abdominal viscera. Knowing the approximate locations helps a physician better interpret abdominal palpatory findi ngs.

2. Ifrotarional preference is present, side-b ending preference will also be presen t and usually ro the same side. Side-bending and rotational preference at the thoracolumbar junction indicates that diaphragmatic funcrion is compromised, and its "dome" is probably Aarrened, in the resting position, on one or both sides.

Abdominal Diaphragmatic Re-doming

For more information on re-doming techniques, see Chapter 68, The Lymphatic System: Lymphatic Manipulative Techniques. Direct or indirect methods of manipulative treatment may be used. Direct myofascial, muscle energy treatment ro re-dome the abdominal diaphragm: Position: The patient is supine and the physician stands beside the patient's hips with his or her dominant hand nearest ro the patient's feet. 1. The physician holds the patient's myofascial tissues of the thoracolumbar region i n the direction of its restriction for rotation. TABLE 50.5. REFLEXES FOR EVALUATING THE LUMBAR REGION

Reflexes Patel lar Ach i l les Cremasteric

Comments

L4 nerve root. 51 nerve root. L 1 and L2. Usua l l y tested only if specific history or physical findi ngs ind icate possible i nvolvement.

as the patient is instructed ro take three or four deep inhalations and exhalations. With this positioning and the patient's respirarory efforts, the diaphragm re-domes itself.

4. The physician retLlrns the thoracolumbar region to a neutral position and rechecks movemeJ1( of that region as the patient takes a deep breath i n and out (also see Chapter 68, The Lymphatic System: Lymphatic Manipulative Tech n iques) .

Hip Drop Test

For additional i n formation on the hip drop test, see Figure 50.20 and Chapter 44, Musculoskeletal Examination, Figure 44. 1 1 . Negative test: The iliac crest o n the unsupported side drops 20 ro 25 degrees, and there is a smooth lumbar curvature roward the weigh t bearing side of the body. Positive test: The iliac crest does not drop 20 ro 25 degrees on the non-weight-bearing side, and there is an angled, uneven, or poor lumbar spinal curve roward the weight-bearing side. A pos itive test indicates that the l umbar andlor thoracolumbar spine has difficulty side-bending roward the weight-bear i ng side of the body (i.e., the side opposite the positive test). Because rotation and side-bending are linked motions, the physician may elect ro screen the lumbar spine using only the segmental rotational test or the hip drop test. Nei ther test is as sensi tive as segmeJ1(al palpation, but when properly performed, a positive finding on either test identifies a need for segmental diagnosis of the lumbar spine. Thoracolumbar Rotation Screen

See Chapter 44, Musculoskeletal Examination, and Table 44.3, ro read about the trunk rotation test. Negative test: Normal rotation is equal motion in both directions-about 90 degrees in both directions. Positive test: Failure ro rotate as far i n one direction as in the other or a qualitatively different end-feel ro each barrier. This

742

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In the thoracic region, a positive compression test is more often associated with finding type I somatic dysfunction in a group of vertebral units, because the thoracic spine can flex more easily rhan it can extend. A group of thoracic, type I somatic dysfunction that resists extension and is flexed will have a positive anterior compression test. Negative test: If the thoracic or lumbar spine does not resist anterior compression, the test is considered to be a negative com pression test. Yet this lumbar spine could still have type I somatic dysfunction. Now if there were a type I I , lumbar non-neutral dys function, the physician may not catch the resistance of this one vertebral unit in five and report a false negative compression test. For this reason, testing for rotational preference of each lumbar vertebra is more time-efficient and will help clarify this possible confusion (see Lumbar Rotation Screen, below). Spinal Lumbosacral Spring Test

wok FIGURE 50.20. A negative left h i p drop test.

suggests a problem that is restricting rotation somewhere in the lumbar spine, especially at the thoracolumbar j unction. Anterior Spinal Compression (Spring) Test

Table 44. 1, Compression Test, in Chapter 44, Musculoskeletal Examination, provides further information about this test. It is a screening examination to determine the ability of the thoracic or lumbar spine to extend. Position: The patient is prone and the physician stands beside the table near the patient's hips. Procedure: The physician intermittently applies anterior p res sure over the spine of the thoracic and lumbar regions of the body. Positive test: Compression is resisted (end-feel is abrupt). This means that the thoracic or lumbar spine will not extend and is flexed. Note that the lumbar spine can normally extend through more degrees than it can flex and still be in the neutral sagit tal plane range of multiple-plane l umbar motion (Fig. 50. 16) . I f the anterior compression test is positive, t h e vertebral u n i t resists extension and probably prefers to flex. Multiple-plane lumbar somatic dysfunction of a vertebral unit with a preference for flex ion is more likely to be symptomatic and to be associated with type II somatic dysfunction in a single vertebral unit. Therefore, if a lumbar compression test is positive, the vertebral unit(s) must be segmentally tested for rotation and side-bending. If a type I I somatic dysfunction involves the L 1 or L2 vertebral unit, there is also the probability that it may be associated with visceral dysfunc tion of the descending colon or a pelvic o rgan; alternately, it may be associated with a psoas syndrome. Testing for the rotational preference of each vertebra is a more efficient way ofscreening the lumbar spine, because it identifies asymmetry in rotation, which can then be correlated with segmental side-bending to provide a specific diagnosis of somatic dysfunction.

This test is a part of some physicians' tests for segmental sacral diagnosis. It is easily confused with the anterior spinal compres sion test, because some physicians (and instructors) say that they "spring" the vertebral column anteriorly when referring to the an terior compression test. Results are used to help diagnose sacral somatic dysfunction and are interpreted in relationship to find ings from segmental testing of the sacrum. Position: The patient is prone, someti mes resting on his or her elbows, and the physician stands to one side near the patient's pelvis. Procedure:

1 . The physician places his or her caudad hand over the lum bosacral region and reinforces it with the palm of the cephalad hand. 2. Repeated anterior and slightly cephalad pressure is appl ied to this region of the spine. Positive test: If no spring to this region of the lumbar spine is found, it is believed to be due to posterior motion of the sacral base, which locks the lumbar spine. Negative test: This is believed to be normal for the lumbar spine or associated with somatic dysfunction of the sacrum, where segmental tests indicate the base has moved anteriorly.

Lumbar Rotation Screen

Additional information on this topic can be found in Chapter 44, Musculoskeletal Examination, Segmental Motion Testing, Passive Lumbar Segmental Motion Testing. Note that if rotational preference of a lumbar vertebra is found in one direcrion wirh restricrion in rotation in the opposite direction, side-bending preference will also be present and must be tested. If preferences for side-bending and rotation occur to the same side, then flexion or extension must also be tested to de termined p reference for sagittal plane motion in those segments. Rotation testing of each of the five lumbar vertebrae is the most accurate and time-efficient method of screening for lumbar so matic dysfunction, because the transverse processes are directly lateral to the spinous process of the lumbar vertebra being tested. The rotational screen also begins segmental lumbar testing.

50. Lumbar Region

FIGURE 50.2 1 . The Thomas test for finding i l iopsoas spasm or contracture.

Paraspinal Palpation for Tissue Texture Changes

See Chapter 44, Musculoskeletal Exam i nation, Palpation for Tis sue Texture Abnormalities and Tenderness and Figures 44. 17. Positive test: Tissue texture asymmetry is palpated. Vertebral units with palpable tissue texture abnormaliry have segmental somatic dysfunction. I f found at the Ll or L2 level, then viscero somatic reflexes from irritation of a kidney, the descending colon, or pelvic organs ( T I O-L2) must also be considered.

743

If Chapm an myofascial tender points for the lumbar region are evaluated ( Fig. 50. 1 8) , palpate for them at the beginning of the physical examination, because motion and repeated palpa tion or stretching of the myofascial tissues in their location will decrease their sensitiviry and diagnostic value; their tenderness to palpation will disappear, at least for a period of time. Chapman points found around the umbilicus may be related ro the blad der, k idney, or adrenal glands. Those over the pubic symphysis may be related ro gonadal tissue. Posterior Chapman points to the large intestine lie in a triangular area on either side of the lower l umbar spine. I f large bowel problems are suspected, do not give lumbar soft tissue treatment until you have palpated the an terior points related to the colon (found in the i liotibial bands) to secure data that would help confirm this suspicion. Chapm an points should be carefully correlated with hisrory, palpation, ten derness of the collateral abdominal ganglia, and spinal somatic dysfunction, as well as with the palpation of the suspected or gan system ro determine the ranking, significance, and value of the tender point in the differential d iagnosis (see Chapter 5 1 , Abdominal Region) . Chapman reflexes are one of the early diag nostic clues ro irritation and dysfunction of viscera.

Thomas Test for Psoas Shortening

Figure 50.2 1 shows this test. Psoas shortening can be acute, chronic, or subacute. (See also Chapter 53, Lower Extremities.) Patiems are tested in the supine position. Positive test: I f the iliopsoas muscle is shortened, the lower extremiry on that side will be unable .to fully extend at the hip (i.e., the thigh and popliteal region do not lie flat on the table). Psoas Test Variations

TREATME NT: LUMBAR SOMATIC DYSFU NCTION Specific manipulative treatment methods and activating forces used to treat somatic dysfunction in any region of the body are found in the differem palpatory diagnosis and treatment chapters of this book. The indications and goals of osteopathic manipu lative treatmem of the total patient include: Treat the patiem according to that patiem's physiologic needs. Reduce or remove symptoms and spinal cord facilitation due to

The patiem may also be tested in the prone or lateral recumbem position. Though a patiem with chronic or subacute shortening of the psoas muscle can usually lie prone, the patient with acute psoas spasm or shortening cannot usually lie p rone flat on the table. In this case, the physician can have the patient turn to the lateral recumbent position and attempt to extend the leg at the hip. Positive test: It is not comfortable for the leg to be in the fully extended position. When the psoas is involved, the patient becomes especially uncomfortable when anterior thigh extension is attempted. If the extension of the thigh produces pain in the posterior sacroiliac joint, also consider dysfunction of the hip or sacroiliac joint on that side.

primary somatic dysfunction. Reduce or remove facilitated spinal cord segments due ro sec ondary somatic dysfunction. Support the body's homeostatic mechanisms during natural stresses (e.g., pregnancy) and illness, preoperatively, and after posroperative complications. Support the body's i mmune system. Provide comprehensive and efficient rotal body treatment. Comfort the patient and help alleviate anxiery during the workup for conditions that may primarily require medical/ surgical treatment. Enhance other medical or surgical treatments. Prevent the likelihood of reoccurrence of the dysfunction.

Tender Points and Trigger Points Relating to the

Clinical Examples: Treatment for " Back Pain"

Lumbar Region

The multifidi next to the spines, the quadratus lumborum m uscle, and/or the gluteus medius attachments to the lateral i liac crest may contain Travell tender points (Fig. 50. 1 1 ) , which can refer pain to the lumbar region. Tender poims for the iliopsoas m uscle are located approximately 1 inch medial ro each anterior superior iliac spine (ASIS) on the anterior side of the body. An i l iopsoas tender point is deep in the abdomen, not on the posterior wall and not in the superficial abdominal wall.

Treatment for Medical/Surgical Etiologies

Any physician who is adept at finding and treating somatic dys function should remember that approximately 1 0% of patiems complaining of back pain will primary have a medical or surgi cal etiology for their complaint. Medical/surgical conditions that refer pain to the lumbar region include: Two surgical emergencies: dissecting abdominal aneurysm and cauda equina syndrome ( 1 4)

744

VII.


Secondary (medical) somatic dysfunction: kidney dysfunc tion, ureteral obstruction, irritation of the left colon , and prostate or bladder irritation Primary cancers that metastasize to bone (most common in patients over 5 0 years of age): thyroid, breast, lung, kidney and prostate

Abdominal Aneurysm

Both anatomic relationships and a good history help more accu rately determine the cause of a patient's complaints. For example, an older, hypertensive patient complaining of severe back pain , numbness of t h e lower extremities, a n d a bruit over the abdomi nal aorta (with or without a palpable abdo minal mass) could have either an abdom inal aneurysm or renal artery stenosis. The ab dominal aorta divides into the common iliac arteries at the level of the umbilicus. The umbilicus is located anterior to and in a hori zontal plane running through the L3-4 disc space. Bruits fro m an abdominal aortic aneurysm are often identified by auscultation near or anterior to the umbilicus. The sudden onset of severe, tearing abdominal pain that radiates through to the back and is associated with palpation of an abdominal mass and the aus cultation of a bruit most likely i ndicates a dissecting abdominal aneurysm. A dissecting abdominal aneurysm is a surgical emer gency; surgical consultation should be i mmediately obtained. A bruit from renal artery stenosis is also auscultated at the midline but higher in the epigastric region, and the abdominal aorta is not enlarged. Any ventral abdominal osteopathic techniques or thrust ac tivations for manipulative treatment of the thoracic, lumbar, or sacral regions should be avoided in these patients. If somatic dys function is present and located in the midcervical region, thoracic inlet, or the abdominal diaphragm, it should be treated using gen tle, indirect methods (if necessary) . Gentle paraspinal inhibition with the patient in the supine position is indicated (or may be tolerated) in nonemergent cases to prepare the patient for s urgery.

Cauda Equina Syndrome

The typical patient with this problem complains of backache and paralysis that begins in the feet and progresses upward. I f asked, h e or she will usually give a history of bladder and/or anal sphincter weakness, because the sphincters are often involved early. Paralysis may develop slowly or occur very rapidly (pro gressing to complete paralysis of the lower extremities within an hour) . Therefore, i mmediate surgical consultation and timely emergency surgical decompression of the nerves is mandatory if full use of the lower extremities is to be achieved. Although surgery is able to completely decompress the nerves, if surgery is delayed too long, motor function of the lower extremities and/or sphincters may never return. Osteopathic manipulative treatment is defin itely secondary to i mmediate surgical care for patients with surgical emergencies, but it is definitely indicated i n the postoperative period, where ii: supports abdominal diaphragmatic function, improvement of lymphatic drainage, and the reduction of postoperative sympa thicotonia of the GI tract (which could progress to paralytic ileus) .

Others

These include uterine spasm or irritation, renal calculi, and or thopedic problems (see Chapter 5 1 , Abdominal Region, and Chapter 52, Pelvis and Sacrum) . When exami ning a patient with low back pain, orthopedic problems must be ruled out. Orthopedists divide the vertebra into three parts to help with the differential diagnosis and treatment considerations-a posterior element, a middle element, and an anterior element (Fig. 50.22). Scott states that Gunnar Anderson does not consider the in tervertebral disc with the middle elements, i nstead placing it with the anterior elements. I n this classification, only the spinal cord and spinal canal remain with the middle elements. In his Orthopedics chapter in the first edition of Foundations for Osteopathic Medicine, Scott mentions the etiologies for back pain (Table 28. 1 ) . Somatic dysfunction of the first two lumbar vertebral units may also be related to viscerosomatic reflexes from left colon or pelvic organ irritation, especially if they are diagnosed as exhibit ing a non-neutral mechanical preference. L 1 and L2 are the only lumbar nerves with white rami that carry sympathetic efferent neurons, the neurons that carry outgoing sympathetic messages. It is possible that somatic dysfunction of either, or both, of these twO vertebral units is a secondary result of viscerosomatic re flexes fro m primary dysfunction irritating the left colon, pelvic splanchnic nerves, or pelvic organs. In these conditions, nocicep tive impulses are transmitted up through the paraspinal sympa thetic chain ganglia to the T 1 2-L2 spinal cord levels. Here, they facilitate the T 1 2-L2 cord segments. Then, through "cross-talk" in the spinal cord with somatic motor nerves in the dorsal horn of the T 1 2-L2 segments, secondary somatic dysfunction develops in the joints and tissues associated with T 1 2-L2 somatic inner vation. The upper lumbar region may also be painful and exhibit somatic dysfunction as a result of primary problems in an organ innervated by parasympathetic sacral nerves, 52-4. For example, although pain fibers fro m the cervix of the uterus refer to the pelvic splanchnic nerve centers (52, 53, and 54), pain fibers from an irritation of the fundus of the uterus refer to the upper lumbar region (see Chapter 5 1 , Abdominal Region). Treatment of Non-MedicaIINon-Surgical Etiologies

The same caution that was given to the physician "specializing" in osteopathic manipulative medicine must be given to an internist or surgeon , but worded differently: "Not all back pai n is due to medical or surgical problems." In fact, most are not. Ni nety percent of patients with back pain have conditions that do not require surgery or primary medical care. Most conditions are due to mechanical dysfunction of the posterior elements of a vertebra (Fig. 50.22) or other distant and/or nonarticular somatic structures functionally related to the lumbar spine, including shoulder dysfunction fro m lumbosacral somatic dysfunction via the latissimus dorsi muscle, and dermatome, myotome, or sclero tome pain referred to the lower extrem ity (see Chapter 53, Lower Extremities, Fig. 53 .30) . It also includes patients with primary somatic dysfunction, strains, sprains, postural decompensation, or overuse syndromes, and patients with hypermobility. Most will have a primary diagnosis of somatic dysfunction and/or pos tural decompensation. Sometimes the decompensation is due to

50. Lumbar Region

745

FIGURE 50.22. Vertebral divisions that h e l p a physician consider possible etiologies for back pain. The vertebra is d ivided into the posterior bony elements, the middle meningeal and neu rologic elements, and the vertebral body and disc (Table 50.7).

TABLE SO.7. POSTERIOR. MIDDLE. AND ANTERIOR SPINAL ELEMENTS RELATED T O BACK PAIN

Elements Posterior Elements-most common Spinous process, tra nsverse processes, lam ina, pedicles, l i gaments and joint capsule, intervertebral joints

Middle Elements Central spinal canal, meninges, spinal cord and nerves

Anterior Elements Posterior longitud i n a l l igament, vertebral body, a nterior longitu d i n a l l igament, and i ntervertebral disk

Possible Etiologies

Somatic dysfunction-TART" Espec i a l ly the " h a lf-dirty dozen" ( 1 5) Age-related and activity-related stra ins-arthritis, overuse Severe or chronic twists Stra ins and spra i ns Spondylosis, overuse, or chronic trauma Spondylol isthesis Severe tra uma and twists Fractures of pedicle, transverse process, or spinous processb Compression of the spinal canal or nerve root Cauda equina syndromeb I ntrinsic I ntradural tumors Meni ngeal infections Extrinsic pressure through foramen and/or the thecal sac Metastatic tumors R u ptured disc with contents free i n spinal canal Neurofibromas Spurs or other symptoms, of aging or degenerative cond itions (osteoarthritis) Benign tumors or fibromas Reflex etiolog ies-visceral dysfunctions and d isease Compression fractures of the vertebral body Vascular causes-a bdom i n a l aneurysmb Traumatic disc d isruption with pressure on nerve root or thecal sac I nfection

aGlossary of osteopathic terminology. AOA Yearbook and Directory. 9 1 st ed, Chicago, 2000:869. b Surgical emergency.

IL:

American Osteopathic Association;

746

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chronic, unrreared somaric dysfuncrion. Somerimes rhe primary eriology arises from an u nlevel sacral base, which is usually asymp romaric unless lerr und iagnosed and unrreared for a sign ificanr lengrh of rime (perhaps years) . Over rime, rhe parienr usually be gins ro complain of localized d iscomforr or pain broughr abour by com pensarory changes rhar are acrually locared cephalad from rhe unlevel sacral base (see Chaprer 44, Posrural Considerarion in rhe Sagirral, Coronal, and Horizonral Planes) . Dirty Half- Dozen

Th is designarion was coined by Phil Greenman ( 1 5) for a c1usrer of somaric findi ngs rhat ofren underlie the complainrs of pa rienrs who have been diagnosed wirh "failed low back syndrome" ( Fig. 50.23). This dysfuncrion includes: Non-neurral lumbar somatic dysfuncrion. Dysfu ncrion of the symphysis pubis (pubic shear) . Restricrion of the anrerior movemenr of the sacral base. This could be eirher a posrerior sacral base or a posrerior back ward rorsion (non-neutral sacral rorarion on an oblique sacral axis) . I n nom inare shear dysfu ncrion. A shorr leg and pelvic rilr syndrome. Muscular im balance of rhe rrunk and lower exrremity (includ ing psoas syndrome) . Over years of pracrice, many parienrs rhar were referred ro me for "failed low back syndrome" were ofren found ro have a unilareral sacral Aexion (sacral shear) rhar had been overlooked. I n nominare shears or sacral shears may be asym promatic ar rheir sire, bur evenrually resulr i n secondary subjective symproms in rhe parienr's lumbar, upper rib, cervical, suboccipiral, o r cranial regions. These are regions of i ncreased srress broughr abour by rhe body's arrem pr ro compensare for rhe persistenr dysfuncrion and rhe pelvic base. Because shears are non-physiologic, rhe body is ofren unable ro remove them wirhour ourside specifi c rrear-

menr; so ir tries ro compensare for thei r presence. A pelvic shear may even preven r successful mani pularive rrearmenr of orher so maric dysfuncrion. The presence of a shear is also associared with the contin uance or rerurn of symproms shorrly afrer orher di agnosed somaric dysfunction has been successfully rreared and removed. When a parient complai ns of pelvic symproms wirh persisrenr and/or recurrenr "usual" sacroiliac somatic dysfunc rion (regardless of receiving "effecrive" manipularive rrearment) , look for other dysfuncrion rhat refers pain ro rhe lumbosacral region, including mechanical, surgical, and/or medical. Iliolumbar Ligament Syndrome

The back pain experienced by a parienr with iliolumbar ligamenr syndrome is locared in rhe sacroiliac, posrerior rhigh, and/or in guinal regions (Fig. 50.24) . In facr, rhe presenring complaint is orren , "I rhink I have a hernia," and rhen rhe parienr poinrs ro the inguinal region. Check for an inguinal hernia, bur regardless of rhe acrual presence or absence of a hernia, palpate the arrach menr of rhe iliolumbar ligamenrs ro rhe ilia for a render point. If rhe iliolumbar ligamenr is stressed and irri rared, irs render poinr will be on rhe iliac crest, locared o n rhe ipsilareral side of rhe com plainr 1 inch superior and lareral ro the undersling of rhe posterior superior iliac spine (Fig. 50.8). This tender poinr in rhe iliolumbar ligamenr may or may nor refer pai n ro the inguinal region. If rhe parienr has a hernia and a render point in rhe ili olumbar ligament, even successful surgical repair of the hernia, wirhout rreating the eriology for the i l iolumbar ligament syn drome, may leave the parienr with contin ued symproms of "rhe inguinal hernia." . Also remember rhar rhe iliolumbar ligamenr is the first lig ament srressed when there is posrural decompensation. So, if a patienr's i l iolumbar ligament is render ro palparion, also check for an u n level sacral base, scoliosis, shorr leg, and so on, and provide correcrive rrearmenr as i ndicared by your diagnostic findings. I njection of a local anesrheric inro rhe render point located at

Psoas Spasm NN

Lumbar

S u perior I n nominate Shear

v�-'-t--,L... -; -

Sacral Rotation on an Oblique Axis

_ NN

_ _

Sacral Shear

Pu bic Shear (Short Leg)

�

P

+J� \ ------------� \ t{ � (� wak

_ __ __ __ __

FIGURE 50.23. The " D i rty Ha lf-Dozen . " This term, popularized by P h i l G reenman, lists the common mechanical etiologies for somatic dysfu nction in patients with "failed low back syndrome. "

50. Lumbar Region

747

relax or sleep. They are also unable ro sit or stand i n one place for any length of time, and are continually shifting ro fi nd a com fortable position when they have ro sit for a period of time. The patient presentation of the latter has been called "theater cocktail syndrome." Hypermobility may be a relative contraindication for the use of thrust-type activation i n the treatment of somatic dysfunction in that region. Patients with this problem usually respond better ro indirect or gentle and specific m uscle energy procedures, be cause these activations produce less stress on structures that are already over-stretched. A region of hyper mobility may need ro be strengthened with graded exercises or treated with a regi men that i ncludes sclerotherapy. Interestingly, areas of hypermobility often resolve when adjacent areas of hypo mobile somatic dys function are treated. I n those cases, the hypermobility was ap parently compensarory for the adjacent hypomobile region. In any case, primary causes of hypermobility, including postural gravitational strain, overuse phenomena, and so on should be sought and treated. Psoas Syndrome FIGURE 50.24. Referra l pain pattern of a patient with an irritated right i l iolu mbar ligament syndrome (see also Fig. 50.8).

the arrachmenr of the l igamenr ro the ilium will often relieve or reduce the pain while definitive diagnosis and specific treatment for the primary problem i s instituted. Meralgia Paresthetica

"The iliopsoas m uscle is the hidden prankster in the sense that it serves many critically i mportant fu nctions, often causes pain, and is relatively i n accessible" (6) . The psoas muscles are attached ro the vertebral bodies and the anterior surface of the transverse processes of the lumbar vertebra. They pass along the superior border of the true pelvis, are j o ined by the il iacus m uscles, pass over the superior ramus of the pubes, and then rurn posteriorly ro insert on the lesser trochanter of each femur via common tendons ( Fig. 5 0 . 2 5 ) .

This condition may or may not be associated with back pain, but it does involve the lumbar region. The patienr complains of numbness, paresthesia, or hypoesthesia i n a fairly large oval region on the lateral side of the thigh, which can cover any portion of the area from the lateral burrock ro the knee. H isrory usually supplies no apparenr clue for its occurrence. Examination of gait, weight bearing posture, and a radiograph of the back may all be normal. This condition is due ro pressure somewhere along the course of the lateral femoral cutaneous nerve (formed from the L2 and L3 nerve roots) . Th is nerve passes through the psoas major m uscle, runs inferolateral on the iliacus muscle, under (and sometimes through) the i nguinal l igamenr j ust medial ro the A S I S , and then passes inro the thigh. Somatic dysfunction may involve the L2 or L3 vertebral units, the psoas muscle, the i n nominate, or the fasciae of the thigh or i n nominate. Manipulative treatment of any of this somatic dysfunction is indicated, i f present. Sometimes, very constrictive clothing (jeans) or some other external mechanical force will have initiated th is condition. Hypermobility

In some sympromatic "back pain" patients, motion of the l umbar region seems un usually free and easy. This can be especially true with extension motion at the L5 level, and this finding suggests hypermobility from relaxed ligamenrs and contributes ro insta bility of the i nvolved vertebral unit. Patients with stressed low back ligaments often complain of severe back d iscomfort that lasts for minutes ro an hour or more when they first lie down ro

FIGURE 50.25. Ful l-blown left psoas syndrome. The patient is forward bent, leans to the left side, and the left foot is everted. Signs and symp toms include: ( 1 ) the key, non·neutral somatic dysfunction at L 1 or L2 that is side-bent left, (2) marked left psoas muscle spasm, (3) rotation of the sacrum on a left oblique axis (often of the non-neutral type). (4) right pelvic side shift, (5) right p i riformis spasm and myofascial ten der poi nt, and (6) pain i n the right h i p, down the back side of the right leg, but not usua l ly past the knee.

748

VII.

Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment

Psoas syndrome is usually initiated when a person assumes any number of positions that shorren the origin and i nsertion of the psoas m uscle for a signifi cant length of time and then gets up quickly, suddenly lengtheni ng the origin and i nsertion, and attempts to assume normal upright activiry. The initial positions that might bring abour this syndrome i nclude sitting i n a soft easy chair or recli ner, bending over fro m the waist for a long period of time, wotking at a desk, or weedi ng in the garden. Psoas syndrome can also be precipitated by overuse, such as doing sit ups with the lower extremities fully extended. Apparenrly, each of these situations creates a neuromuscular imbalance that results in psoas muscle hypertonici ry. The subsequent formation of somatic dysfunction then affects the psoas muscle and the lumbar spine. Once a patient realizes that he o r she has been in one of these posi tions, the possibiliry of ini tiating a psoas syndrome can usually be avoided i f he or she slowly returns ro a neutral postural pos I tion. The physician m ust be aware that there are organic causes for psoas tension or spasm, and if suspected, these must be ruled out by history and/or physical exam ination and special tests. These include: Femoral bursitis Arthritis of the hip Diverticulosis of the colon Ureteral calculi Prostatitis Cancer of the descending or sigmoid colon Salpingitis The key somatic dysfunction initiating or perpetuating psoas syndrome is believed to be a type I I (non-neutral) somatic dys fu nction (F Rx Sx) usually occurring in the L 1 or L2 vertebral unit, where "x" is the side of side-bending of the somatic dysfunc tion. If this key somatic dysfunction remains, the patien t's symp toms may progress to full-blown psoas syndrome (Fig. 50.25). Symptoms of this syndrome include: The key, non-neutral (rype 1 I ) somatic dysfunction at Ll or L2 Sacral somatic dysfunction on an oblique axis, usually to the side of lumbar side-bending Pelvic shift to the opposite side of the greatest psoas spasm Hypertoniciry of the piriformis muscle that is opposite the side of greatest psoas spasm Sciatic nerve irritation on the side of the piriformis spasm Gluteal muscular and posterior thigh pain that does not go past the knee, on the side of the piriformis muscle spasm Man ipulative treatment is preceded by ruling out psoas in volvement caused by one of the organic etiologies previously listed. EFfective treatment of the "key" somatic dysfunction (usu ally Found at L 1 or L2) is essential for the patient's com fort and For effective, long-lasting effects of manipulative treatment, regardless of the admi nistration of other i ndicated medicines, chemotherapy, radiation, or s u rgery. Removing somatic dysfunc tion, wherever i t occurs in the body, reduces afferent load to the spinal cord From secondary somatic sources and lessens the seg mental activiry of the primary facilitated spi nal cord segments.

This makes the patient more comfortable and supports the body's homeostatic and defense mechan isms, thus hastening recovery. Radiculopathy

Radiculopathy is a general diagnosis that involves several etiologic conditions affecting a nerve root. " Radicular" pain describes pain that fol lows the distribution of a n involved nerve root. Common mechanisms include cond itions that produce pressure (pressure radiculopathy) or i nAam mation (radiculitis) of the nerve root. The lumbar region is a common site for radiculopathies. Multi ple, specific etiologies exist for this condition, and di agnosis can be difficult. Etiologies incl ude a ruptured disc with material from the nucleus pulposus pressing on the nerve root or cord, and pressure exerted by bone tumors, exostoses, spinal stenosis, or irritation from an infection. Radiculopathy is often precipi tated or aggravated by acute somatic dysfunction, espe cially if the intervertebral foramen and/or the spinal cord had al ready been compromised by some chronic process. A ruptured and protruding disc producing pressure on the nerve roOt is oFten the first condition that the physician con siders when a patient presents with pain referred into the lower extremiry. As mentioned in the Functional anatomy section of this chapter, the L4 and L5 discs are at greatest risk for rupture, as they undergo the most lumbar motion and experience signiF icant functional and/or postural stress. Also, the width of the postetior longitudinal ligament at L4 and L5 is only one-half the width it was at L l , producing a posterolateral weakness over the intervertebral disc at each of these sites (Fig. 50.7). Because the pedicles of a lumbar vertebra are located on the superolateral one-third of th� lumbar vertebral body, a lumbar nerve winds around a pedicle and passes through its foramen, before i t passes over the disc of that vertebral unit (Fig. 50.3). It is therefore more common to see the L5 nerve irritated by pressure from a ruptured L4 herniated disc, and the S I nerve root irritated by pressure from a ruptured L5 herniated disc. Remember that it is not a reported "bulging disc" that produces symptoms. It is the sign ificant pressure of a bulging or ruptured disc on a nerve root that is responsible for the patient's complaints, and it is helpful if magnetic resonance i maging indicates this connection at the site of the pressure. Lumbar radiculopathy produces paresthesia in a dermatomal pattern. These are located on the anterior portion of the thigh, leg, and/or foot (Fig. 50. 1 3) . Myotomal distribution also results in decreased or absent deep tendon reAexes, muscle weakness, and atrophy of the muscles associated with the level of the rup tured disc (Figs. 50.26 and 50.27). Sclerotomal pain associated with discogenic disease is referred to the pelvis and over the lower extremiry, as seen in Chapter 53, Lower Extremities, Fig ure 53.30. It also predisposes to trigger points in the involved musculature. I f any one of these three effects is seen (paresthesias, reflex changes, and muscle atrophy) and involve the same nerve root or roots, conservative care with adequate follow-up is indicated. A poor response to conservative treatment indicates that more aggressive care is indicated to prevent permanent weakness or loss ofleg function; a consultation is recommended for these patients. Surgical consultation (orthopedic and/or neurologic) and spe cial tests are indicated if certain conditions are present. These

50. Lumbar Region

81 Tibialis anterior muscle

Conservative care includes reduction of as many of the possi ble contributing facrors as is practical. This may include specific treatment of postural imbalance and somatic dysfunction, ade quate relief of pain , treatment of contributing or primary medical facrors, and reduction of any other mechanical, structural, or psy chological stresses. Anaromically, the contents of the in tervertebral foramen fill only one-third of the cross-section of the foramen, so it seems that the nerve roots should have plenty of room. Remem ber, 90% of low back pain is due ro mechanical causes ( 1 1 ) . Studies have shown that probably only 5 % of patients that actually have ruptured discs require surgery ( 1 4) . Osteopath ic manipulation is effective in i mproving biomechanical function and is a primary treatment for radiculopathy due ro functional causes. Removal of somatic dysfunction may be j ust enough ro make a patient with a ruptured d isc comfortable or asympromatic. Furthermore, re moval of adjacent hypo mobile somatic dysfunction may elimi nate lumbar vertebral units that are exhibiting hyper mobility stress.

Abduct h i p

G l uteus m e d i us muscle

Walk on heel with foot inverted

Physician offers

L4

resistance

Extensor hallucis longus muscle

Extensor digitorum

t

longus and brevis muscles

Patient exe rts effort (strength test)

FIGURE 50.26. Tests for L4 n e rve dysfu nction.

include: ro 8 weeks of conservative care that has not been accompa nied by steady progress roward reversal of and/or resolution of the symproms and signs • Poor clinical response associated with any two or all three of the following: paresthesia, reAex changes, and muscle atrophy • If the symproms i ncrease in intensity despite good ongoing conservative care

749

• G

Walk on heels

FIGURE 50.27. Tests for LS nerve dysfu nction.

750

V!1.

Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment

As a pariem gers older, several i nfirmiries commonly compro mise an imervenebral foramen and disc: Arrhriris Ligamenr hypemophy Disuse arrophy Disc degenerarion M uscle imbalance Inherenr rissue q ualiries Somaric dysfuncrion Man ipularion is also indicared in rhe 1 0% of parienrs wirh medical o r surgical problems. Ir makes rhe parienr more com fonable and normal izes local biophysiologic responses while rhe specific primary care is being adminisrered. Removal of somaric dysfuncrion supporrs rhe body's self-healing mechanisms during recovery from primary medical or surgical condirions. Sympa rheric rone can be reduced, rhe rhoracic inler fascia normal ized, and rhe diaphragm domed, preparing rhe parienr's own sysrems and defenses for a s urgery and/or aiding in posrsurgical or medi cal recovery. Realize rhar mere "physician frusrrarion" from poor resulrs while using some combi narion of conservarive rrearmenr on a parienr wirh back pain is nor, by irself, an i ndicarion for recommending s urgery. Adequare pain reliefis necessary ro prevem reflex m uscle spasm and guarding. Failure ro adequarely comrol pain usually leads ro increased disabiliry and morbidiry, bur care musr be raken nor ro produce dependency or addicrion . Muscle relaxanrs and physical rherapy can be helpful ro rhe pariem's conservarive care. The physician should expecr rhar effecrive conservarive crear menr of a parienr will be accompanied by progressive reducrion of subjecrive and objecrive signs and symproms, and will be associ ared wirh obvious improvemem in rhe parienr. The key ro good resulrs wirh conservarive rrearmenr is ro provide specific forms of acceprable rrearmenr rhar are i ndicared by rhe parhophysiol ogy and funcrional srarus of rhe parienr, ro moniror progress, ro expecr sready improvemem, and ro modify diagnosric pro cedures and rrearmenr and/or ger a consuirarion as ir becomes clin ically indicared. Ir is unreasonable ro expecr a parienr who has been receiving your besr conservarive care for a long rime and who has failed ro make any significanr objecrive and subjecrive change ro suddenly ger bener wirh adminisrrarion of "more of rhe saine."

rhe complai nr bur also rhe funcrional and reciprocal relarionships wirhin rhe resr of rhe body as rhey relare ro rhe lumbar region. This chaprer is nor meanr ro provide comprehensive rrearmenr of all lumbar complain rs, bur ro presenr represenrarive, common exam ples obrained rhrough clinical experience rhar illuscrare how os reoparhic rhinki ng is used in rhe care of parienrs wirh lumbar pain . Despire r h e facr rhar mechanical problems (including somaric dysfuncrion) are responsible for mosr complainrs ofback pai n , rhe physician m usr always consider and be ready ro rrear dysfuncrion in regions rhar have funcrional connecrions ro rhe back. The arrending physician should crear or find an inrernisr or surgeon consulranr who will rrear rhe parienr for any primary medical or surgical problems and emergencies. Do nor feel inferior for asking for consulrarions rhar are needed. The l u mbar region is a frequenr sire of srrain, pain, and dis abiliry. There are many myofascial and neural inrerconnecrions berween rhe lumbar region and orher regions of rhe body. For rhe besr resulrs, rrearmenr offered musr be direcred roward rhe primary cause and nor merely ar rhe symprom of a backache or a back problem.

REFERE NCES I . Deyo RA. Low-back pain. Sci Am. 1 99 8;279:48-53. 2 . Anderson G BJ . Epidemiological fearures of chronic low-back pain (re view). Lancet. 1 999;354 : 5 8 1 -5 8 5 . 3. Taylor V M, Deyo RA , Cherkin DC, et a l . Low-back pain hospital ization: Recent U ni ted States trends and regional variations. Spine 1 994; I 9: I 207- 1 2 I 2. 4 . H ar t L G , Deyo RA, Cherkin DC. Physician office visits for low back pain. Spine. 1 99 5 ;20 : 1 1 - 1 9 . . 5 . Williams PL, Warwick RW, Dyson M , et al. Grays Anatomy, 37th ed. Edinburgh, Scotland: Churchill Livingsrone; 1 989. 6 . Travell J G , Simon D G . Myofoscial Pain and Dysfilflction: Tbe Trigger

Point Manual The Lower Extremities, vol. I I . Baltimore, M D : Williams

& Wilkins; 1 99 2. 7 . Travell J G , Simon D G . Myofoscial Pain and Dysfilflction: The Trigger

Point Manual, vol. I . Baltimore, M D: Williams & Wilkins; 1 999. 8 . Hoppenfeld S, Hutton R. Orthopaedic Neurology, A Diagnostic Guide to

Neurologic Levels. Philadelphia, PA: J B Lippincott Co; 1 977. 9 . Moore KL. Clinical OrientedAnatomy, 2nd ed. Balti more, M D : Williams

& Wi l k i ns; 1 98 5 . 1 0. Warwick R , Peter WL Grays Anatomy, 3 5 th British ed. Philadelphia, PA: WE Saunders; 1 973:222.

I I. Borenstein DJ , Wiesel S W. Low Back Pain. Philadelphia, PA: WE Saunders; 1 989.

CONCLUSIONS

1 2. Glossary of osteopathic terminology. AOA Yearbook and Directory, 9 I St ed. Ch icago, lL: American Osteopathic Association; 2000:869. 1 3. White AA, Panjabi M M . Clinical Biomechanics of the Spine, 2nd ed.

This chaprer presenrs some of rhe unique rhoughr processes used ro evaluare rhe lumbar region and how rhese rhoughr processes can be used ro diagnose and crear parienrs wirh lumbar com plainrs. The physician should consider nor only rhe lumbar sire of

P hi ladelphia, PA: JB Lippincott, 1 990:4 5 . 1 4. Borenstein D G , Wiesel Sw. Low Back Pain: Medical Diagnosis and

Comprehensive Management. Philadelphia, PA: WE Saunders; 1 989. 1 5 . Greenman PE. Principles ofManual Medicine, 2nd ed. Baltimore, M D : Williams & Wilkins; 1 996.

THE ABDOMINAL REGION RAYMOND J. HRUBY

KEY CONCEPTS • • • •

• •

Osteopathic historical perspective on the abdomen The abdominal region defined Functional anatomy Supportive evidence for the use of osteopathic manipulation in the treatment plan for abdominal disorders Osteopathic evaluation of the abdomen Osteopathic manipulative approaches and example techniques for the abdomen

HISTORICAL PERSPECTIVE AND SUPPORTIVE EVIDENCE

Osteopathic manipulative techniques can be used as part of a complete treatmenr approach to abdominal visceral problems. Such techniques have been part of osteopathic practice since the time of Andrew Taylor Still, the founder of osteopathic medicine. One early description of abdominal visceral treatmenr by Still is that of his first case of "flux," or dysentery, in a 4-year-old boy. He describes his examination of the child, noting that the child's back was hot while the abdomen was cold to the touch. In writing abom his treatment, he states: I began at the base of the brain, and thought by pressures and rubbings I could push some of the hot ro the cold places, and in so doing I found rigid and loose places on the muscles and ligamenr5 of the whole spine, while the lumbar was in a very congested condition. I worked for a few minutes on that philosophy, and rold the mother ro report next day, and if I could do anything more for her boy J would cheerfully do so. She came early next morning with the news that her child was well

(1).

Still described having treated many other similar cases with a high degree of success. His knowledge of the structure-function relationships involved with abdominal conditions was extensive enough to warrant an entire chapter of one of his books being devoted ro this ropic (2). Other osteopathic physicians since the time of Still have pro moted the use of osteopathic manipulative techniques directed

toward the abdominal viscera. Hazzard described how to exam ine the abdomen, and discussed treatment approaches for various abdominal visceral diseases (3). Conrad (4) devoted a section of his book ro diseases of the abdomen, specifically diseases of the stomach, intestines, liver, kidneys, and spleen. He described and illustrated specific osteopathic manual techniques for these or gans. In a rather extensive treatise on the abdomen, McConnell (5) talked about the osteopathic approach from the ventral plane of the body, and described "ventral technique." Tender points, described as "gangliform contractions," were noted by Frank Chapman, DO, and came to be known as "Chapman's reflexes." The only known reference text on this topic was published by Owens (6). In later years other osteopathic researchers published stud ies illustrating the use of osteopathic manipulative techniques for abdominal conditions. For example, Hermann (7) demon strated that osteopathic manipulative treatment (OMT) prior ro abdominal surgery greatly reduced the incidence of posropera tive ileus. He also demonstrated that OMT could be successfully used to treat postoperative ileus when it did occur. In a recent study, Radjieski (8) demonstrated the use of OMT could signif icantly reduce the length of hospital stay in patients with acute pancreatitis. Researchers in other health care professions have also noted the clinical relationship between the soma and the viscera. As an example, Pikalov (9) found using spinal manipulative techniques as part of the treatment plan for duodenal ulcer disease resulted in pain relief and clinical remission much sooner than conventional medical treatment alone. Travel! and Simons (10) have noted that abdominal myofascial trigger points may produce visceral symproms such as diarrhea, vomiting, belching, food intolerance, and infantile colic. Barral has published extensively on the use of manual techniques for treatment of the abdominal viscera (11,12). Other authors in this area include Finet (13) and Lossing (see Chapter 69). Thus it becomes apparent that optimum treatment of abdom inal visceral conditions requires an understanding of the underly ing structure-function relationships and of the segmental viscero somatic reflex phenomena that are involved. An understanding of osteopathic philosophy and principles, and the ability to use OMT as part of a complete treatment approach to abdominal dis ease, is one of the most unique characteristics of the osteopathic physician.


752

Xiphoid process

T8 T9 --

IAbdomenl L3-4 -----

superior and dorsal boundary includes the sacrum, coccyx, and the piriformis and coccygeus muscles; and its inferior bound ary includes the levator ani muscles and fascial coverings (which together Form the pelvic diaphragm). For Further information re garding the Functional anatomy (skeletal, muscles and ligaments, vasculature and lymphatics, nerves) of the thoracic region, ribs, lumbar region, true pelvis, and the perineal region as related to the abdominal region see Chapters 48, 49, 50, and 52. The abdominal structures of interest in this chapter are the stomach, small intestine, large intestine, liver, gallbladder, spleen, pancreas, kidney, parts of the ureters, suprarenal glands and nu merous blood and lymph vessels, lymph nodes, and nerves. The lower ureters, the urinary bladder, and internal genitalia are not covered in this chapter. See Chapter 28 for discussion of these particular organs. Skeletal

The skeletal elements of the abdomen are the lumbar vertebrae, the sacrum, coccyx, and the innominate bones (Fig. 5l.1). De tailed descriptions of these skeletal elements are given in Chapters 48, 50, and 52. Ligaments, Muscles, and Fasciae ------LL- The abdomlno pelvIs of the true pelvis the perineum

FIGURE 51.1. Boundaries and skeletal elements of the abdomen.

DEFINITION

The abdomen may be defined simply as the region of the trunk below the thoracic diaphragm. This area (Fig. 51.1) consists of rwo pans: an upper part, the abdomen proper, and a lower part, the lesser pelvis (14). These rwo areas are continuous at the plane of the inlet of the lesser pelvis_ This inlet is bounded by the sacral promontory, the arcuate lines of the innominate bones, the pubic crests, and the upper border of the symphysis pubis.

FUNCTIONAL ANATOMY

The abdomen proper is bounded superiorly by the thoracolum bar diaphragm; inferiorly it becomes continuous with the pelvis or, as some anatomists describe it, the abdominopelvic portion of the abdominal cavity (15), by way of the superior aperture of the lesser or true pelvis. Anteriorly the abdomen is bounded by the abdominal muscles, which include the rectus abdominis, the pyramidales, the external obliques, the internal obliques, and the transversus abdominis. Posteriorly the abdomen is bounded by the lower thoracic and the lumbar vertebrae, the crura of the di aphragm, the psoas and quadratus lumborum muscles, and the posterior parts of the iliac bones. The lesser peLvis or abdominopelvic portion of the abdomen is shaped somewhat like an inverted cone. Irs anterolateraL bound ary consists of those parts of the hip bones below the arcuate lines and the pubic crests, and the obturator internus muscles; its

As noted earlier, the muscles of the abdominal cavity include the rectus abdominis, the pyramidales, the external obliques, the internal obliques, and the transversus abdominis, along with the diaphragm, the psoas, and quadratus lumborum muscles. The muscles of the abdominal region have associated fascial sheaths. The deep fascial layers have names associated with the various abdominal regions. Table 51.1 shows these fascial layers and their associated abdominal regions. The peritoneum is a large serous membrane that consists of rwo layers: the parietaL layer, which lines the abdominal wall, and a vis ceraL layer, which is reflected over the abdominal viscera. The pari etal peritoneum angles from the posterior wall of the abdomen to form very defined mesenteric connections to (he abdominal viscera. These mesenteries carry the sympathetic and parasympa thetic fibers and arteries to the viscera. They also carry visceral . afferent fibers, veins, and lymphatic vessels away from the viscera. The visceral peritoneum is sensitive to stretch. It produces visceral pain only when the distention of the viscus exceeds the length of the visceral peritoneum on the outside of the mesentery. The root of the mesentery for approximately 30 feet of small intestines is only 6 inches long and is located on the posterior wall TABLE 51.1. ABDOMINAL REGIONS AND THEIR ASSOCI ATED DEEP FASCIAL LAYERS Region Internal surface of the transversus

Fascial Layer Transversalis fascia

abdominis Inferior surface of thoracolumbar

Diaphragmatic fascia

diaphragm Psoas and iliac areas

Iliac fascia

Anterior surface of the quadratus

Anterior layer of the

lumborum muscles Muscles of the pelvis

thoracolumbar fascia Pelvis fascia

51. The AbdominaL Region

753

ture that lies just to the left of the thoracolumbar junction at about the level of the first lumbar vertebra. It receives lymphatic vessels that drain interstitial fluids from all the abdominal organs, the pelvic organs, the lower extremities, and all of the superficial lymphatic vessels located below a horizontal plane of the body running through the umbilicus. The superficial lymphatic vessels drain lymph into superficial inguinal nodes. Lymph then travels into the deep nodes, the deep trunks along the common iliac ar teries and the aorta, and finally into the cisterna chyli. It should be noted that lymph from the ovary, testicles, and prostate does not drain into the inguinal nodes but drains into the deep pelvic nodes.

Nerves

v FIGURE 51.2. Roots of the abdominal mesenteries.

of the abdominal cavity, posterior to a point about 1 inch to the left of and 1 inch above the umbilicus (Fig. 51.2). The root of the mesentery runs inferolaterally to a second point just anterior to the right sacroiliac joint. Mental visualization of these mesenteries allows a physician to determine more accurately the origin of palpable masses and the origin of auscultated abnormal sounds. It is also important when performing visceral manipulation to free fascial pathways and improve visceral function.

Primary sympathetic fibers for innervation of all organs below the diaphragm, except the descending colon and pelvic organs, pass from the intermediolateral cells in the thoracic spinal cord through the thoracoabdominal diaphragm. In the abdomen these primary fibers enter the celiac, superior mesenteric, and the infe rior mesenteric collateral ganglia where they synapse (Fig. 51.5). Secondary or postganglionic fibers continue on to innervate spe cific groups of organs in the abdomen and pelvis. Parasympa thetic innervation is supplied from the craniosacral outflow. All abdominal organs down to the mid transverse colon are supplied by the vagus nerve (cranial nerve X); the rest of the abdominal organs and all of the pelvic viscera receive their parasympathetic innervation from the pelvic splanchnic nerves (52-4).

Visceral Pain

Visceral afferent impulses travel back to the cord using the same course used by the sympathetic efferent nerves to that organ (Fig. 51.6). This pain tends to be vague and gnawing, deep, poorly localized, and midabdominal.

Vasculature and Lymphatics The thoracic aorta lies along the anterior and left anterolateral side of the thoracic vertebrae. It enters the abdominal cavity through the aortic hiatus in the abdominal diaphragm at the level ante rior to the 12th thoracic vertebra. Here it becomes the abdom inal aorta. Irs main abdominal branches are the celiac, superior mesenteric, renal, and inferior mesenteric arteries. Various small veins and plexuses in the pelvis eventually flow into the external and internal iliac veins. The two pairs of external and internal iliac veins unite to form the left and right common iliac veins, and these in turn unite to form the inferior vena cava, which conveys blood to the right atrium of the heart (Fig. 51.3). The veins that colleer blood from the digestive tract, spleen, pan creas, and gallbladder join to form the portal vein. The portal vein carries blood to the liver, where this vein branches out into a series of very small vessels called sinusoids. From here, hepatic veins convey the blood to the inferior vena cava. The left lymphatic duct (the thoracic duct) drains interstitial fluids from the lower extremities, the pelvic and abdominal vis cera, the left arm, and the left side of the head (Fig. 51.4). It begins as the cisterna chyli, a 2-inch, yellowish, cylindrical struc-

Viscerosomatic Pain

Visceral afferent fibers from the root of the mesentery report to the somatic cord segment of that organ's sympathetic innervation. This type of sensory input produces the paraspinal tissue changes that help the physician to locate the viscus that is most likely dys functional. The tissue changes are tenderness, asymmetry, 1'd.nge of motion differences, and tissue texture changes (TART). The pain and tissue texture changes are primarily localized at the paraspinal level consistent with the organ's sympathetic innerva tion (Figs. 51.7 and 51.8).

Somatic Pain Caused by the Percutaneous Reflex of Morley

This type of somatic pain is usually located directly over the inflamed organ and is produced by direct contiguous irritation of the parietal peritoneum and the abdominal wall (Fig. 51.9). It is responsible for rebound tenderness and abdominal guarding associated with more severe abdominal pain.

754

Vfl. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment

Heart

( Inferior vena cava

Portal vein

mesenteric vein Middle colic vein Superior mesenteric vien Superior left colic vein

Right colic vein

rectal vein

Middle and inferior rectal veins drain into the systemic venous drainage system

rectal veins drain Into the systemic venous drainage system

\ \ )

FIGURE 51.3. Venous drainage: portal venous system for the viscera.

TOPOGRAPHIC ANATOMY

There are certain surface landmarks of the abdomen that are palpable (16). These landmarks (Fig. 51.10) include the: • • • • • • • •

Costal margins Xiphoid process Iliac crests Anterior superior iliac spines Pubic crests and tubercles Inguinal ligaments Umbilicus Linea alba

For purposes of locating abdominal structures and describing abnormalities, the abdomen is conventionally divided into four quadrants (Fig. 51.11). Another method divides the regions of the

abdomen into nine sections (Fig. 5l.12A). Either method may be used, although division into quadrants is most commonly seen. The organs with which we are concerned in the abdomen are the following (Fig. 51.l2B): • • • • • • • • • •

Stomach Liver Gallbladder Pancreas Spleen Kidneys Urinary bladder Small intestine Colon Aorta and common iliac arteries

The adrenal glands are nOt palpable. The internal reproductive organs are considered in Chapters 28 and 31.

51. The Abdominal Region

755

Somesthetic Cortex

1

Thalamus

Viscera FIGURE 51.6. Neurologic pathway of visceral pain (afferent fibers).

DIAGNOSIS FIGURE 51.4. Main lymphatic ducts of the body.

Patient History

While beyond the scope of this chapter, it must be emphasized that a thorough hisrory is a critical element in making a correct diagnosis of a patient's abdominal problem. The hisrory should include at least the following information:

Head

1. Chief complaint 2. Hisrory of the chief complaint 3. Past medical hisrory 4. Past surgical hisrory 5. Current medications 6. Nutritional hisrory 7. Allergies Arms

8. Family and social history 9. Review of systems

a. Upper GI tract

Y.:l

\

b. Small intestines and right half of colon

�\

- U mbilicuS

-

Left half of colon

FIGURE 51.5. Primary sympathetic (efferent) nerves of the body.

FIGURE 51.7. Neurologic pathway of viscerosomatic pain.

756

VI! Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment

Head Xiphist&rnal joint Xiphoid process -':--'-:--"----:�-..:-:r

Costal cartilages

Arms

1 2

Level of umbilicus

3

__

------

Iliac crest

\

- - _ . , - ' "

-

'

.

4

Iliac fossa

Visceral Afferents (sympathetic pathways)

spine Inguinal lig.

FIGURE 51.8. Visceral afferent fibers.

Pubic

The reader is referred to standard textbooks on patient inter viewing for more information on this topic.

{

\\ Pecen pubisTubercle Crest

----

Symphysis --,,--:::r--'

A rch

---.,--�

Physical Examination

A complete physical examination is performed with special em phasis on regions that are spotlighted by the history or that might have functional association with the symptoms expressed by the patienr.ln this chapter, only the more important points as related to a patient with abdominal symptoms are considered.

FIGURE 51.9. Neurologic pathway of pain from the percutaneous re

flex of Morley.

FIGURE 51.10. The abdominal landmarks.

General

Before beginning the abdominal examination, care must be taken to ensure that the patient is as relaxed as possible and in a com fortable position. The examination of the abdomen is commonly done with the patient in the supine position, resting comfortably on an examination table or bed. A pillow supporrs the patient's head; a patient with increased thoracic kyphosis may require more than one pillow for support of the head and shoulders. A pillow may be placed under the patient's knees for additional comfort. If orthopnea is present, raise and support the trunk with a back rest to relax the abdominal muscles (J 7). The patient should be draped in a manner that allows the abdomen to be ex posed from the xiphoid region to the pubes. The examining room temperature should be adjusted for the patient's comfort, and the toom should be adequately illuminated for the performance of the examination. The physician may stand on either side of the patient for the examination. The only instruments required for performing the abdominal examination are the physician's warm hands and warm stethoscope head. The examination should employ the methods of physical examination in the following sequence: observation, auscultation, palpation, and percussion.

51. The Abdominal Region

v '"

/

",'

.

757

paralytic ileus. The midline of the abdomen between the xiphoid process and the umbilicus is auscultated for bruits. These could indicate an aneurysm and/or renal artery stenosis. The perium bilical region and the junction between the middle and outer two-thirds of the inguinal region are auscultated for a bruit that could be associated with a significant atherosclerosis of the com mon iliac or femoral artery. Palpation

RUQ /

'LUQ ,

RLQ

v FIGURE 51.11. The four-quadrant abdomen.

The osteoparhic physician includes examination for the elements of somatic dysfunction commonly noted by the TART acronym. Observation

For this parr of the examination, the examiner should be seated in a chair at the side of the patient so that the examiner's head is only slightly higher than the abdomen. Ideally, there should be a single source of light that shines across the patient's abdomen toward the examiner, or lengthwise over the patient ( 17). The abdomen is observed for the following: l.

Symmetry

2. Contour 3. Scars 4. Pulsarions 5. Visible masses 6. Engorged veins 7. Visible perisralsis

Palpation of the abdomen begins with a touch that is light yet firm, using the palmar surfaces of the approximated fingers to contact the abdominal wall. The physician lightly palpates each quadrant, checking for tenderness, any cutaneous or subcuta neous masses, and any unusual sensitivity. If the patient is appre hensive or is unable to relax during palpation of the abdomen, it is useful to ask the patient to Aex his or her hips and knees in order to facilitate relaxation of the abdominal muscles. During light palpation the physician can assess the abdominal wall for somatic dysfunction. Each quadrant of the abdomen can be palpated for abnormal myofascial tension, and the presence of tender points such as counterstrain points (see Chaprer 63), Chapman reAex points (Fig. 5 1. 13; also see Chapter 67), or Travell trigger points (see Chapter 66). One should note that Chapman reAex points related to abdominal visceral pathology are located next to the sternum in the intercostal spaces of ribs 5 through 1 1 and at the tip of rib 12. After performing light palpation, the osteopathic physician proceeds to deep palpation of the abdomen. Each quadrant is examined for tenderness, masses, or enlarged organs. At this time the physician also assesses the deep fasciae and soft tissues of the abdomen, looking for abnormal tissue tensions that might indi cate disturbance related to the collateral ganglia or mesenteries. The mobility and motility of the various abdominal organs may be assessed according to the theory and techniques described by Sutherland (18), Barral (1l), and others (see Chapter 69). Percussion

Percussion of the abdomen is more commonly performed in the asymptomatic patient, since, in the interest of patient comfort, painful conditions of the abdomen may preclude the use of per cussion. Ordinarily percussion is used to outline rhe borders and help to determine the approximate size and position of solid or gans, such as the liver, and hollow Auid-filled organs such as the urinary bladder. In general, the hollow viscera that occupy most of the abdomen contain gas and are usually resonant to percussion.

8. Unusual pigmentarion 9. Hair distribution 10. Distention Auscultation

Auscultate the four quadrants of the abdomen to determine the presence, location, frequency, and pitch of peristaltic waves. This could reveal the intermittent, low-pitched, occasional slow gurgle that is normal, or the high-pitched, tinkling sounds of develop ing obstruction. Bowel sounds may be absent, indicating possible

TREATMENT GOALS

As with OMT to any other body region, OMT should be applied to the abdominal region with specific goals in mind. The goals of treatment will vary with each individual patient. Some of these goals include: •

Addressing asymmetries, motion restrictions, and tissue tex ture abnormalities that are viscerosomatic reAections of home ostatic disturbances

758


..

2t4

Ri9ht

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hypochodriac region

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4

5 Epigastric region

TPP - - - --:-

Right lumbar

Um.9ilical

region

region

--+-- Left lumbar region Left iliac

Right iliac region ---+-..,.-

Hypogastric

,

-�+- region

/

region

• • • • • • • •

Decreasing or eliminating pain Removing segmental motion restrictions Improving altered skeletal vertebral unit and myofascial mo tion arising from aberrant visceral and autonomic activity Decreasing or eliminating segmental facilitation Decreasing or eliminating trigger point and tender point activity Decreasing pathophysiologic musculoskeletal and neuroreAex ive factors inAuencing circulation Enhancing musculoskeletal and neuroreAexive-mediated cir culatory functions Improving organ function Altering any or all of the previously mentioned situations as either contributing to, or predictive of, future health problems

APPROACHES TO THE OSTEOPATHIC TREATMENT OF THE ABDOMEN

We may consider three ways to approach the abdomen in order to address structure-function relationships: I.

from the back. Any spinal somatic dysfunctions that may

relate to an abdominal problem should be treated in order to im prove spinal motion and therefore restore normal nerve function in segmentally related areas. This approach includes typical ma nipulative methods such as high velocityllow amplitude (HVLA), muscle energy, counterstrain, and others. Paraspinal rib raising and paraspinal inhibition are used effectively for treatment of sympathicotonia.

•

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v •

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{� ./-

Q)

()

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a..

Joint Position - Distance Or X - Axis

2

Key:

N

R

P

A

tures. It is also the end point of perm itted passive motion. The range of normal active motion occurs between the phys iologic barriers. With motion loss in somatic dysFunction, the restrictive or pathologic barrier is the end point of permitted motion. A normal joint has a midline or neutral point within its range of motion. In somatic dysFunction, there is frequently a positional change (or asymmetry) in the joint that shifts its neutral to a new midline. Motion loss occurs in the range of normal physiologic motion. The range between the physiologic barrier and the anatomic barrier is not as finite as the illustration depicts. There is some Aexibility of the boundaries.

These principles describe motion loss in somatic dysfunction and a new position that is identified on examination as asymmetry or positional change. I nappropriate lay terminology is sometimes used to describe this positional change, for example, out of place. This kind of term may lead to a misunderstanding of the nature of motion loss in somatic dysfunction and the positional change as sociated with this motion loss. I nappropriate lay terms to describe treatment as an adjustment (of position) or putting it back fur ther complicate understandi ng. Thrust technique is designed ro remove motion loss in somatic dysfunction. A positional change from the somatic dysfunction position (Fig. 56.1) to the normal neutral or midline is the result of effective treatment. Treatment involves the dynamics of motion, not static positional change.

P

1

2

Somat-ic dysFunction exhibits a change in quantity and quality of motion. Quantity of motion involves the following general principles: 1. Motion beyond the anaromic barrier damages anaromic struc

N

P

A P R N

I

P

Bind

Ease

A

I I

Anatomic barrier Physiologic barrier Restrictive or "pathologic" barrier Midline or original neutral point of motion New midline in plane with somatic dysfunction

2 3

Motion loss in somatic dysfunction Range between physiologic and anatomic barriers

o FIGURE

=

Motion loss

56.1. Somatic dysfunction:

quality and

quantity of joint

motion.

the joint through a range of motion. A joint with somatic dys function exhibits an asymmetric quality of motion. If the y axis of the graph is changed to tension rather than Force, it emphasizes a different component of motion in somatic dysfunction. There is i ncreased tension in the dysfunctional joint, as if both agonist and antagonist are too tight. Motion in a direction of balanced tension is the basis of functional technique, which is described elsewhere (3). Motion characteristics using an example of rotational rem·ic tion of the atlas can be described as: l. AA RR (the atlas on the axis is rotated right, i.e., posi tion) 2. Freer rotation righ t 3. Restriction of left rotation =

Quality of Motion

To the experienced examiner, these qualitative changes are the clue to eval uating motion characteristics of somatic dysfunction. Motion is asymmetric with restriction in one direction and freer motion in the other direction. The terms ease and bind are some times used to describe the asymmetric motion. Movement toward the restrictive barrier exhibits bind, and moving away from the barrier exhibits ease. The qualitative aspects of motion can be depicted on the same graph (Fig. 56.1) used to illustrate quantity, with the x axis defin ing joint position and the y axis defining operator force to move

Somatic dysfunction can be described in three ways: 1. Where is it? ("The posterior aspect of the transverse process of the atlas is more prominent on the right." This is static position that describes an asymmetry, and is not sufficient for providing a HVLA technique.) 2. What will it do? (AA RR. Active or passive motion testing indicates the direction of the ease of motion for the joint. Example: The atlas is rotated to the right. Set-up for a HVLA =

854

VI! Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment

technique would be to rotate the axis to the left, i.e., opposite the diagnosis, to the restrictive barrier.) 3. What won't it do? (AA restricted RL. Active or passive mo tion testing indicates the direction i n which the joint is re stricted. Set-up for a HYLA technique would be to rotate the axis to the left, i.e., the same direction as the "restriction" diagnosis, to the restrictive barrier.) =

These examples illustrate that somatic dysfunction can be named in two ways. The com mon, classic method states the mo tion that the joint prefers (i.e., AA RR) ' The second method states the restricted motions that are present. When using this second method, the formula or description must be preceded by the word "restricted" or "restricted in" (i.e., AA restricted RL) ' =

=

There are some spinal joints that tend to be loose. C5 and C6 become hypermobile (and arthritic) . This process is maintained by a stiff, flexed upper thoracic spine requiring a compensatory cervical lordosis. In the l umbar spine, the l umbosacral (LS) region tends to become hypermobile. A flexed upper lumbar spine asso ciated with chronic psoas tension maintains LS dysfunction (4) . Be aware of the possibility of unstable joints. Reevaluation of motion after treatment will reveal excess freedom of motion. Management involves modifying the activity that contributes to instabi lity, mobilizing adjacent hypomobile joints, and prescrib ing active rehabilitation exercises.

HIGH-VELOCITY/LOW-AMPLITUDE TREATMENT CLASSIFICATION AND MECHANISMS

Direct method of treatment 2. Requires specific diagnosis of the joint dysfunction before each treatment 3. Set-up: motion is carried in the direction of its restriction to the restrictive barrier in all planes 4. Activation: high-velocityllow-amplitude thrust l.

Unstable Hypermobile Joint

Some joints are unstable and hypermobile. Within the numer ous joi nts of the spine, a pattern of alternating hypo mobility and hypermobility may exist. The loose, hypermobile j oints are over worked while the stiff, hypomobile joints escape excess motion. A normal physiologic reaction to a painful hypermobile joint is for muscles surrounding the joint to splint the joint and protect it from excess motion. Physical examination reveals restriction of motion. Underneath that protective muscle splinting is an unstable joint. A high-velocity thrust technique may work, as evidenced by a decrease in pain and improvement in motion. Unfortunately, the treatment contributes to the joint instability. The more HYLA technique is used, the looser the joint becomes.

MECHANISM OF T HRUST TECHNIQUE ACTION

The mechanism of thrust technique action is shown in Figure 56.2. The answer to the question of what maintains re striction of joint motion has been and is being explored by osteo pathic physicians and scientists. I n some cases, a joint gets stuck

(Gamma and alpha motor neuron inhibition due to "stretch" of spindle and Golgi apparatus mechanisms) A

P

o

A

I-II.I I

I I EXAMPlE E-T

R P

(X)

I

Upper

A p

KE¥'------

= Anatomical barrier =Physiological barrier R =Restrictive barrier (Xl Is start point of manipulation 0= Usual" neutral" for this joint

R (X)

Bone

�-----i--�-,r-------------W�L . --�--P FIGURE 56.2. Proposed mechanism of HVLA thrust technique action.

56. Thrust (High- VeLocity/Low-AmpLitude) Techniques

the same way an old loose window or drawer may get stuck: half open and half closed, in a position no longer parallel to the track.' The sacroil iac joint is a good example of this type of restriction. A properly di rected mechanical force frees the joint. As with the stuck drawer, the proper force is not directly in or out, which is the major motion of the drawer. The proper force is an oblique or side force. Remember this in extremity tech niques, where the minor motions or restoration of joint play is the object, not a di rect force against the major motion of a joint. For example, if a wrist is restricted in extension, treatment might involve anterior or posterior translation of the carpal bones. For mechanisms maintaining joint restriction, abnormal mus cle activity is usually involved. Muscles maintain joint restriction. The palpatory findings in somatic dysfu nction include tissue tex ture abnormal ity. Muscles are hypertonic and sometimes boggy and stri ngy. When the joint restriction is treated, there is an im mediate change in the muscles and an im mediate change in the quality and quantity of motion. This change means an immedi ate change in neural activity. How does the thrust change neural activi ty? A likely answer lies in the mechanoreceptor in the j oint capsule. A sudden stretch or change of position of the joint alters the afferent output of these mechanoreceptors, resul ting in release of muscle hypertonicity. This is discussed in the osteopathic and scientific literature on proprioceptors and somatic dysfunction (5-9). Pop or click: Numerous studies have focused on the pop. One widely held hypothesis states that the sudden distraction of joint surfaces produces a nitrogen bubble, along with noise and increased freedom of motion (I 0) . Osteopathic physicians prefer to focus on joint function and dysfunction and not on the noise. The objective of thrust technique is to overcome joint restriction. Always retest motion after the treatment. Although the pop or click is usually ind icative of success, it is possible that an unrelated joint made the noise and rhe restricted joint remained u naltered. It is also possible to have a successful treatment without any noise. Keep your focus on the patient and the joint restriction.

CLINICAL APPLICATION OF HIGH-VELOCITY/LOW-AMP LITUDE MANIPULATIVE TREATMENT Indications

Thrust technique is a method of specific joint mobilization. Proper use of thrust technique requires an assessment of restric tion of joint motion before each manipulative treatment pro cedure is performed, along with the conclusion that treatment of this joint restriction will benefit the patient (for example, re duce pai n, free motion, improve biomechanical function, reduce somatovisceral reflex) . The performance of thrust technique requires an understand ing of somatic dysfunction and the barrier concept. Thrust technique is indicated for treatment of motion loss in somatic dysfunction. Thrust technique is ordinarily not indicated for treatment of joint restriction due to anatomic/pathologic changes, such as traumatic con tracture, advanced degenerative joint disease, or ankylosis.

855

End-Feel at Restrictive Barrier

The use of direct technique requires engaging the barrier. The final activating force is a physician force: high-velocity/low ampl itude. Figure 56. 1 , depicting the force necessary to move a joint to the barrier, is a graphic illustration of end-feel. As the barrier is engaged, increasing amounts of force are necessary and the distance decreases. The term barrier may be misleading if it is in terpreted as a wall or rigid obstacle to be overcome with a push. As the joint reaches the barrier, restraints in the form of tight mus cles and fascia serve to inhibit further motion. We are pulling agai nst restraints rather than push ing against some anatomic structure. The barrier involves a three-dimensional matrix, not just a single plane of motion. We can define motion in the three car dinal planes as flexion-extension, rotation, and side-bending. To be complete, there are components of translatory motion that should be considered. These are fore-aft translation, side-to-side translation, and compression-distraction. All of these single mo tions are combined into a single force vector when executing the tech nique. However, for purposes of diagnosis, each of these components can be tested separately. For a high-velocity tech nique [Q be effective, the barrier must feel solid. If the barrier feels rubbery and indistinct, thrust tech nique may be ineffective.

Barrier Engagement

Experienced physicians develop skills to engage the barrier quickly. They sense how the tissues are responding [Q the force bei ng applied and make subtle alterations in the direction offorce to effectively engage the barrier in all planes. The novice takes more time by engaging one plane at a time. Engaging the barrier with accuracy and confidence is a skill acquired with practice and experience.

Accumulation of Force at Restriction

With a proper diagnosis, initial positioning engages the barrier. Forces must be applied so that they accumulate at the restricted joints. In the spinal area, the reference is a vertebral unit: two bones and the connections (joints) between them. Forces applied from above to the superior vertebra meet forces applied to the inferior vertebra. Forces from above and from below meet at the restricted joint. Depending on the technique, force may be applied at one site; the opposing counterforce is resistance of inertia of body mass, resistance of the table, or other resistance. In all cases, direct the force at the restriction. Specificity of a technique is a measure of how accurately the force accumulates at the restriction. Force that does not accumulate at the lesion is dissipated through other parts of the body. This could result in iatrogenic side effect. The greater the specificity, the lesser the force needed, and the potential for untoward side effects is minimized.

856

VJI. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment

Final Corrective Force Velocity and Amplitude

HVLA thrust techniques use a short, quick thrust. High velocity does not mean high force, and it does not mean high amplitude. Once the barrier is engaged, the fi nal force is applied from that position. Do not back off before delivering the corrective thrust. Likewise, do not carry the force through a great distance. Am pli tude means distance. The amplitude is low, a small fraction of an inch. High amplitude defeats proper localization of force and decreases the likelihood of achieving the desired effect. Do not be overly tentative and apply a low-velocity force with an increase of force and amplitude. These efforts are often un successful. The proper application has been described as a tack hammer blow, sudden but not forceful. The term impulse ap plied to HVLA tech nique recognizes that the force is a sudden acceleration and deceleration. Experience and practice are very helpful in knowing how to apply the force. Some thrust techniques are not executed at high velocity. Con sider an experience where you set up the patient to treat a j oin t restriction, the joint goes click, a n d t h e restriction is released as you are positioning the patient and localizing forces. Some times you tease a joint with carefully and slowly applied forces. Again, experience is very beneficial i n applying the proper force. Although we describe HVLA thrust technique, the actual force may be modified to fit the patient's needs.

Methods Used to Improve Effectiveness of High-Velocity/Low-Amplitude Techniques

Pa tien t Relaxa tion during Thrust Technique

The patient should be as relaxed as possible when applying the corrective force. The more tense the patient, the greater the force necessary, and the greater the risk of side effect or failure to over come the motion restriction. If the patient feels com fortable and secure with the physician's hands, relaxation is not a problem. If the patient feels insecure, muscles will be tight rather than relaxed. If the technique is hurting the patient, muscles will in voluntarily tighten. Nonverbal clues, such as a facial grimace, can alert the physician to a problem. A skilled physician senses when the patient is relaxed and when he or she is not. The exhalation phase of respiration is the relaxation phase, and the final force is often applied during exhalation.

Divert the Patien t's A tten tion

When using a thrust tech nique to treat cervical somatic dysfunc tion, some practi tioners divert attention by instructing the patient to cross his or her legs. This may help in some cases, but it is not an adequate substitute for the physician's hands transmitting a sense of control, comfort, and confidence. This skill comes with practice and experience. It is possible to distract a patien t and apply a corrective force when the patient does not anticipate it. However, if the technique is applied too quickly, forces may not be properly localized. A patien t who has experienced a painful thrust in the past cannot be fooled.

Dose of Thrust Technique

The compassionate physician may err on the side of overdose. Give the patient time to respond to the treatment; the sicker the patient, the less the dose. Older patients respond more slowly; young patients respond more quickly ( 1 1 ) . For hospitalized patien ts, daily osteopath ic man ipulative ther apy (OMT) may be appropriate, but daily thrust technique may be an overdose. When treating hospital patients on a daily ba sis, Larson (N.]. Larson, personal commun ication, 1 967, 1 978) would vary the technique so he did not repeat the same technique on a given area. With the spectrum of techniques available, there should be no reason to overdose a patient on high-velocity tech n ique. The more specific and precise the technique is, the less iatrogenic the side effect.

Precautions and Contraindications

Most of the published precautions about OMT imply forceful HVLA thrust. Instead of presenting a list of absolutes, think in terms of risk/benefit relationships. If the risk of harming the pa tient exceeds the potential therapeutic benefit, the tech nique is not indicated. Risk also relates to the skill of the physician. There is more risk with an unskilled physician. [f forceful, direct tech n iques may harm the patient, gentle indirect release tech niques m ight be safe. Neurologic complications from thrust manipulation can be fatal or result in permanent neurologic impairment. Cervical ma nipulation has been associated with vertebral basilar thrombosis ( 1 2) . Dislocation of the dens associated with rupture or laxity of the transverse ligament of the atlas can cause death or quadriple gia. In the low back, massive protrusion of a disc can produce cauda equina syndrome with loss of bowel, bladder, and sexual function. Pathologic fractures can result from osteoporotic or metastatic bone. Excess force may injure fragile tissues. Joints could be sprained. Arthritic spurs could be broken off. There may be psychological contraindications to the use of HVLA. Apprehension on the part of the patien t is a relative con trai ndication. Make sure the patient understands what i s expected during and after treatment.

Exaggera tion Thrust Technique

Some practitioners of manual medicine use a form of thrust tech nique in which the direction of force is away from the. restrictive barrier. An example of this method follows: If T3 is extended, extension is free (freer motion), and flexion is restricted. The exaggeration method (technique) involves thrusting on T3 to extend it suddenly and forcibly. This form of technique is poten tially damaging to the ligamentous structure, producing hyper mobility. I n addition, the patient may experience an increase of symptoms with a prolongation of somatic dysfunction. This is es pecially true for patients with extended thoracic dysfunction that is misdiagnosed as flexed dysfunction, and an extension force is applied. The exaggeration thrust techn ique is not taught in U.S. colleges of osteopathic medicine.

56. Thrust (High- Velocity/Lo w-A mplitude) Techniques

857

Guidelines for Safety

1. 2. 3. 4. 5. 6. 7. S. 9. 1 0. 11.

Be aware of possible compl ications. Make a diagnosis. A palpatory examination is a prerequisite for treatment. Listen with your hands and fingers. If it doesn't feel right, back off and collect more data. If the barrier doesn't feel right, don't thrust, but select an alternate technique. Emphasize specificity, not force. Ask permission to treat. If response to treatment does not meet your expectations, reevaluate the patient. Somatic dysfunction with joint restriction is the indication. Pain is not an indication for high-velocity manipulation. Somatic dysfunction often coexists with orthopedic disease (spondylosis, disc degeneration, spondylolysis). Be aware of the total picture.

FIGURE 56.3. Occ i p itoatlantal tec h n i q u e with side-bending focus.

Beneficial Use of High-Velocityl Low-Amplitude Thrust Technique

Thrust technique is a very efficient use of physician's time in treating a patient, as long as the physician has met the prerequi site of an effective skill level. When a patient is able to tolerate thrust tech nique, the results are long lasting rather than tem porary. The patient usually experiences immediate relief, with decreased pain and increased freedom of motion. For years, osteo pathic physicians have treated patients using thrust techniques, and these patients continue to seek the services of an osteopathic physician.

3. 4.

5. 6.

HIGH-VELOCITY/LOW-AMPLITUDE TREAT MENT TECHNIQUES BY REGION AND DIAGNOSIS

7.

interphalangeal (PIP) joint of his or her left index finger is placed on the bony calvaria (left occiput) , taking care to avoid the mastoid portion of the temporal bone. Mild extension is added and is limited to the O-A j oint, taking care to avoid hyperextension. The physician side bends the patient's head to the left by translation downward (caudally) with the left MP (or PIP) joint and slightly upward with the right hand. The restrictive barrier in left side-bending and right rotation is localized. The patient is asked to take a big breath in and exhale. At the end of exhalation, a high-velocityllow-amplitude thrust to increase the side-bending component is directed through the left M P (or PIP joint) by translation of the occiput toward the patien t's righ t eye. Retest the range of motion.

Cervicals

Atypical Cervicals: Occipito-Atlantal Joint, Side-Bending Focus

A typical Cervicals: Atlanto-Axial Joint, Neutral

Diagnosis

The atlas is rotated right in relationship to the axis and moves more easily in this direction AA=RR AA restricted RL

The occiput is side bent right, rotated left in relationship to the arias (posterior occiput on the left) . OA SRRL or CO S RRL OA restricted SLRR or CO restricted SLRR =

=

=

Diagnosis

=

=

Position Position

The patient is supine, and the physician stands to the left of the patient at the head of the table ( Fig. 56.3).

The patient is supine, and the physician stands to the right of the patient at the head of the table (Fig. 56.4) . Procedure

Procedure

To restore range of motion to the occipital-atlantal (OA) joint so that in resetting itself, appropriate physiologic motion is restored: 1 . The physician's right hand cups the patient's chin with the palm at the zygomatic process. 2. The physician's metacarpophalangeal ( M P) joint or proximal

To restore physiologic range of motion to the atlanto-axial (A-A) joint so that in resetting itself, there is a physiologic increase in left rotation: 1.

The fingers and palm of the physician's left hand grasps the patient's chin with the palm or the forearm at the patient's left zygomatic process.

858


FIGURE 56.4. Atlanto-axial technique.

2. The proximal phalanx of the physician's right index finger is placed by the soft tissue next to the patient's A-A joint, with the thumb contacting the patient's lateral aspect of the face in the region of the right zygomatic process, avoiding the mandible. 3. The patien t's head is rotated to the left with enough flexion extension and/or side-bending to engage the restrictive barrier. (Note the resilience of the end-feeL) 4. The patien t is asked to inhale and exhale. 5. At the end of the patient's exhalation, the physician applies a high-velocity/low-amplitude thrust in a left rotational pattern, focusing the force with the right index finger as a fulcrum. 6. Retest the range of motion.

FIGURE 56.5. Tech n i q u e for cervica ls

(2-7 with side-bending focus.

5. The physician side bends the patient's head and neck to the right until localized at the C3-4 joint space. 6. The physician rotates the head and neck to the left down to C3 to obtai n a facet lock down to the somatic dysfunction, con tinually adjusting the side-bending and extension to maintain localization at C3. 7. The physician applies a high-velocity/low amplirude right side-bending thrust by translatory motion toward the left through the right index finger M P or P I P joint contact, aiming the thrust in a vector toward the opposite shoulder. 8 . Retest the range of motion.

Typical Cervicals (C2-7), Side-Bending Focus Diagnosis to

C3 is flexed, side-bent to the left, rotated left in relationship C4, and moves more easily in these directions. C3 F SI.RL C3 restricted E SRRR =

=

Typical Cervicals (C2-7), Rotational Focus Diagnosis

C6 is flexed, side-bent right, rotated right in relationship to C7, and moves more easily in these directions C6 F SR RR C6 restricted E SLRL =

Position

The patient is supine, and the physician stands to the right side of the patient at the head of the table (Fig. 56.5) . Procedure

restore physiologic range of motion to the C3-4 vertebral unit so that in resetting itself, appropriate physiologic motion is restored:

=

Position

The patient is supine, and the physician stands to the right of the patient at the head of the table (Fig. 56.6).

To

1 . The physician's left palm and fingers cup the patient's chin with the palm or forearm supporting the patient's head in the area of the zygomatic process. 2. The MP or P l P joint of the physician's right index finger is placed at the soft tissue next to the artiCular pillar of C3. 3. The physician flexes the patient's head and neck down to the C3-4 joint space. 4. To address the sagittal plane restriction, the physician intro duces a mild extension by adding a small amount of anterior translation th rough the C3 fulcrum contact.

Procedure

To restore physiologic range of motion to the C6 vertebral unit so that in resetting itself, appropriate physiologic motion is restored: 1 . The physician's palm and fingers of the left hand cup the pa tient's chin with the palm and forearm supporting the patient's head i n the area of the zygomatic process. 2. The M P or P I P joint of the physician's right index finger is placed at the soft tissue next to the articular pillar of C6. 3. The physician flexes the patient's head and neck down to C6 and then induces a small amount of extension by applying an anterior translation of C6 at the index finger (fulcrum contact) .

56. Thrust (High- Velocity/Low-Amplitude) Techniques

859

Procedure

To restore physiologic range of motion to the T-7 joint so that i n resetting itself, appropriate physiologic extension is restored:

FIGURE 56.6. Technique for cervicals

(2-7 with rotation focus.

4. The physician rotates the head and neck to the left (down to and including the C6 segment) to the restrictive barrier. Side bending left is achieved by keeping the patient's left temple close to the table. 5. The physician applies a high-velociryllow amplitude left to tational thrust with the vector aimed at the opposite eye and in the plane of the facets using the right hand contact. 6. Retest for motion.

1 . The physician asks the patient to cross his or her arms over the chest, with the arm on the opposite side opposite the physician superior, and to grasp the lateral portion of each shoulder. 2. The physician supports the patient's head and neck with the cephalad hand and flexes the patient to a point where the caudad hand can palpate motion at the dysfunctional vertebra and the joint space below it. 3. The physician makes a bilateral fulcrum with his or her thenar eminence and flexed fingers of his or her caudad hand. This fulcrum straddles the spinous p rocesses and is placed to con tact the soft tissues overlying both transverse processes of the dysfunctional vertebral unit. I 4. The physician positions the patient's elbows in his or her epi gastric area (or a small pillow is placed between the patient's elbows and the physician's epigastric area). The physician lo calizes the flexion force to the midline by transferring a por tion of his or her body weight until motion is focused over the caudad, fulcrum hand. 5. The patient is asked to inhale and exhale. 6. The physician applies a high-velociry/low-amplirude thrust by momentarily dropping his or her body weight with a bending of the knees, producing force with a vector straight toward the fulcrum (usually straight down toward the floor) . 7. Retest the range of motion.

Thoracic

Thoracic Single Plane: Flexion Diagnosis

T6 is flexed relative to T7 and flexes more easily T6=F T6=restricted E

Thoracic Single Plane: Extension Diagnosis

T6 is extended relative to T7 and extends more easily. T6 = E T6 restricted F =

Position

The patient is supine, and the physician stands on either side of the patient, facing the head (Fig. 56.7) .

Position

The patient is supine, and the physician stands on either side of the patient facing the head. Procedure

To restore physiologic range of motion to the T6-7 joint so that in resetting itself, appropriate physiologic flexion is restored:

1 Use

of the hand as a fulcrum (at spinal segment level) depends on the

thrust itself. In a flexion somatic dysfunction, some physicians will have the bilateral fulcrum at the level of the dysfunctional segment. This places the effective fulcrum at the level of the joint space as they roll the patient over it during the thruSt maneuver. Other physicians will stabilize the segment below the dysfunctional vertebra and obtain the same effect with their thrust by less cephalad motion during rhe roll. Either way, the biomechanics of the thrust necessitate a confrontation of rhe barrier, with a gapping action at the FIGURE 56.7. Hand placement for thoracic s u p i ne tec h n i q u e .

dysfunctional joint level, reestablishing normal motion.

Vl!. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment

860

1 . The physician asks the patient to cross his or her arms over the chest, with the arm on the opposite side of the physician superior, and to grasp the lateral portion of each shoulder. 2. The physician supports the patient's head and neck with the cephalad hand and flexes the patient to a point where the caudad hand can palpate motion at the dysfunctional vertebra and the joint space below it. 3. The physician makes a bilateral fulcrum with his or her thenar eminence and flexed fingers of his or her caudad hand. This fulcrum straddles the spinous processes and is placed to contact the soft tissues overlying both transverse processes. 2 4. The physician positions the patient's elbows in his or her epi gastric area (or a small p illow is placed between the patient's elbows and the physician's epigastric area) . The physician lo calizes the flexion force to the midline by transferring a por tion of his or her body weight until motion is focused over the caudad, fulcrum hand. 5. The patient is asked to inhale and exhale. 6. The physician applies a high-velocityllow-amplitude thrust by momentarily dtopping his or her body weight with a bending of the knees, producing force with a vector approximately 45 degrees cephalad and posterior at the fulcrum. 7. Retest the range of motion. Thoracic Multiple Plane: Type I Diagnosis

Dexrroscoliosis (left convexity) with left side-bending and right rotation T7 is at the apex of the curve, side-bent left, rotated right i n relationship to TS, and moves more easily in these directions T7 N SL RR T7 restricted N S R RL =

=

Position

The patient is supine, and the physician stands on the left side of the patient (the side opposite the posterior transverse process) ( Fig. 56.S). Procedure

To restore physiologic motion to the T7 -S joint: 1 . The physician has the patient cross his or her arms over the chest, with the arm on the opposite side of the physician superior, and grasp the lateral portion of each shoulder.

FIGURE 56.8. Thoracic m u l tiple p l a n e tech n i q ue, type I .

2. The physician's cephalad hand rotates the patient's opposite shoulder and thorax toward him or her. 3 . The physician reaches across the patient and places the thenar eminence of the open flat caudad hand on the patient's right T7 transverse process (this is the transverse process that is rela tively posterior in position) . This is to be used as the fulcrum. 4. The physician supports the patient's head, neck, and shoulders with the cephalad hand and flexes the patient through T7 to the dysfunctional joint space (T7-S) . 5 . The physician positions the patient's elbows in his or her epi gastric area (or a small pillow is placed between the patient's elbows and the physician's epigastric area). 6. The physician side bends the patient's spine right, down to the T7 to TS j unction, and the side-bending, Aexion, and rotation forces are localized at the T7 fulcrum by adjusting his or her body weight through his or her epigastric region and the patient's elbows. 7. The patient is asked to inhale, and the physician increases the localization as the patient exhales. S. At the end of exhalation, the physician applies a high velocity/low-amplitude thrust through the epigastric contact, aimed straight down toward the fulcrum hand (usually straight down toward the floor). This vector passes through the pa tient's elbows, around the thorax, and to the T7 fulcrum. This is accomplished more by a momentary drop of the physician's weight then a squeezing or compression of the patient. 9. Retest the range of motion. Note: These techniques are sometimes referred to by their colloquial name, the Kirksville Krunch.

2 Use

of the hand as a fu lcrum (at spi nal segment level) depends on

the thrust itself. In a Aexion somatic dysfunction, some physicians will

have the bilateral fulcrum at the level of the dysfunctional segment. Th is

Thoracic Multiple Plane: Type I/, Flexion

patient over i t during the thrust maneuver. Other physicians will stabi

Diagnosis

places the effective fulcrum at the level of the joint space as they roll the

lize the segment below the dysfunctional vertebra and obtain the same ef fect with their thrust by less cephalad motion during the roll. Either way,

the biomechanics of the thrust necessitate a confrontation of the barrier,

with a gapping action at the dysfunctional joint level, reestablish i ng notmal motion.

T5 is flexed, side bent right, and rotated right in relationship to T6, and moves more easily in these directions T5 F SR RR T5 restricted E SLRI. =

=


861

is accomplished more by a momentary drop of the physician's weight than a squeezing or compression of the patient. 9. Retest the range of motion. Multiple Plane: Type II, Extension Diagnosis

T7 is extended, side-bent right, rotated right in relationship to TS, and moves more easily in these directions T7 E S R RR T7 restricted F S L RL =

=

Position

FIGURE 56.9. Thoracic multiple plane tec h n i q ue, type I I, flex i o n .

Position

The patient is supine, and the physician stands at the left side of the patient (the side opposite the posterior transverse process of the somatic dysfunction) (Fig. 56.9). Procedure

The patient is supine, and the physician stands on the left side of the patient (the side opposite the posterior transverse process (Fig. 56. 1 0) . Procedure

To restore physiologic range of motion to the T7 -S joint: l.

2.

To restore physiologic motion to the T5-6 joint: 1. The physician asks the patient to place his or her hands behind the neck with fingers interlaced. This can also be done by asking the patient to cross his or her arms over the chest, with the arm on the opposite side of the physician superior, and to grasp the lateral portion of each shoulder. 2. The physician uses his or her cephalad hand to rotate the patient's opposite shoulder and thorax toward him or her. 3. The physician reaches across the patient and places the thenar eminence of the open, flat caudad hand on the patient's right T5 transverse process (this is the transverse process that is rela tively posterior in position). This is to be used as the fulcrum. 4. The physician supports the patient's head, neck, and shoulders with the cephalad hand and flexes the patient through T5 to the dysfunctional joint (T5-6). 5 . The physician positions the patient's elbows in his or her epi gastric area (or a small pillow is placed between the patient's elbows and the physician's epigastric area) . 6. The physician places the cephalad hand under the patient's neck and cervicothoracic junction to induce a component of left side-bending at the T5-6 joint space. The side bending, flexion, and rotation forces are localized at the T7 fulcrum (thenar eminence) by adjusting his or her body weight through his or her epigastric region and the patient's elbows. 7. The patient is asked to deeply inhale and exhale. The physician increases localization as the patient exhales. S. At the end of exhalation, the physician applies a high velocity/low-amplitude thrust through the epigastric contact, aimed straight down toward the fulcrum hand (usually straight down toward the floor) . This vector passes through the pa tient's elbows, around the thorax, and to the T7 fulcrum. This

3.

4.

5.

6.

The physician asks the patient to interlace his or her hands behind the neck. (This can also be done with the arms crossed over the chest.) The physician's cephalad hand is used to rotate the patient's opposite shoulder and thorax toward him or her. The physician reaches across and under the patient with his or her caudad hand to contact the right transverse process of TS with the thenar eminence. This will be used as a fulcrum. Note that this is the transverse process of the segment below the dysfunctional joint space. The patient's head, neck, and shoulders are supported by the physician's cephalad hand, and the patient's spine is flexed down through T7 to the dysfunctional j oint space (T7-S). The physician localizes the forces over the fulcrum (thenar eminence) by adj usting his or her weight over the patien t's elbows through the epigastric contact. The cephalad hand under the patien t's neck and cervicotho racic junction is used to induce a component of left side bending at the T7-S joint space.

FIGURE 56.10. Thoracic mUltiple p l a n e tech n i que, type II, extension.

862


7. The patient is i nstructed to deeply inhale and exhale. The . physician increases localization as the patient exhales. S. A high-velocity/low-amplitude thrust toward your fulcrum is applied at the end of exhalation. The thrust is i n a vector aimed 45 degrees between the floor and the patient's head. The thrust is produced more by a momentary drop of your body weight than by squeezing or compression of the patient. 9. Retest the range of motion.

Multiple Plane: Crossed Hand, Midthoracic Diagnosis

TS is flexed, side-bent right, rotated right in relationship ro T9, and moves more easily in these directions TS F S R RR TS restricted E S L RL =

than one cycle as you localize your forces. Pressure through the hand �ver the posterior transverse process is in a cephalad and downward (toward the floor) direction. Pressure through the T9 hand is caudad and downward (toward the floor). 5. Rotation is induced by the posteroanterior forces. A trans latory force is also induced to the entire region by moving the hands toward you, therefore decreasing the dysfunctional side-bending. 6. A high-velocityllow-amplitude thrust in the directions already specified is applied by using a momentary drop of the physi cian's body weight to transmit the force through wrists and elbows that are held rigid. 7. Retest the range of motion. Note: This commonly used thoracic technique has earned the sobriquet of the Texas Twist.

=

Position

The patient is prone, and the physician stands on the right side of the patient (the side of the posterior transverse process) (Fig. 56. 1 1 ) . Note: A pillow may be placed under the under the thorax to increase thoracic kyphosis.

Multiple Plane: Crossed Hand, Upper Thoracic (T1 -4J Diagnosis

T l is flexed, side-bent left, rotated left in relationship to T2, and moves more easily in these directions Tl F S L RL T l restricted E SR RR =

=

Procedure

To resrore physiologic range of motion to the TS-9 joint: l . The patient is supine with his or her arms at the sides. 2. The physician places his or her caudad hand over the TS vertebra, fingers pointing toward the patient's head, and the hypothenar eminence or pisiform region contacting its right transverse process (this transverse process is posterior), and moves the contact i nto a more cephalad position. 3. The left (opposite) transverse process of the segment (T9) be low the dysfunctional joint space is contacted with the thenar eminence of the physician's cephalad hand, fingers point to ward the patient's feet, and moves this contact into a more caudad position. This establishes the crossed-arm technique. 4. The patient is asked to inhale, then exhale, through more

FIGURE 56. 1 1 . T horacic tec h n i q u e with c rossed h a n d .

Position

The patient is prone, and the physician stands on the left side of the patient at the head of the table (Fig. 56. 1 2) . Procedure

To restore physiologic range of motion to the T l -2 joint: 1. The physician side bends the patient's neck ro the right (side of restricted side-bending) through the level ofT I to the dys functional joint space, and places the patient's chin on the table. 2. The physician's right hand slightly rotates the patient's head to the left to obtain ligamentous tension locking. 3. The right hand of the physician is on the left side of the

FIGURE 56. 1 2 . Upper thoracic tech n i q u e with crossed h a n d .


863

patient's head and the hypothenar eminence (pisiform region) or thenar eminence of his or her left hand is placed over the left rransverse process ofT l . This is the crossed hand position. 4. The patienr is asked ro inhale and exhale several times as the physician takes up the tissue slack, localizing forces. 5. A high-velocityllow-amplitude thrust is applied through the pisiform with its vecror directed in a lateral, posteroanterior (toward the Aoor), and caudad direction. This side bends the patient in a direction opposite the dysfunctional side-bending. The hand on the head is used to stabilize it as the thrust is be ing applied and transmitted through the Tl transverse process. The posteroanrerior force on the patienr's left transverse pro cess of T l induces right rotation while the stabilizing hand on the head effects a sl ight relative rotation in an opposite direction. 6. Retest the range of motion. Multiple Pla ne, Pillow Fulcrum: Flexion Diagnosis

T4 is Aexed, side-bent right, rotated right in relationship ro T5, and moves more easily in these directions T4 = F SRRR T4 = restricted E SRRR Position

The patient is seated (or standing), and the physician stands behind the patient (Fig. 56. 1 3) .

FIGURE 56.13. Thoracic multiple p l a n e techn ique, flexion.

Procedure

To resrore physiologic range of motion to the T4-5 j oint: 1.

2.

3.

4.

5. 6.

7.

8.

The patient places his or her hands behind the neck with the fingers interlaced. To control the movements of the patient, the physician places one arm under the axilla on one side of the patient and places the fingers of that extremity on the dorsal aspect of the patient's wrist. The physician places a small pillow berween his or her epi gastric region (or chest) and the right transverse process of T4. The physician puts his or her other arm under the patient's other axilla and places the fingers of that hand on the dorsal aspect of the patient's wrist. Note: Do not use the hand con tacts ro pull down and induce spinal Aexion (the hand only rests on the patient's wrists). Extension is i nduced down ro and including T4, using your epigastric region and the pillow as your fulcrum . The physician induces left side-bending through right trans larory motion at the level of the pillow fulcrum. The pressure of the pillow itself will direct rotation of the patient's vertebra to the left. The patient is asked to inhale and exhale, relax the shoulders and back, and "let the tummy hang." As the patient relaxes, the localization at the fulcrum must be retained. At the end of expiration, ask the patient to bring the elbows

together. As you feel localization occur in the tissues at the fulcrum, use an anterior and superior high-velocity/low amplitude thrust through your epigastrium and the pillow. Si m ultaneously induce superior and posterior traction through your arms (a lifting motion). Some physicians have developed an epigastric muscular contraction that they use to direct the thrust. 9. Retest the range of motion. Multiple Plane, Pillow Fulcrum: Extension Diagnosis

T6 is extended, side-bent left, rotated left in relationship to T7, and moves more easily in these directions T6 E S L RL T6 restricted F SR RR =

=

Position

The patient is seated (or standing), and the physician stands behind the patient (Fig. 56. 1 4) . Procedure

To resrore physiologic range of motion

to

the T6-7 joint :

1 . The patient places his or her hands behind the neck with the fi ngers interlaced. 2. To conrrol the movements of the patient, place one arm under

864


FIGURE 56.15. R i b

1 techn ique, prone.

upward and backward where the arms contact the patient's axilla (a lifting motion) . 9. Retest the range of motion. Ribs

Rib 1 : Prone Diagnosis

FIGURE 56.14. T horacic m u l t i p l e p l a n e technique, extension.

3.

4.

5.

6.

7. 8.

the axilla on on� side of the patient and place the fingers of that extremiry on the dorsal aspect of the patient's wrist. The physician places a small pillow berween his or her epi gastric region (or chest) and the segmem to be treated (T6 vertebral unit). The physician puts h is or her other arm under the patient's other axilla and places the fingers of that hand on the dorsal aspect of the patient's wrist. Note: Do not use the hand con tacts to pull down and induce spinal Aexion (the hand only rests on the patient's wrists). The physician induces Aexion of the patient's spine by poste rior translation at T6. This is accomplished when the patient slumps forward, letting the "tummy drop toward the Aoor," and when the physician pulls the patient's upper body back ward over the pillow fulcrum. The physician induces right side-bending through left trans latory motion at T6. The pressure of the pillow contact itself will induce right rotation. The patient inhales and exhales, relaxes the shoulders and back, and "lets the tummy drop toward the Aoor." At end-expiration, the physician asks the patient to bring the elbows together. As localization occurs in the tissues anterior to the pillow fulcrum, an anterior and superior high-velociry/low-amplitude thrust through the epigastrium and the pillow is applied. Simultaneously, the physician lifts

Rib 1 elevated on the left (superior shear, superior translation) Posterior portion (tubercle) ofleft rib 1 appears elevated, with surrounding tissue texture changes and tenderness Cervicothoracic j unction is usually side-bent right3 Elevated left rib 1 Caudad motion of right rib I tubercle is restricted when pres sure is applied Position

The patient is prone, and the physician stands to the right side of the patient at the head of the table (Fig. 56. 1 5) . Procedure

To restore physiologic range of motion to the T 1 I rib 1 costover tebral joint: 1 . The physician places his or her right hand on the left side of the patient's head and the thenar eminence or hypothenar eminence (pisiform region) of his or her left hand over the tu bercle of the left rib 1 . Note: The physician's arms are crossed, with the right arm superior. 2. Using the chin as a pivot, the patient's head is rotated left to obtain ligamentous tension locking. 3. The physician then side bends the patient's head and neck to the right through the level of T 1 to the dysfunctional joint space.

3These same findi ngs are also present with a fascial dysfunction involving

presence of left side-bend i ng and rotation at the cervicothoracic junction (thoracic inlet).

56. Thrust (High- Velocity/Low-A mplitude) Techniques

865

4. The patient is asked ro inhale and exhale several times. The physician takes up the tissue slack as the patient exhales, lo calizing the forces. 5. The physician applies a high-velocityllow-amplitude thrust through his or her left thenar eminence contact with the vec ror directed in a posteroanterior and caudad direction. The hand on the head stabilizes it as the thrust with the other hand is transmitted through the tubercle of the patient's first rib. A small amount of right rotation ro Tl is induced by slight opposite rotarory motions through the pisiform or thenar em inence on the left transverse process of T I while the hand on the head induces slight rotation i n an opposite direction. 6. Retest the range of motion. Rib 1: Supine

FIGURE 5 6 . 1 6 . Rib

1 techniq ue, supine.

Diagnosis

Rib 1 elevated on the right (superior shear, superior transla tion) Posterior portion (tubercle) of right rib 1 appears elevated, with surrounding tissue texture changes and tenderness Cervicothoracic junction is usually side bent left4 Elevated right rib I Caudad motion of right rib 1 tubercle is restricted when pres sure is applied Position

The patient is supine, and the physician stands at the head of the table (Fig. 56. 1 6) .

Rib 1: Seated Diagnosis

Right rib 1 is elevated on the right (superior shear, superior translation) Posterior portion (tubercle) of right rib 1 appears elevated, with surrounding tissue texture changes and tenderness Cervicothoracic j u nction is usually side bent left5 Elevated right rib 1 Caudad motion of right rib 1 tubercle when pressure is applied Position

Procedure

To resrore physiologic range of motion to the T l Irib I cosrover tebral joint: 1.

2. 3. 4. 5. 6. 7.

8.

The physician places the M P or PIP joint of his or her right index finger on the upper surface of the tubercle of the right first ri b. The physician's left hand cups the left side of the patient's head. The physician rotates the patient's head and neck left co the level of the Tl /rib 1 joint space. The patient's head and neck are then side bent right co the level of the tubercle. The patient's head and neck are then flexed co the level ofT l . The patient is asked ro inhale and exhale. The physician lo calizes the forces as the patient exhales. A high-velocityllow-amplitude thrust with the physician's right hand contact is directed medially, inferior, and poste rior. The index finger of this hand is the fulcrum that side bends the head and neck co the right by using a component of flexion and slight rotation co the left. Retest the range of motion.

4These same findings are also present with a fascial dysfunction i nvolving

presence of right side-bending and rotation ar rhe cervicorhoracic j uncrion (rhoracic inlet).

The patient is seated, and the physician stands behind the patient (Fig. 56. 1 7) . Procedure

1 . The physician places his or her left foot on the table and drapes the patient's left arm over a pillow that has been placed on the physician's left knee or thigh. 2. The physician's left elbow is placed in front of the patient's shoulder with the forearm contacting the left side of the pa tient's face and the hand over the cop of the head. 3. The physician's right palm is placed on the patient's right shoulder with the first metacarpophalangeal j oint contacting the tubercle of rib 1 . 4. The patient's head and neck are slowly rotated and side bent right CO the level of the rib, with simultaneous downward pres sure on the rib. A slight translacory movement of the patient left and posteriorly (using the physician's left knee contact) may aid in localization. 5. The patient is asked co inhale and exhale. The physician lo calizes the forces as the patient exhales. Sometimes a slight rotation of the head and neck co the left may further free the first rib head.

5These same findings are also presenr wirh a fascial dysfuncrion involving

p resence of lefr side-bending and roration ar rhe cervicothoracic j u ncrion (thoracic inler).

866

ViI. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment

'FIGURE 56. 1 7. R i b

1 techn ique, seated . FIGURE 56.18. R i b

6. A high-velociryllow-amplirude thrust is performed through the physician's right MP joint, with a vector directed pos teroinferiorly and medially while right side-bending/rotation of the neck is slightly increased. 7. Retest the range of motion. Rib 2: Seated Diagnosis

Righ t rib 2 is elevated on the right Posterior portion (tubercle) of right rib 2 appears elevated, with surrounding tissue texture changes and tenderness Right rib 2 is elevated Caudad motion of right rib 2 tubercle when pressure is appl ied

2 techniq ue, seated.

to the right to the level of the rib (reducing inAuence of the scalenes) while exerting simultaneous downward pressure on the patient's right first rib with the fulcrum. The rotation movemenr ceases when the rib exh ibits less resistance to this downward pressure. 5. The patient is asked inhale and exhale. The physician localizes forces as the patient exhales. 6. A h igh-velociryllow-ampli rude thrust applied through the physician's right M P joint contact is directed inferiorly and medially with a small posterior vector. 7. Retest the range of motion. Ribs 2- 1 0, Inhala tion or Exhalation: Supine

Position

The patient is seated, and the physician stands behind the patienr ( Fig. 56. 1 8) . Procedure

restore physiologic range of motion to the rib 2 costotransverse joint:

To

The physician places his or her left foot on the table and drapes the patient's left arm over a pillow that has been placed on the left knee or thigh of the physician. 2. The physician places his or her left elbow in front of the patient's left shoulder with the forearm contacting the left side of the patient's face and places the hand over the top of the patient's head. 3. The physician's right hand (dorsum up) is placed on the patient's right shoulder with the thumb contacting the ru bercle of the patient's rib 2 . The thumb contact is the fulcrum. 4. The patient's head and neck are slowly rotated left, disengaging the rib head as T 1 rotates away from it. The region is side bent I.

Diagnosis

Exhalation lesion: the

. . IS more promInent

posterior inferior border of the rib angle

inhalation lesion: the posterior superior border of the rib angle is more prominent Exhalation rib Inhalation rib Rib restricted in exhalation (If an inhalation lesion, exhalation motion is restricted) Rib restricted in inhalation (I fan exhalation lesion, inhalation motion is restricted) Position

The patient is supine, and the physician stands on the opposite side of the patient's dysfunctional rib. Procedure

To restore physiologic range of motion to the costovertebral joinr : 1 . The physician asks the patient to cross his or her arms with the opposi te arm superior and the hands on the lateral aspects of


867

the shoulders. (This can also be accomplished with the hands interlaced behind the neck.) 2. The physician's cephalad hand rotates the patient's opposite shoulder and thorax: toward him or her. 3. The physician reaches across and under the patient, placing the thenar emi nence of his or her caudad hand posterior to the posterior angle of the dysfunctional rib. 6 4. With the patient's head, neck, and shoulders supported by the physician's cephalad hand, the patient's spine is flexed toward, and slightly side bent away from the dysfunctional rib. 5. Forces are localized by rolling the patien t's body over the fulcrum, past the midline, focusing the weight between the epigastrium and the thenar eminence. A pillow between the physician's epigastric region and the patient's elbows may be used if desired. 6. The patient is asked to deeply inhale, and the physician in creases the localization as the patient exhales. 7. A high-velocityllow-amplitude thrust at the end of exhala tion is delivered through the physician's epigastric contact and the patient's thorax:. The thrust has a vector that is directed straight down and is produced more by a momentary drop of your body weight than by squeezing or compression of the patient. 8. Retest the rib angle for tenderness and for motion during breathing.

FIGURE 56.19. Ribs

3.

4.

Ribs 2- 1 0: Crossed Hand, Prone Diagnosis

Rib 8 on the right is held in exhalation Lateral or anterior elevation (during inhalation) in comparison with the corresponding contralateral rib (Rib 8 major motion bucket-handle mechanics; minor mo tion pump-handle mechanics) Exhalation right rib 8 Right rib 8 restricted in inhalation

5. 6.

=

=

Position

The patient is prone, and the physician stands o n the side of the patient's dysfunctional rib (Fig. 56. 1 9) . Procedure

To restore physiologic range of motion to the rib at the costover tebral articulation, allowing free lateral and anterior elevation of the rib during the inhalation phase: 1 . Ask the patient turn his or her head away and place arms at the sides. 2. The physician moves the patient's torso and, if necessary, hips

7.

8.

2- 1 0 technique, prone.

away from him or her to induce left side-bending, with the apex at the level of the dysfunctional rib. The physician's hypothenar eminence or pisiform region of the right hand contacts the posterior right eighth rib, with fingers pointing caudad. The palmar surface of the physician's left hand contacts the paravertebral area over the opposite rib (left rib 8), with fingers pointing toward the patient's head. This hand will serve as a stabilizing force. (This is a crossed-arm technique.) The patient is asked to inhale, then exhale through more than one cycle as the physician localizes the forces. Pressure is applied i n a caudad and anterior vector with the physician's right hand and toward the floor over the rib and paravertebral area with the left hand. At end of exhalation, a high-velocity/low-amplitude thrust is applied with the physician's right hand contan and has a vector that is directed caudally and anteriorly. Retest the range of motion.

Ribs 1 1 and 1 2: Prone Diagnosis

Rib l I on the right is held in inhalation; its position is more posterior than that of the opposite rib The tenth intercostal space is decreased in comparison to the contralateral side Inhalation right 1 1 th rib Right 1 1 th rib is restricted exhalation (anterior caliper motion on exhalation but it will rotate backward on inspiration) and decreased lowering during exhalation (bucket-handle motion)

6The actual contact and vecror of force applied ro this portion of the rib ro

engage the barrier benefits from applying pump-handle mechanics (where,

in inhalation, the anterior portion of the rib is elevated while it is depressed in back) . Apply your conract in a manner that takes the slack out of the soft

tissues and posterior costal articulations, drawing inferiorly on the superior rib border for exhalation somatic dysfunction, or pushing superiorly o n the

inferior border fo r inhalation somatic dysfunction.

Position

The patient is prone, and the physician stands to the left side (opposite the dysfunctional rib) of the patient, at the level of the patient's hip (Fig. 56.20).

868


Thoracolumbar Region

Type I: Lateral Recumbent (Posterior Transverse Process Down) (n O-L5) Diagnosis

L3 is at the apex of a left side-bending group curve (dextro rocoscoliosis), side-bent left, rotated right in relationship ro L4, and moves more easily in these directions L3 N S L RR L3 restricted N SR RL =

=

Position

The patient is lateral recumbent, posterior transverse pro cess down, and the physician stands in front of the patient (Fig. 56. 2 1 ) . FIGURE 56.20. R i bs

1 1 - 1 2 tec h n i q ue, prone.

Procedure

To resrore left side-bending and left rotation with the patient in a (sagittal) neutral position:

Procedure

1.

To rescore physiologic range of motion co the rib at its coscovertt bral articulation so that it will exhibit both anterior and posterior rotacory caliper motion and increased lateral depression (bucket handle) during exhalation:

2.

l . The physician side bends left the patient's thorax by pulling fi rst the feet, then the shoulders, co the left. The convexiry has its apex at the dysfunctional rib. 2 . For this inhalation rib treatment, the patient's right arm is at his or her side. (If th is were treatment for a right exhalation right 1 1 th rib, the right arm would be hyperabducted co the side of the patien t's head.) 3. The physician contacts the most medial aspect of the patient's right rib 1 1 with the thenar eminence of the cephalad hand. 4. The physician's caudad hand grasps the patient's opposite an terior superior iliac spine. 5. A longitudinal stretch is applied between the hand contacts sufficient co take the slack out of the tissues. This will usually lift the hip off the table by a few inches. 6. The physician's cephalad hand pushes the right 1 1 th rib ante rior, lateral, and superior, localizing the disengagement force on the rib. 7. The patient is asked co inhale and then exhale. The physician further localizes the forces as the patient exhales. 8. At end of exhalation, a h igh-velociry/low-amplitude thrust is appl ied through the thenar eminence of the physician's cepha lad hand with a veccor di rected anteriorly, laterally, and superi orly. Alternative: Ask the patient to cough instead of applying the thrust. 9. Retest the range of motion. Note: The hip is used co pull the lateral aspect of the rib pos teroi nferiorly through stretch of the quadratus lumborum muscle and associated fascia. The cephalad hand's superior thrust will corque the medial aspect of the rib around an effective fulcrum, which is slightly lateral co your hand.

3.

4. 5. 6. 7. 8.

The physician flexes the patient's legs until motion is palpable at the L3-4 joint space. The inferior leg (the leg next ro the table) is straightened. The foot of the superior leg is placed behind the knee of the inferior leg. The physician anteriorly rotates the patient's rorso by pulling anteriorly on the right (lower) arm until rotacory motion is palpable at L3 . That same arm is then pulled caudad ro induce right side bending down ro the L3-4 joint space. The physician's caudad forearm is placed over the area infe rior co the patient's iliac crest. The physician's cephalad forearm is placed in the patient's uppermost axilla. The fingers of one or both hands monicor the forces localized ar the L3-4 articulation. The patient is asked co inhale and exhale. The physician con tinues co localize the forces as the patient exhales and observes

FIGURE 56.21 . Lumbar type I tech n i q u e, posterior tra nsverse process down.


the direction in which the pelvis moves with exhalation. The structure of the patient's facets determines the optimal di recrion of thrust. I f the primary motion observed is rotation, then the thrust will have more of a rotatory component. If the primary motion is side-bending, then the thrust should have more of a side-bending component. 9. A high-velociryllow-amplirude thrust is applied with the physician's caudad forearm contact and has a vector toward the physician's knees. The thrust is by momentarily drop ping the patient's body weight, thereby rotating the lumbar region left and side-bending right up through L3. Although the cephalad arm mainly serves as a stabilizing force, it may simultaneously add a small component of left rotation and right side-bending. Note: Too much torsion by opposite mo tions can inj ure the patient's shoulder region. 1 0. Retest the range of motion. Type I: La teral Recumbent (Posterior Transverse Process Up) (T1 O-L5)

4.

5. 6. 7.

8.

9. 1 0.

Diagnosis

L3 is at the apex of a left side-bending group curve (dextro roroscoliosis), is side-bent left, rotated right in relationship to L4, and moves more easily in these directions L3 N SLRR L3 restricted N SLRR =

11.

869

The physician places the forearm of his or her caudad arm over an area inferior to the iliac crest. The physician places his or her cephalad forearm in the pa tient's uppermost axilla. The fingers of one or both hands monitor motion at the L3-4 articulation. Using slight anterosuperior pressure through h is or her cau dad forearm, the physician rotates the patient's h ips and lum bar spine to the left to the point where rotation at L4 is pal pated. Simultaneously, the thoracolumbar spine is rotated to the right by light pressure through the forearm that is contacting the patient's axilla. The physician slightly rotates the patient toward him or her while maintaining the localization (side-bending, Aexion, rotation). The patient is asked to inhale and exhale. The physician takes up tissue slack and maintains localization during exhalation. A high-velociryllow-amplirude thrust through the physi cian's caudad forearm, by momentarily dropping his or her body weight, is directed toward the table, producing right side-bending. The physician's cephalad arm mainly stabil izes the patient's torso, although a slight simultaneous compo nent of left rotation and right side-bending may occur. Retest the range of motion.

=

Position

The patient is lateral recumbent with the posterior transverse process of the dysfunctional unit "up." The physician stands in front of the patient (Fig. 56.22). Procedure

To restore physiologic range of motion to the L3-4 joint: 1 . The physician Aexes the patient's legs until motion is palpated at the L3-4 joint space. 2. The inferior leg is straightened, and the foot of the superior leg is placed behind the knee of the other leg. 3. The physician pulls the patient's left arm superiorly and slightly forward to reduce left side-bending (and/or induce right side-bending) .

FIGURE 56.22. Lumbar type I tech n i q ue, posterior transverse process up.

Type I/, Extension: La teral Recumbent (Posterior Transverse Process Up) (T1 0-L5) Diagnosis

L3 is extended, side-bent right, rotated right in relationship to L4, and moves more easily in these directions L3 E SR RR L3 restricted F SLRL =

=

Position

The patient is left lateral recumbent, and the physician stands in front of the patient (Fig. 56.23). Procedure

To restore physiologic range of motion to the L3-4 joint:

F I G U R E 5 6 . 2 3 . L u m b a r type I I tech n i q ue, posterior transverse process up.

870


1 . The physician flexes the patient's legs until motion is palpated at the dysfunctional transverse process (L3). 2. The inferior leg is straightened and the superior (upper most) foot is hooked into the lower leg's popliteal fossa. 3. The physician rotates the patient's torso (by pulling the left arm) down to, but not including, the dysfunctional vertebral segment as the caudad hand monitors the posteriorly rotated transverse process. 4. The physician places his or her caudad forearm on the pa tient's il iac crest j ust superior to the posterior superior iliac spines (PSIS). At least one finger continues to monitor the dysfunctional segment. 5. The physician's cephalad arm is placed in the patient's axilla beneath the patient's upper arm to stabilize the thorax. 6. The patient is slightly rotated toward the physician while lo calization is continued (side-bending, flexion, rotation) . 7. The patient is asked to inhale and exhale. The physician takes up tissue slack and maintains localization during exhalation. 8. The physician performs a high-velocity/low-amplitude thrust through the caudad forearm by momentarily dropping his or her body weight toward the floor, thereby side bending the lumbar region to the left. The physician's cephalad arm mainly stabilizes the torso, although a slight simultaneous component of right rotation and right side-bending may occur. 9. Retest the range of motion. Type I/, Extension: La teral Recumbent (Posterior Transverse Process Down) (T1 O-L5) Diagnosis

L3 is extended, side-bent right, rotated right in relationship to L4, and moves more easily in these directions L3 E SR RR L3 restricted F SLRL =

=

Procedure

1 . The patient's legs are flexed until motion is palpable at the L3-4 joint space. 2. The inferior leg is straightened and the foot is placed behind the knee of the other leg. 3. The physician pulls the patient's right arm cephalad and up ward to induce left side-bending to the L3-4 joint space. If additional flexion is desired, the thoracic area may be brought anteriorly through a pull on the shoulder. 4. The physician places his or her caudad forearm inferior to the patient's iliac crest. 5. The physician's cephalad forearm is placed in the patient's uppermost axilla. 6. The patient is asked to inhale and exhale. The physician mon irors motion at the L3-4 articulation while taking up tissue slack and maintaining localization during exhalation. 7. A high-velocityllow-amplitude thrust through the physician's caudad forearm contact is directed roward the patient's head and downward to encourage L3 side-bending. The patient's cephalad arm functions as a stabil izer of the patient's upper torso during the thrust. 8. Retest the range of motion. Note: This produces left side-bending and right rotation of the pelvis (rotation roward the physician). The rotation of the pelvis is transmirred through L4, giving a relative left rotation ro L3. Type /I, Flexion: Lateral Recumbent (Posterior Transverse Process Down) (T1 0-L5) Diagnosis

L 1 is side-bent right, rotated right in relationship ro L2, and moves more easily in these directions Ll F SR RR L1 restricted E SL RL =

=

Position

The patient is right lateral recumbent (posterior transverse pro cess down) , and the physician stands in front of the patient (Fig. 56. 24) .

Position

FIGURE 56.24. Thoracolumbar type II tec h n i q ue, posterior transverse process down.

FIGURE 56.25. Lumbar type I I tec h n i q u e : flexed, posterior transverse process down.

The patient is right lateral recumbent (posterior transverse pro cess down) , and the physician stands in front of the patient (Fig. 56.25).

56 Thrust (High- Velocity/Low-Amplitude) Techniques

87 1

ProcedUIe

To restore physiologic range of motion to the L l -2 joint: I.

2. 3.

4.

5. 6. 7. 8.

9.

1 0.

The physician flexes the patient's legs until motion can be palpated at the L J -2 joint space. This locks the lower lumbar facets. The inferior leg is straightened, and the foot of the superior leg is placed behind the other leg. The physician induces extension to the L l -2 joint space by pushing his or her elbow of the caudad arm in a posterior direction while palpating the Ll area for motion using the caudad hand. The physician then pulls the patient's right arm cephalad and upward to induce left side-bending and rotation down to the L J -2 joint space. Be sure not to rotate below L l . The physician places his o r her caudad forearm inferior to the patient's iliac crest. The cephalad forearm is placed in the patient's uppermost axilla. The patient is asked to rotate his or her head to the left to rotate the neck and trunk to the left. The patient is asked to inhale and exhale. The physician monitors motion at the L3-4 articulation while taking up tissue slack and maintaining localization during exhalation. The physician performs a high-velocity/low-amplitude thrust with his or her caudad forearm contact. Direction of the vector of force is toward the patient's head and down ward. This rotates the patient's pelvis toward the physician, producing left lumbar side-bending and right rotation of the pelvis. The rotation of the pelvis is transmitted through L2, giving a relative left rotation to L I . The physician's cephalad arm functions as a stabilizer of the upper torso. Retest the range of motion.

Pelvis

Anterior Sacrum, Right (Left Rota tion on Left Oblique Axis) Diagnosis

The sacral sulcus is deep on the right, with associated tissue texture changes and tenderness The left inferolateral angle is posterior (the sacrum is effectively rotated left, side-bent right) Right anterior sacrum (or) Sacrum rotated left on a left oblique axis Posterior motion at the right sacral sulcus is restricted when anterior pressure is applied to the left inferolateral angle Sacrum restricted in rotating right on a left oblique axis Position

The patient is left lateral recumbem, and the physician srands in front of the patient (Fig. 56.26).

FIGURE 56.26. Anterior sacrum right tech n ique.

I.

2. 3.

4.

5. 6.

7.

The physician flexes the patient's hips un til motion is palpated at the patient's right sacral sulcus. The physician drops the patient's upper leg and foot off the side of the table to induce left side-bending. The flexor surface of the physician's caudad forearm is placed parallel to the lower spine, posterior to and crossing the il iac crest. This will brace the pelvis. The physician's cephalad forearm is placed through the pa tient's uppermost axilla, with the hand posterior and inferior to the patient's shoulder and the elbow braced against the an terior portion of the patient's shoulder. The shoulder is rotated posteriorly to stabilize the patient. The patient is asked to inhale and exhale. The physician mon itors the localization of forces at the end of exhalation. A high-velocity/low-amplitude thrust with the physician's cau dad arm is performed and follows a circular motion with the ilium, rotating it anteriorly from behind. Retest the range of motion.

Posterior Sacrum, Left (Left Rota tion on Left Oblique Axis) Diagnosis

Tissue texture change and tenderness at the left inferior pole of the SI joint The sacral sulcus is deep on the right The left inferolateral angle is posterior (the sacrum is effectively rotated left, side-bent right) Posterior sacrum, left (or) Left sacral rotation on a left oblique axis Restricted: Cephalad and downward motion at the left inferior pole of the SI joint when anterior pressure is applied to the left inferolateral angle (or) Restricted in rotation right on a left oblique axis Position

Procedure

To restore physiologic range of motion to the sacroiliac joint:

The patient is supine, and the physician stands on the righr side of the patient (Figs. 56.27 and 56.28).

872


5. 6. 7.

8.

FIGURE 56.27. Posterior sacrum left tec h n i q u e show i n g hand place ment on the patient's chest.

hand may need to be used to stabilize the shoulder during this rotation to avoid Aexion. The physician's caudad hand is placed over the left il iac crest. Right rotatior, is continued from above until the force is felt ro accumulate at the left iliac crest. A high-velocity/low-amplitude rotarory thrust with the physi cian's cephalad arm rotates the opposite shoulder anteriorly from behind while a small counterforce is exerted on the far ilium through the physician's caudad hand. Note: increased force at the ilium will rarely increase the effectiveness of this technique. Retest the range of motion.

Note: A posterior sacrum (right) has the same motion descrip tion as an anterior sacrum (left) (rotated right, side-bent left) , but the restriction and tissue change is dominant on the poste rior sacrum side. The technique localizes force to the posterior sacrum side. Anteriorly Rota ted Ilium (Innominate)

Procedure

rotate the sacrum right and side-bend it left by applying force from above down through the sacrum with a counterforce on the left ilium, localizing force co the left sacroiliac j oint:

To

The physician moves the patient's shoulders so that his or her upper rorso is side-bent left and the shoulder closest co the physician is in the center of the table. 2. The patient is asked co interlace his or her fingers behind the neck. 3. The physician inserts his or her cephalad hand through the posterior aspect of the opposite axilla so that the dorsum of the hand is contacting the sternum (Fig. 56.27). 4. Right rotation of the patient is i ntroduced through the physi cian's cephalad arm, pivoting the patient around the shoulder closest to him or her. Do not Aex the patient. The caudad 1.

Diagnosis

Standing Aexion test is positive on the side of dysfunction The anterior superior iliac spine (ASIS) is more caudad on the dysfunctional side The ipsilateral pubic ramus is more caudad (not always detectable) The ipsilateral PS IS is more cephalad Anterior innominate (or) Innomi nate anterior Restricted in backward rotation (posterior) of the ilium about a transverse axis Position

The patient is lateral recumbent, and the physician stands facing the patient ( Fig. 56. 29) . Procedure

To mobilize the ilium in a posterior rotatory fashion to eliminate the restriction of motion:

FIGURE 56.28. Posterior sacrum left tec h n i q u e showing hand place ment on the ASIS of i l i u m ( h i p bone).

F I G U R E 56.29. Anteriorly rotated i l i u m tech nique.


1 . The physician flexes the patient's legs to 90 degrees and then drops the upper leg off the table in front of the lower leg. 2. The physician contacts the ilium with his or her caudad fore arm on a line berween the PSIS and the greater trochanter; the thenar eminence of the physician's cephalad hand is placed on the anterior surface of the ASIS. 3. Firm pressure is applied with the physician's caudad hand contact in a direction that follows the line of the upper femur. The physician should feel as though this force is posteriorly rotating the entire innominate (i.e., backward. rotation on the transverse axis). 4. The physician's cephalad hand places a force on the upper shoulder, carrying the shoulder backward until force is local ized to the SI joint. 5 . The patient is asked to inhale and exhale. The physician lo calizes forces as the patient exhales. 6. At end-exhalation, a h igh-velocity/low-amplitude anterior ro tatory thrust is applied that is directed down the shaft of the femur. Because the thrust is below the axis of rotation, the ilium rotates posteriorly. 7. Retest the position and range of motion.

873

Procedure 1.

2.

3. 4.

5. 6. 7.

The physician straightens the patient's lower leg and flexes the hip and knee of the upper leg. The foot of that leg is placed in the popliteal fossa of the lower leg. The physician contacts the PSIS of the upper ilium with the palmar surface of his or her caudad forearm (or thenar eminence). The physician's cephalad hand or forearm is placed on the patient's upper shoulder to stabilize the patient. The physician applies firm pressure on the PSIS with his or her caudad hand contact, directed toward the patient's umbilicus. The physician should sense this force is anteriorly rotating the entire innominate (i.e., forward rotation on the transverse axis) . The patient is asked to inhale and exhale. The physician lo calizes forces as the patient exhales. At end-exhalation, apply a high-velocity/low-amplitude ante rior rotatory thrust directed toward the umbilicus. Retest the position and range of motion.

Superior Iliac Shear (Upslipped Innomina te) Diagnosis

Posteriorly Rotated Ilium (Innomina te) Diagnosis

Standing flexion test is positive on the side of dysfunction The ASI S is more cephalad The ipsilateral pubic ramus is more cephalad (may not be detectable) The ipsilateral PSIS is more caudad Posterior innominate (or) Innominate posterior Restricted anterior rotation of the ilium about a transverse axis

The standing flexion test is positive on the dysfunctional side The ASIS, pubic ramus, and PSI S are all superior on the dysfunctional side Superior innominate shear (or) Upslipped innominate Restricted downward motion of the innominate

Position

The patient is supine, and the physician stands at the feet of the patient (Figs. 56.3 1 and 56.32).

Position

The patient is lateral recumbent, dysfunctional side up, and the physician stands facing the patient (Fig. 56.30).

FIGURE 56.30. Posteriorly rotated i l i u m tech nique.

FIGURE 56.3 1 . Superior i l iac shear tec h n i que.

874


FIGURE 5 6 . 3 3 . Posterior rad i a l head tec h n ique. FIGURE 56.32. Superior i l iac shear tech n i q ue.

Procedure

To mobil ize the S1 joint so that increased downward motion is possible: 1 . The physician grasps the patien c's leg on the dysfunctional side superior to the ankle. 2. The patieJ1 ('s leg is flexed sl ightly, and traction and internal rotation of the leg are applied. 3. The patieJ1( is asked to relax the knee and then the hip. The physician instructs the patient to i nhale and exhale as he or she local izes the traction forces to the ilium. 4. On end-exhalation, the physician applies a high-velocityllow ampli tude tractional force (tug) to the leg. 5. Retest the range of motion. Upper Extremity

Posterior Radial Hea d Diagnosis

Tenderness over the radial head Posterior glide of the radial head is free Posterior radial head (or) Radial head posterior Radial head restricted in anterior glide Position

The patient is seated, and the physician stands on the dysfunc tional side of the patienc ( Fig. 56.33). Procedure To

increase the range of anterior glide:

The physician grasps the patient's flexed elbow with one hand, placi ng his or her thumb over the posterolateral aspect of the radial head. 2. The physician grasps the wrist with his or her other hand so that the thumb is over the patient's dorsum of the distal ulna. I.

3. The physician supinates the patient's wrist with his or her distal hand while extending the elbow with his or her proximal hand. 4. JUSt before reaching complete extension, a high-velocityllow amplitude thrust is applied on the radial head through the physician's thumb and is di rected in a ventral direction. Simul taneously with this thrust, the physician's distal hand provides a slight i ncrease in the supination of the patient's forearm . 5 . Retest the range of motion. Alternate method: If the radial head restriction is greater in pronation, treat with the forearm pronated. Abducted Elbow (Humeroulnar) Diagnosis

The angle berween the ulna and humerus is increased (in creased carrying angle) Abduction places pressure on the proximal radius, forcing it distally in relation to the ulna and producing radiocarpal adduction Abducted elbow (or) Ulnar abduction with medial glide Restricted ulnar adduction and radiocarpal abduction Position

The patient is seated, and the physician stands on the dysfunc tional side in front of the patient (Fig. 56.34). P rocedure

To increase adduction of the elbow and radiocarpal abduction: Note: Elbow restriction should be treated before wrist rest[Jct)ons. 1 . The physician places the patient's wrist of the dysfunctional extremity berween his or her arm and lateral chest wall. 2. The physician grasps the elbow with both hands, thumbs in the antecubital region over the proximal radius and ulna, avoiding direct pressure over the ulnar nerve.

56. Thrust (High- Velocity/Low-Amp litude) Techniques

875

FIGURE 56.35. Wrist tech n iq u e .

Note: Elbow restriction should be treated before wrist restric tions. l. FIGURE 56.34. Abducted e l bow tec h n i q u e .

2. 3. With the elbow close to ful l extension (slight flexion i s required to avoid extension locking), the physician applies a lateral translatory force to take the ulna into adduction (a varus force) . 4. A high-velocity/low-amplitude thrust is applied in the same vector when the physician reaches the restrictive barrier. 5. Retest the range of motion.

3. 4.

5. Wrist Diagnosis

Increased adduction, abduction, flexion, or extension of the wrist The position of the involved bones may not be demonstrably altered, but motion will be freer in one direction and restricted if attempted in the opposite direction Wrist abducted, adducted, flexed, or extended Radiocarpal abduction with medial carpal glide (or) radio carpal adduction with lateral carpal glide, (or) radiocarpal flexion with dorsal carpal glide, (or) radiocarpal extension with anterior carpal glide Wrist or radiocarpal joint restricted in motion opposite to the increased or free motion This example: wrist flexed (or) Radiocarpal j oint flexed with dorsal carpal glide Position

The patient is seated or supine, and the physician sits or stands facing the patient (Fig. 56.35). Procedure

To restore physiologic range of motion to the radiocarpal joint:

The physician grasps the patient's dysfunctional wrist with both hands, with the fingers under the palm of the hand on the medial and lateral sides. The physician's thumbs are on the dorsal surface of the pa tient's hand, with the pads over the dorsal surface of the carpal bones. (Usually the l unate has the somatic dysfunction .) The physician applies traction and continues it while produc ing circumduction of the patient's wrist. The physician continues the traction and completes the mo tion by dorsiflexing the wrist as the thumbs press fi rmly down ward (anteriorly) on the carpal bones. Retest the range of motion.

Note: This is actually an articulatory technique that usually works smoothly, especially if the traction is steady and continuous throughout. If the physician feels it is necessary, a thrust with minimal force can be added as the restrictive barrier is reached. This technique may be modified to treat the restrictions ofmotion of other individual carpal bones by superimposing the thumbs over the involved carpal bone and exerting the final man ipulation (see step four above) that will mechanically reverse the glide that is present, as determined by the diagnosis. Lower Extremity

Posterior Fibular Head Diagnosis

Palpable muscle/connective tissue tension in the interosseous region between the tibia and fibula Possible posterior displacement of the fibular head; posterior glide is free Posterior fibular head (with posterior glide of fibular head) (or) fibular head posterior Fibular head restricted in anterior glide This example: posterior right fibular head (with posterior glide of fibular head)

816


an anterior cou nterforce to the fibular head with the fi rst M P joint of the cephalad hand. 6. Retest the range of motion. Note: This technique can be done prone with slight modifi catIons. An terior Fibular Head Diagnosis

Palpable muscle/connective tissue tension in the interosseous region between the tibia and fibula Possible anterior displacement of the fibular head; anterior glide is free Anterior fibular head (or) Fibular head anterior Fibular head restricted in posterior glide This example: anterior right fibular head Position

The patient is supine, and the physician stands at the foot of the table on the side opposite the dysfunction (Fig. 56.37). Procedure

To increase the posterior glide of the fibular head: l.

2. 3. 4. FIGURE 56.36. Posterior f i b u l a r head tech n iq u e .

Position

5.

The patient is supine, and the physician stands by the table on the dysfunctional side of the patient ( Fig. 56.36) . Procedure

6.

The physician places a pil low below the patien t's dysfunctional knee to avoid locking it in extension. The physician grasps the leg immediately proximal to the ankle with his or her caudad hand. The thenar eminence of the physician's cephalad hand is placed on the anterior aspect of the patient's fibular head. The physician internally rotates the patient's ankle to draw the distal fibula anteriorly (and move the fibular head to its restrictive barrier through the reciprocal motion principle). The physician's cephalad hand applies a high-velocityllow amplitude thrust in a posterolateral vector to the fibular head while the caudad hand simultaneously applies a slight internal rotation counterforce to the ankle. Retest the range of motion.

To increase the anterior glide of the fibular head: I.

2.

3. 4.

5.

The physician Aexes the dysfunctional hip and knee. The physician's cephalad hand is placed in the patient's popli teal space, palm upward, with its fi rst M P joint posterior to the fibular head. (Avoid direct pressure over the common peroneal nerve.) The physician grasps the patient's leg proximal to the ankle with his or her caudad hand. The patient's knee is Aexed to the point where the physician feels pressure of the fibular head on his or her fi rst M P joint. The physician simultaneously externally rotates the ankle us ing the caudal hand contact at the ankle to further localize at the fibular head. The physician applies a high-velocity/low-amplitude thrust by Aexing the leg with his or her caudad hand while applying

FIGURE 56.37. Anterior f i b u l a r head tec h n i q u e .

56. Thrust (High- Velocity/Low-A mplitude) Techniques Anterior Lateral Malleolus Diagnosis

The lateral malleolus (distal fibula) has free anterior glide relative [0 the distal tibia The distal medial border of the talus is more prominent Anterior lateral malleolus Lateral malleolus restricted in posterior glide This exanlple: Anterior right lateral malleolus

877

3. The physician accumulates posterior force on the lateral malle olus by dorsi flexing the foot and applying posterior pressure with the thumbs. 4. Prior [0 full dorsiflexion, the physician applies a high velocity/low-amplitude posterior thrust through his or her thumbs [0 the patient's lateral malleolus. 5. Retest the range of motion. Posterior La tera l Malleolus

Position

The patient is supine, and the physician stands at the foot of the table (Fig. 56.38) . Procedure

To increase posterior motion of the lateral malleolus: The physician grasps the heel with the cupped fingers of the lateral hand. The physician's palm is on the lateral aspect of the heel and the thumb is i n contact with the anterior surface of the lateral malleolus. 2. The physician's other hand grasps the medial side of the ankle, reinforcing the fi rst thumb by placing i ts thumb on [Op of it. 1.

Diagnosis

The lateral malleolus (distal fibula) has free posterior glide relative to the distal tibia The anterior portion of the talus is displaced in a lateral direction Posterior lateral malleolus Lateral malleolus is restricted in anterior glide Position

The patient is prone, and the physician stands at the foot of the table (Fig. 56.39) . Procedure

To increase anterior glide of the lateral malleolus: 1 . The physician grasps the dorsum of the patient's foot with the cupped fi ngers of his or her lateral hand. The thumb is in contact with the posterior surface of the patient's lateral malleolus. 2. The physician's other hand grasps the medial side of the ankle, reinforcing the fi rst thumb by placing its thumb on [OP of it. 3. The physician accumulates an anterior force on the patient's lateral malleolus by plantar flexing the foot and applyi ng an terior pressure with the thumbs. 4. Prior to ful l plantar flexion, the physician applies a high velocityllow-amplitude anterior thrust through his or her thumbs [0 the patient's lateral malleolus. 5. Retest the range of motion.

FIGURE 56.38. Anterior lateral m a l leolus tech n i q ue .

F I G U R E 5 6 . 3 9 . Posterior lateral m a l l e o l u s techn i q ue.

878


FIGURE 56.40. Anterior tibia on talus.

Talotibial Joint: Anterior Tibia on Talus Diagnosis

Tibia is anterior on the talus The ankle prefers dorsiflexion Anterior tibia on talus Talus restricted in gliding posteriorly on the talus (the ankle is restricted in plantar flexion) Position

The patient is supine, and the physician stands at the foot of the table to the side of the somatic dysfunction (Fig. 56.40) . Procedure

To restore physiologic range of motion to the tibiotalar joint (true ankle) , specifically to restore ful l plantar flexion of the ankle (posterior glide of the tibia over the talus) : 1 . The physician grasps the patient's heel and applies traction to it, dorsiflexing the ankle. 2. The physician's other hand grasps the distal end of the tibia, palm over its anterior surface near the talotibial joint, and applies posterior pressure (down, toward the table) . 3 . The physician applies a high-velocity/low-amplitude posterior thrust posteriorly through his or her distal tibial contact as the foot is dorsiflexed with the other hand on the heel. 4. Retest the range of talotibial motion. Talus in Plan tar Flexion: Ankle Tug Diagnosis

Tibia is posterior on the talus The ankle prefers plantar flexion Tal us in plantar flexion (or) Talus plantar flexed with anterior glide Tibia is restricted in gliding anteriorly on the talus The ankle is restricted in dorsiflexion

FIGURE 56.41 . I n verted talus (plantar flexion of talus).

Procedure

To restore physiologic range of motion to the tibiotalar joint (true ankle) , specifically to restore full dorsiflexion of the ankle (anterior glide of the tibia over the talus) : 1 . The physician grasps the patient's foot, curling his or her fifth or fourth finger over the dorsal surface of the head of the talus. The physician also grasps the foot with the other hand and clasps his or her fingers so that the fifth or fourth finger supports the same finger of the opposite hand (over the talar head) . 2. The physician's thumbs are placed over the ball of the foot and the patient's foot is dorsiflexed at the ankle. This dorsiflexion of the ankle is maintained throughout this technique. 3. Traction is applied with continued dorsiflexion and slight eversion at the ankle, until all joint play is out of the ankle joint. 4. The physician applies a high-velocityllow-amplitude tug to re-seat the talus in the mortise of the ankle. 5. Retest the range of talotibial motion. Note: This type of somatic dysfunction may be accompanied by tissue congestion and spasm of the peroneus muscles andlor fibular head somatic dysfunction. Hiss Plantar Whip: Cuboid Diagnosis

The cuboid is displaced inferiorly with the medial edge gliding laterally, flattening the lateral longitudinal arch There is palpable tenderness on the plantar surface of the cuboid Cuboid everted with plantar glide Cuboid is restricted in dorsal glide (motion toward the dorsal surface of the foot) Position

Position

The patien t is supine, and the physician stands at the end of the table (Fig. 56.4 1 ) .

The patient is prone, and the physician stands at the foot of the table, or the patient is standing, and the physician stands or sits behind the patient (Fig. 56.42).

56 Thrust (High- Velocity/Low-A mplitude) Techniques

879

Position

Same as for the cuboid tech nique. Procedure

The physician places his or her thumb on the lateral margin of the plantar surface of the navicular bone and rei nforces that thumb with the other thumb. 2. The whip-like thrust is directed straight down. The thu mb position will direct the force medially. (For preparation, see Hiss Whip: Navicular.) I.

Hiss Plantar Whip: Cuneiforms Diagnosis

The cuneiform bone glides inferiorly (toward the plantar sur face, usually the second of the three bones FIGURE 56.42. Hiss plantar w h i p tec h n i q u e .

Procedure

To restore the cuboid to its appropriate position: 1.

2.

3. 4.

5.

[n the patienr prone position: The physician moves the dys functional leg off the table. In the patienr standing position: The physician asks the patienr to flex the knee on the dys functional side. The physician grasps the patienr's foot with both hands. The thumb of the hand on the lateral side of the patienr's foot is placed on the soft tissues over the medial planrar edge of the patienr's cuboid bone, and the thumb of the other hand lies over the fi rst th umb for reinforcement. The physician induces a series ofoscillating motions, swinging the foot to produce plantar flexion. A high-velociry/low-amplirude thrust is applied by perform ing a whip-like motion in the same direction as above (i.e., the foot is pulled toward the physician in the final motion while the thumbs impart a sudden downward and lateral motion, thrusting the cuboid toward the dorsolateral surface of the patient's foot). Retest the range of motion.

Note: This same tech nique may be used with variations for other somatic dysfunction of the foot (navicular, cuneiforms, metatarsal bases) , as follows.

Position

Same as for the cuboid or navicular techniques. Procedure

1 . The physician places his or her thumb on the plantar su rface of the appropriate cuneiform. 2. The whip-like thrust is directed straight down toward the floor. (For preparation, see H iss Whip: Navicular.)

CONCLUSION

The ultimate effective use of these techniques demands consider able knowledge, skill, and experience. The general principles of HVLA thrust technique are to: Idenrify the motion restriction of somatic dysfunction. 2. Engage the barrier. 3. Apply the activating force, a HVLA thrust. 4. Reevaluate. l.

Careful execution ofhigh-velociry/Jow-amplirude thrust tech niques in the areas presenred can help patients and bring them healing from dysfunction.

REFERENCES I . The G lossary Review Committee of the Educational Council on Osteo pathic Principles. G lossary of Osteopathic Termin ology. I n : Allen TW,

Hiss Plantar Whip: Navicular Diagnosis

The navicular bone is displaced inferiorly, with the lateral edge gliding medially, flattening the lateral longitudinal arch There is palpable tenderness on the planrar surface of the navicular bone Navicular inverted with plantar glide Navicular is restricted in dorsal glide (motion toward the dor sal surface of the foot)

ed. A OA Yearbook and DirectO/y o/Osteopathic Physicians. Chicago, I L:

American Osteopathic Association; 1 994. 2. Greenman PE. Principles o/ManuaI Medicine. Baltimore, M D : Williams & Wilkins; 1 989:94. 3. Bowles CH. Functional tech nique: a modern perspective. I n : Beal MC, ed.

The Principles 0/ Palpatory DiagnoJis and Maniplliative

Technique. Newark, O H : American Academy of Osteopathy; 1 992:

1 74- 1 78 . 4. Hargrove-Wilson. Symposi um: manipulative treatmen t. Met! J A ust. 1 967;24:274-280. 5 . Kappler R . Role of psoas mechanism in low back pain. J Am Osteopath Assoc. 1 973;72.

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6. Korr 1 M . The Collected Papers of Irwin Korr Colorado Springs, CO: American Academy of Osteopathy; 1 979. 7. Korr 1M. Proprioceprors and somatic dysfunction. JAm Osteopath Assoc. 1 97 5 ;74:638-650. 8. Parrerson M . A theoretical neurophysiologic mechanism for faci l i tated segment. J Am Osteopath Assoc. 1 978;77(5):399. 9. Parrerson M . A model mechanism for spinal segmenral facilitation. JAm Osteopath Assoc. 1 976; ( 1 ) :62-72.

1 0. Van Buskirk R. Nociceptive reflexes and the somatic dysfuncrion: a model. J Am Osteopath Assoc. 1 990;(9) :792-809. 1 1 . Kimberly PE. Formulating a prescription of osteopathic manipulative treatment. In: Beal Me, ed. The Principles ofPalpatory Diagnosis andMa nipulative Technique. Newark, OH: American Academy of Osteopathy;

1 992: 1 46- 1 52. 1 2. Hamann G, Haass A, Kujat D, et al. Cervicocephalic artery dissection and chiropractic manipulation. Lancet. 1 993;20:34(8847):764-765 .

MUSCLE ENERGY TECHNIQUES WALTER C. EHRENFEUCHTER MARK SANDHOUSE

HISTORY KEY CONCEPTS • • • • • •

Definition of muscle energy technique Uses of muscle energy technique History of muscle energy technique Physiologic principles of various muscle energy techniques Steps of muscle energy treatment Efficiency factors and contraindications to muscle energy technique

DEFINITION

Muscle energy technique has been defined as a form of osteo pathic manipulative treatment in which the patient's muscles are actively used on request, from a precisely controlled posi tion, in a specific direction, and against a distinctly executed counterforce. Muscle energy techniques involve the patient's active cooper ation to contract a muscle or muscles, inhale or exhale, or move one bone of a joint in a specific direction relative to the adja cent bone. For these reasons, muscle energy cannot be used if the patient IS III a coma, uncooperative, too young to cooperate, or unresponsive (8) .

TECHNICAL PRINCIPLES IN MUSCLE ENERGY TREATMENT

Muscle energy procedures attempt to shorten or lengthen the distance between the origin and insertion of certain muscles, depending on how they are applied. The goals are to: • • • • • •

Decrease muscle hypertoniciry Lengthen muscle fibers Reduce the restraint of movement Produce joint mobilization Improve respiratory and circulatory function Strengthen the weaker side if there is an asymmetry

Muscle energy is a system of osteopathic diagnosis and treatment with roots extending back to AndrewTaylor Still. Dr. Still did not record the way that he treated, preferring to insist that his students conduct an exhaustive study of anatomy while absorbing the os teopathic philosophy. He told students that if they knew anatomy and understood osteopathic philosophy, they would know what to do. As the osteopathic profession sought to increase the ef ficiency of teaching students how to treat patients, certain key individuals made contributions by developing a particular type of technique into a plan. Fred Mitchell, Sr. contributed by de veloping a plan of diagnosis and treatment that he called muscle energy because of its reliance on active patient effort through muscular contraction. M itchell ( 1 ) credited Kettler as the first to focus (his) atten tion on the importance of the vast amount of tissue involved between joints, muscle, and fascia, and the changes it undergoes in the lesioning process. Kettler also emphasized that without es tahlishing bilateral myofascial harmony, the lesion pattern is not obliterated and returns again and again. Mitchell also quoted A. T. Still, showing that he knew about this: "The attempt to restore joint integrity before soothingly restoring muscle and ligamen tous normality was putting the cart before the horse" (1) . Some soutces allege that muscle energy techniques are an out growth of a method developed by T. J. Ruddy (2) called re sistive duction. In Ruddy's method, the physician offers resis tance to the patient's active movement but the patient is required to move quickly, often at a rate of 60 excursions per minute, or equal to the patient's pulse rate. Ruddy's purpose in ask ing the patient to contract muscle quickly and repetitively was twofold: 1 . To increase blood (and other tissue fluid) movements to re move metabolic waste products from the cells and circulate oxygen. 2. To tone inactive muscles that might be weak. Mitchell and Kettler must have been unaware of the proprio ceptive neuromuscular facilitation (PN F) techniques developed by Kabat, KnOtt, and Voss at the Kabat-Kaiser Institute dur ing the late 1940s. These techniques were not widely known.

VII.

882

PNF uses skills to reeducate muscle for several reasons ( 3): "To gain in hib ition in musc les w hich may b e in a pro tec tive

spasm.

"

"To impro ve range (of mo tion ) at an in terverteb ral level.

Mitchell first published his work in the Yearboo k of the Amer ic an Academy of Osteo pathy in 1958 after receiving requests for a written description of the work he had developed in the 1 940s and 1950s. He described one method of correction that used the effort of an extrinsic guiding operator as the activating force plus the intrinsic respiratory and muscular cooperation of the pa tient. He wrote about the direct method treatments of soft tissues (with attention to fasciae) and treatment using Neidner's fascial release prior to articular correction. Muscular energy technique, he wrote, with its many ramifications, is a most useful tool in preparation of the soft tissues. Ligamentous stretching may also be of use before articular correction is attempted ( 1 ) . Lewit and Simons (4) wrote that the use o f post-isometric re laxation was pioneered by Fred Mitchell Sr. and clearly described by F. L. Mitchell J r. as a mobilization technique that applies gen tle force to improve "articulation" and thereby restore previously restricted movement. Later authors believed that Mitchell's mus cle energy approach did this more quickly than PNF techniques. Probably because Mitchell's work was not recorded in indexed allopathic literature, Travell and Simons (5) credited Lewit in their text by stating that the concept of applying post-isometric relaxation in the treatment of myofascial pain was presented for the first time in a North American journal in 1 984. Mitchell taught his techniques in tutorials to numerous physi cians. The first 5-day Mitchell tutorial was held in Fort Dodge, Iowa, in 1970 and was attended by John Goodridge, Philip Greenman, Rolland Miller, Devota Nowland, Edward Stiles, and Sara Sutton-all osteopathic physicians. Several tutorials fol lowed across the country. In 1 972, Mitchell's examination and treatment procedures were videotaped at Michigan State Univer sity's College of Osteopathic Medicine. After Mitchell's death in 1974, the American Academy of Osteopathy organized a com minee of physicians who had taken a tutorial with Mitchell and developed a manual for the presentation of 5-day courses to fa miliarize others with Mitchell's work. Additional tutorials were conducted for new faculty at the newly established colleges of osteopathic medicine from 1 977 to 1 981. The five earlier es tablished osteopathic colleges began to integrate muscle energy procedures inco their curriculum. In 1979, Mitchell J r., Moran, and Pruzzo (6) published the manual that was and is still used as a reference in most osteopathic medical colleges. In 1 999, Fred Mitchell, J r. completed publication of an exhaustive text on the muscle energy approach (7). Muscle energy diagnostic and treat ment procedures developed by Fred Mitchell, Sr. are currently a standard part of the osteopathic manipulative medicine curricu lum and are also used by many physical therapists.

DIAGNOSIS

Before a therapeutic procedure is performed, the patient should be examined for asymmetry of joint motion, quality and range of motion, muscle tone and strength, and tissue texture changes.

Localized tenderness in muscle and connective tissue elements may also provide valuable diagnostic information. Some positional asymmetries in the static state suggest asym metrical movements. Use functional assessment to confirm the static state suggested and indicate the true direction of force re quired to balance the cone or increase the range of motion. Often, the movement of the bones at a joint is restrained rather than im peded by obstacles in its path. Palpatory Exercise in Diagnosis

The following exercise in diagnosis develops a sense of the initial resistance. This has also been referred co as the "feather edge" of the restrictive barrier. 1 . With one hand, grasp the foot and ankle of a supine patient to abduct the lower extremity. Close your eyes to enhance your focus. Rather than using your eyes, sense through the hand, forearm, and upper arm of the hand that is abducting. 2. Take the limb into abduction slowly, carefully sensing when resistance fi rst occurs. 3. Open your eyes when you first feel resistance, observing how many degrees of an arc the patient's limb has negotiated. 4. Perform the same evaluation on the other leg and compare to see which had resistance occurring sooner, as indicated by the lesser of the two arcs.

PHYSIOLOGIC PRINCIPLES OF MUSCLE ENERGY Post-Isometric Relaxation

Goal To accomplish muscle relaxation.

Physiologic Basis Mitchell J r. (9) postulated that immediately after an isometric contraction, the neuromuscular apparatus is in a refractory state during which passive stretching may be performed without en countering strong myotatic reflex opposition. All the operator needs to do is resist the contraction and then take up the slack in the muscles during the relaxed refraccory period. With muscle contraction, there may also be increased tension on the Golgi or gan ptoprioceptors in the tendons; this inhibits the active muscle's contraction.

Force of Contraction Sustained gentle pressure (10 to 20 pounds of pressure) . Joint Mobilization Using Muscle Force

Goal To accomplish restoration of joint motion in an articular dys function.

57. MuscL e Energy T echniques

Physiologic Basis

Reciprocal Inhibition

Distortion of articular relationships and motion loss results in a reflex hypertonicity of the musculature crossing the dysfunc tional joint, similar to thrust ( HVLA) technique. This increase in muscle tone tends to compress the joint surfaces, and re sults in thinning of the intervening layer of synovial fluid and adherence of the joint surfaces. Restoration of motion to the articulation results in a gapping, or reseating of the distorted joint relations with reflex relaxation of the previously hypertonic musculature.

Goal

883

To lengthen a muscle shortened by cramp or acute spasm.

Physiologic Basis When a gentle contraction is initiated in the agonist muscle, there is a reflex relaxation of that muscle's antagonistic group.

Force of Contraction Force of Contraction Maximal muscle contraction that can be comfortably resisted by the physician (30 to 50 pounds of pressure).

Very gentle (think ounces, not pounds of pressure). Crossed Extensor Reflex

Goal

Goal

Used in the extremities where the muscle that requires treatment is in an area so severely injured (e.g., fractures or burns) that it is directly unmanipulable or inaccessible.

To produce improved body physiology using the patient's volun tary respiratory motion.

Physiologic Basis

Respiratory Assistance

Physiologic Basis The muscular forces involved in these techniques are generated by the simple act of breathing. This may involve the direct use of the respiratory muscles themselves, or motion transmitted to the spine, pelvis, and extremities in response to ventilation mo tions. The physician usually applies a fulcrum against which the respiratory forces can work.

Force of Contraction Exaggerated respiratory motion.

This form of muscle energy technique uses the learned cross pattern locomotion reflexes engrammed into the central nervous system. When the flexor muscle in one extremity is contracted voluntarily, the flexor muscle in the contralateral extremity relaxes and the extensor contracts.

Force of Contraction Very gentle (think ounces not pounds of pressure).

SEQUENTIAL STEPS OF MUSCLE ENERGY TREATMENT Diagnosis

Oculocephalogyric Reflex

Goal To affect reflex muscle contractions using eye motion.

Physiologic Basis Functional muscle groups are contracted in response to voluntary eye motion on the part of the patient. These eye movements reflexively affect the cervical and truncal musculature as the body attempts to follow the lead provided by eye motion. It can be used to produce very gentle post-isometric relaxation or reciprocal inhibition.

Force of Contraction Exceptionally gentle.

The physician should make an accurate diagnosis prior to initi ating any treatment sequence. Although a diagnosis of somatic dysfunction from the muscle energy perspective has some unique elements, they are well described in the chapters on regional ex amination of the body. The reader is referred to those chapters to learn the appropriate diagnostic techniques. Sequence

Based on an accurate diagnosis, a muscle energy procedure follows these principles: 1 . The physician positions the body part to be treated at the position of initial resistance. It is important that only the "feather edge" of the restrictive barrier is engaged for maxi mal efficacy of these techniques. 2. The physician instructs the patient about his or her partic ipation and helps the patient to obtain an effective direc tion of movement for the limb, trunk, or head. The patient

884

VII Osteopathic Considerations in Palpatory Diag nosis and Manipulative Treatment

is instructed in the intensity and duration of the muscle contraction. 3. The physician directs the patient to contract the appropriate muscle(s) or muscle group. 4. The physician uses counterforce in opposition to and equal to the patient's muscle contraction. 5. The physician maintains forces until an appropriate patient con traction is perceived at the critical articulation or area. This generally takes 3 to 5 seconds, but the duration varies with the size of the muscle being treated. G. The patient is directed to relax by gently ceasing the contrac tion while the physician simultaneously matches the decrease in patient force. 7. The physician allows the patient to relax and senses the tissue relaxation with his or her own proprioceptors. 8. The physician takes up the slack permitted by the procedure. The slack is allowed by the decreased tension in the tight muscle, allowing it to be passively lengthened. The physician notes increased range of motion. 9. Steps one through eight are repeated 3 to 5 times until the best possible increase in motion is obtained. The quality of response often peaks at the third excursion, with diminishing reru rn th erea fter. 10. The physician reevaluates the original dysfunction.

EFFICIENCY FACTORS

Good results depend on accurate diagnosis, appropriate levels of force, and sufficient localization. Poor results are most often caused by inaccurate diagnosis, improperly localized forces, or forces that are too strong. Diagnosis

An inaccurate diagnosis may lead to inappropriate treatment and does not achieve the desired improvement in the patient's con dition. Even if a segmental diagnosis is accurate, complicating factors and the entire clinical picture of the patiem need to be considered. For example, a careful diagnosis may indicate that side-bending is restricted at a segment superior to the one iden tified for treatment; this then interferes with the localization re quired, and the superior segment may need to be treated before the inferior segment. Localization

The localization of force is more important than the intensity of force. Localization depends on the physician's palpatory per ception of movement (or resistance to movement) at or about a specific articulation. Such perception enables the physician to make subtle assessments about a dysfunction and create variations of suggested treatment procedures. Monitoring the localization of forces and confining the direc tion of force by the diagnosed muscle group to the level of somatic dysfunction are important to achieve desired results. When the

physician introduces motion into an articulation that is a seg ment or two below the dysfunctional one, the probability of success greatly decreases because the forces have been directed to the wrong muscles.

Amount of Force

Using excessive force is the most common mistake made in ap plying muscle energy technique. This is not a wrestling match between patient and physician. Excessive force recruits other mus cles to assist in stabilization of the body part being treated and may completely negate the intent of the technique. Excessive forces used on older patients may result in tendon avulsion from bone.

Asymmetrical Muscle Strength

Where asymmetry of range of motion occurs, consider and test the possibility of asymmetrical strength. Some ranges of motion may be asymmetrical because of weakness of a group of muscles rather than the shortness of the antagonist group. If asymmetry of muscle strength is present, employ a method to increase the strength of the weak muscle group. Progressive resistance exer cises are used to strengthen weakened muscle groups. If weakness and shortness occur in different muscle groups but on the same side, attend to the shortness first. Jull and Janda (10) feel the agonists spontaneously increase their strength if the shortened or hypertonic fibers are lengthened.

CONTRAINOICATIONS

Post-isometric-type techniques should not be applied to acutely injured or painful muscles. These would be berter treated using a reciprocal inhibition technique. Muscle energy techniques should not be requested of a patient with low vitality that could further be compromised by adding active muscular exertion. Examples include a postsurgical patient or a patient in an intensive care unit immediately after a myocardial infarction.

CONCLUSION

Muscle energy techniques are primarily used as stand-alone tech niques for the treatment of somatic dysfunction. They can also be helpful in preparing the soft tissue about an articulation before using a high-velocityllow-amplitude (HV LA) technique. Muscle energy procedures are used to lengthen muscles that are short ened and inappropriately contracted (hypertonic) or to increase coordination of musculoskeletal tissues. The procedures can also be used to strengthen muscles that are weak (hypotonic) and thereby reduce pain, improve symmetry of articular mobility, and enhance a more appropriate circulation of body fluids. AJ though these are some of the most common uses, muscle energy technique can be combined with any of the other osteopathic manipulative techniques in total patient management.

57. Muscle Energy T echniques MUSCLE ENERGY TECHNIQUES Spinal Segmental Somatic Dysfunction

Each of the following techniques will address somatic dysfunction between spinal segments. In all cases, these employ post-isometric relaxation techniques (in the cervical spine, oculocephalogyric re flexes may also be used). Very precise localization oHorces is nec essary to make these techniques work effectively. It is important to remember that you will be making large voluntary muscles contract to create reflex contractions of the involuntary segmen tal musculature. It is these small muscles that the muscle energy technique' is directed toward.

Lumbar Dysfunction-Multiple Plane (Fig. 57. 1) Diagnosis Position: L5 FRRSR; L5 (a type II dysfunction) is flexed, rotated right, and side bent right. R estriction: L5 is restricted in extension, right rotation, and right side-bending. Type of Muscle Energy Post-isometric relaxation. Treatment Position Patient: Lateral recumbent and lying with the rotational compo nent closest to the table (in this case on the right side). The hips are flexed 45 degrees and the knees are flexed 90 degrees. Phy sician: Standing facing the patient. Procedure 1. The physician palpates the interspinous space between L5 and S 1 with the cephalad hand.

885

4. The patient's pelvis is rotated anteriorly until the initial resis tance reaches the segment to be treated. 5. The L5-S 1 interspinous space is now palpated with the physi cian's caudad hand while the patient's upper shoulder is car ried posteriorly again until the initial resistance reaches the segment ro be treated. 6. The patient is instructed to "pull gently forward with your shoulder." This contraction is held for a full 3 to 5 seconds. After 2 seconds of relaxation, the shoulder is carried posteriorly until a new restrictive barrier is met. 7. The patient is then instructed to "pull your hip gently back ward." This contraction is held for a full 3 to 5 seconds. After 2 seconds of relaxation, the hip is carried forward until a new restrictive barrier is met. S.

Each sequence of contractionlrelaxationlrepositioning is re peated three to five times or as long as further segmental mo tion is being gained. If coordinated enough, the patient may contract muscles at both the hip and shoulder simultaneously.

9. Success of the technique is determined by reevaluating seg mental motion at the dysfunctional lumbar segment.

Lum bar Dysfunction-Multiple Plane (Fig. 57.2) Diagnosis Position: L3NRRSL; L3 is at the apex of a type I group dysfunction and is rotated right and side bent left. R estriction: L3 is restricted NRLSR. Type of Muscle Energy Post-isometric relaxation.

2. The patient's lumbar spine is passively flexed and extended by flexing and extending the hips until the dysfunctional segment is positioned in neutral relative to flexion and extension. 3. The patient's upper leg is flexed slightly further at the hip and dropped off the side of the table cephalad to the lower leg.

FIGURE 57.1. Treatment for l u mbar, type (lateral recumbent position).

II segmental dysfunction

FIGURE 57.2. Treatment for lumbar, type I segmental dysfunction (seated position).

886

VII. Osteopathic Considerations in Palp atory D iagnosis and Manipulative Treatment

Treatment Position Patient: Seated, patient may straddle the table. The left hand is placed behind the neck and the right hand on the left elbow. (This position would be reversed for a dysfunction with the opposite rotational component.) Phy sician: Standing behind the patient on the side opposite the rotational component of the segmental dysfunction (in this case, the left) .

Procedure 1. Place the heel of your right hand over the right transverse process of L3 and exert an anterior pressure.

2. Place your left arm under the patient's left upper arm and your hand on rop of the patient's right upper arm. 3. The patient's trunk is Aexed forward until a very slight gapping is felt berween the spinous processes of L3 and L4. 4 . The patient's trunk is then rotated to the left and side bent to the right until the initial sense of restriction is palpated at the L3 level. 5. The patient is instructed to, "pull your right shoulder back ward and up toward the ceiling." 6. This contraction is maintained for a full 3 to 5 seconds. 7. Direct the patient to relax, simultaneously ceasing your counterforce. 8. Wait 2 seconds for the tissues to relax, and then rotate L3 fur ther to the left and side bend it further to the right, engaging the new restrictive barrier. 9. Steps five, six, seven, and eight are repeated three to five times. 10. Success of the technique is determined by rechecking seg mental motion at the L3 level.

FIGURE 57.3. Treatment for upper thoracic. type II dysfu nction.

2. Place your right hand over the patient's left parietal bone. Use this hand ro produce Aexion, right rotation, and right side-bending at T4 on T5 to the point of initial resistance. 3. The patient is instructed to "lift your head up into my hand." This should create an isometric force in a direction that would appear to exaggerate the dysfunction. 4. This contraction is maintained for a full 3 to 5 seconds.

Upper Thoracic Dysfunction (T1 -6) -Multiple Plane (Fig. 57.3) Diagnosis Type II dysfunction. Position:T4ERLSL;T4 is extended, side bent left, and rotated left. R estriction:T4 restricted FRRSR; there is restriction of Aexion, right rotation, and right side-bending at T4. Type of Muscle Energy Post-isometric relaxation. Treatment Position Patient: Seated. Phy sician: Standing behind and to the right of the patient. Procedure 1. Place the pads of the fingers of your left hand over the left paravertebral musculature with the palmar surface of your fingers positioned as follows: middle finger berween the spinous processes ofT4 andT 5 , index finger berween the spi nous processes of T3 and T4, and ring finger berween the spinous processes ofT5 and T6.

5 . Direct the patient to relax, simultaneously ceasing your counterforce. 6. Wait 2 seconds for the tissues to relax, then move the patient's head and neck in a direction that would correct the dysfunc tion in all three planes of motion until new restrictive barriers are engaged. 7. Steps three, four, five, and six are repeated three to five times. 8. Success of the technique is determined by retesting segmental motion berween T4 and T5.

Lower Thoracic Spine (T6-12) -Multiple Plane (Fig. 57.4) Diagnosis Type I dysfunction. Position:T5-9NRRSL;T5-9 is neutral, rotated right, and side bent left. R estriction:T5-9 restricted NRLSR; there is restriction of left rotation and right side-bending at segments T5-9. Type of Muscle Energy Post-isometric relaxation.

887

57 Mus cle Energy T echniques

B

A FIGURE 57.4. Treatment for lower thoracic, type I dysfunction. A: a nterior and (B) posterior views.

Treatment Position Patient: Seated with the left hand behind the neck and the right hand on the left elbow. (This position would be reversed for a dysfunction with the opposite rotational component.) Phys ician: Stands behind the patient on the side opposite the rotational component of the dysfunction (in this case, the left). Procedure 1. Place the pads of the fingers of your right hand over the right paravertebral musculature with the palmar surface of your fingers positioned as follows: middle finger between the spinous processes of T7 and TS, index finger between the spinous processes ofTG and T7, and the ring finger between the spinous processes of TS and T9. Localization of forces is directed at the segment that is the middle or apex of the group dysfunction.

further to the left and side bend it further gaging the new restrictive barrier.

to

the right, en

9. Steps five, six, seven, and eight are repeated three tImes.

to

five

10. Success of the technique is determined by rechecking seg mental motion in the T5 to T9 range.

Typical Cervicals-Multiple Plane (Fig. 57. 5) The typical cervical spinal segments include C2 to CG. C7 tends to act more like an upper thoracic segment, as its inferior facets are more oriented to the coronal plane. Diagnosis Pos ition: C5NRLSL; C5 is neutral, rotated left, and side bent left.

2. Place your left arm under the patient's left upper arm and your hand on top of the patient's right upper arm. 3. The patient's trunk is flexed forward until a very slight gapping is felt between the spinous processes of T7 and TS. 4. The patient's trunk is then rotated to the left and side bent to the right until the initial sense of restriction is palpated at the T7leveL 5. The patient is instructed to "pull your shoulder backward and up toward the ceiling." G. This contraction is maintained for a full 3 to 5 seconds. 7. Direct the patient to relax, simultaneously ceasing your counterforce. S. Wait 2 seconds for the tissues to relax, and then rotate T7

FIGURE 57.5. Treatment for cervical segmental dysfunction «(2 to (6).

888

VI1. Osteopathic Considerations in PaLpatory Diag nosis and Manipulative Treatment

R estriction:C5 is restricted in RRSR; right rotation and right side-bending are restricted atC5. Type of Muscle Energy Post-isometric relaxation and oculocephalogyric reflex.

Treatment Position Patient: Supine. Phy sician: Seated at the corner of the head of the table. Procedure I. Cradle the head and neck in both hands with the middle or index fingers palpating the C5-6 facet joints.

2. Lift the head forward until you straighten the cervical spine. 3. Let the neck extend backward untilC5 is positioned in neu tral relative roC6. 4 . Rotate C5 ro the right until initial resistance ro segmental motion is palpated. Side-bending will occur auromatically because side-bending and rotation are coupled motions in the cervical spine. (The left hand is more supportive of the head and neck as the right hand monirors motion at the facet joint.) 5. Instruct the patient ro "turn your head gently ro the left." (To use the oculocephalogyric reflex, instruct the patient ro look hard ro the left.) 6. Exert an equal counterforce through the fingers and hands. 7. Maintain this contraction for a full 3 ro 5 seconds. 8. Direct the patient ro relax the muscular effort, simultane ously ceasing your counterforce. 9. Wait 2 seconds for the tissues ro relax, and then rotate C5 until the next restrictive barrier is engaged. 10 . Repeat steps five, six, seven, eight, and nine three ro five times. 1 1 . Success of the technique is determined by retesting segmental motion at theC5-6 level.

Occipito-Atlantal Joint-Single Plane (Fig. 57. 6) Diagnosis Position: O-A E; O-A extended; occiput (CO) is extended on the atlas (Cl) R estriction: 0 E restriction; O-A restricted F; O-A restriction of flexion; occipital (CO) restriction of flexion on the atlas (Cl). Type of Muscle Energy Post-isometric relaxation and oculocephalogyric reflex. Treatment Position Patient: Supine. Phy sician: Seated at the head of the table. Procedure 1 . Place one hand under the occiput with the fingers in contact with the suboccipital musculature.

2. Place your other hand on the forehead over the meropic suture. 3. Forward bend the occiput ro initial resistance of the occiput on the atlas. 4. Direct the patient ro "lift the chin roward the ceiling," ex tending the occiput in relation ro the atlas. T ( o use the ocu locephalogyric reflex, ask the patient ro look hard roward the rop of his or her head.) This action needs ro generate only a few ounces of force. 5. Exert an equal amount of counterforce through your hand and fingers.The physician should be able ro palpate the con traction of the suboccipital muscles with the fingers beneath the occiput. 6. This contraction is maintained for a full 3 ro 5 seconds. 7. Direct the patient ro relax the muscular effort, simultane ously ceasing your counterforce. 8. Wait 2 seconds for the tissues ro relax, and then nod the head forward by drawing cephalad with the occipital hand until the new motion barrier is reached. 9. Steps four, five, six, seven, and eight are repeated three ro five times 10 . Success of the technique is determined by retesting segmental occipiro-atlantal motion.

Occipito-Atlantal Joint-Single Plane (Fig. 57. 7) Diagnosis Position: O-A F; O-A flexed; occiput (CO) is flexed on the atlas (Cl); 0 F. R estriction: O-A restricted E; O-A restriction of extension; occiput (CO) restriction of extension on the atlas (Cl). Type of Muscle Energy Post-isometric relaxation and oculocephalogyric reflex.

FIGURE 57.6. Treatment for occipito-atla ntal dysfunction-extended occiput.

Treatment Position Patient: Supine. Phy sician: Seated at the head of the table.

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889

FIGURE 57.8. Treatment for occipito-atlantal dysfunction-multiple FIGURE 57.7. Treatment for occip ito-atlantal dysfunction-flexed

plane.

occiput.

Procedure 1. Place one hand under the occiput with the pads of the fingers contacting the suboccipital musculature.

2. Place your other hand on the forehead over the metopic suture. 3. The physician extends the occiput to initial resistance of the occiput on the atlas. 4. Direct the patient to "tuck your chin toward your throat." (To use the oculocephalogyric reflex, ask the patient look hard toward his or her feet.) 5. Exert an equal amount of counterforce through the hand and fingers. The physician should be able to feel the relax ation of the suboccipital muscles with the fingers beneath the occiput. 6. This contraction is maintained for a full 3 to 5 seconds. 7. Direct the patient to relax the muscular effort, simultane ously ceasing your counterforce.

Treatment Position Patient: Supine. Phy sician: Seated at the head of the table. Procedure 1. The physician's right hand is placed under the occiput with the distal pad of one finger (index or middle finger) of right hand against the posterolateral portion of the patient's right O-A joint to monitor tissue response and movement at that area.

2. Place the palmar surface of the left hand and fingers against the left side of the patient's head. 3. The physician flexes the occiput to initial resistance, then side bends the occiput to the right until increasing tension is felt de veloping in the right suboccipital musculature. This automat ically creates left rotation of the occiput because side-bending and rotation are coupled motions at this segment. 4. Instruct the patient to "nod your head backwards so that your chin lifts up toward the ceiling." (To use the oculocephalogyric reflex, ask the patient look up toward the top of the head and then to the left.)

8. Wait 2 seconds for the tissues to relax, and then nod the head backward by pressing caudad with the occipital hand until the new motion barrier is reached.

5. This contraction is maintained for a full 3 to 5 seconds.

9. Steps four, five, six, seven, and eight are repeated three to five times.

6. Direct the patient to relax the muscular effort, simultaneously ceasing your counterforce.

10. Success of the technique is determined by retesting segmental occipito-atlanta] motion.

7. Wait 2 seconds for the tissues to relax. Maintaining the posi tion of side-bending, nod the head forward by drawing cepha lad with the hand beneath the occiput until a new motion barrier is reached. 8. Steps four, five, six, and seven are repeated three to five times.

Occipito-Atlantal Joint-Multiplane (Fig 57.8) Diagnosis Position: O-A E SL RR; occiput (CO) is extended, side-bent left, and rotated right on the atlas (C1); 0 (CO) E SL RR. R estriction: O-A restricted F SR RL; occipital (CO) restriction of flexion, side-bending right, and rotation left on atlas (Cl).

Type of Muscle Energy Post-isometric relaxation and oculocephalogyric reflex.

9. Success of the technique is determined by retesting segmental occipito-atlantal motion.

Atlanto-Axial Dysfunction (Fig. 57. 9) Diagnosis Position: AA RR; Cl RR; atlas (Cl) is rotated right on the axis (C2) . R estriction: AA restricted RL; atlas (Cl) is restricted in left rotation on the axis (C2).

890


FIGURE 57.9. Treatment for atlanta-axial dysfu nction.

Type of Muscle Energy Post-isometric relaxation and oculocephalogyric reflex. Treatment Position Patient: Supine. Physician: Seated at the head of the table. Procedure J. Grasp the patient's head between your two hands taking care not to occlude the ear canals.

2. Flex the patient's head and neck forward until the regional motion barrier for flexion is engaged. This effectively locks out rotation at all cervical segments except at Cl-2. 3. While maintaining this flexion, the head is rotated toward the left until the initial resistance is felt. 4. The patient is then instructed to "gently turn your head to the right." (To use the oculocephalogyric reflex, ask the patient to look hard to the right.) 5. Direct the patient to relax the muscular effort, simultaneously ceasing your counterforce. 6. Wait 2 seconds for the tissues to relax, then, maintaining flex ion, rotate the head further toward the restrictive barrier. 7. Steps four, five, and six are repeated three to five times.

8. CAUTION: Do not attempt to perform a thrust technique on an atlanto-axial dysfunction in this flexed forward position, as serious injury could result. 9. Success of the technique is determined by retesting segmental motion at the atlanto-axial level. Costal Somatic Dysfunction

In general, costal somatic dysfunction is divided into two groups: ribs held in inhalation and ribs held in exhalation. The key word here is held. In the muscle energy system of treatment, it is be lieved that muscle hypertonicity is responsible for the costal mo-

FIGURE 57.10. Treatment for elevated fi rst rib.

tion loss. For this reason, when a group of ribs is found to be held in exhalation, it is prudent to treat the lowest rib first, as it may also be drawing several of the ribs above it downward. Likewise, when a group of ribs is found to be held in inhalation, the upper rib would be treated first, as it may be drawing several of the ribs below it upward.

Rib Dysfunction-Elevated First Rib (Fig. 57. 1 0) Diagnosis Position: Elevated right first rib; the first rib elevates fully with inhalation and does not move appreciably with exhalation. Restriction: The right first rib exhibits restricted motion with exhalation. Type of Muscle Energy Respiratory assistance. Treatment Position Patient: Seated on the side of the table with left arm draped over the physician's thigh. Physician: Standing behind the patient. The physician's left foot is on the table next to the patient's hip. Procedure 1. The metacarpophalangeal joint of the physician's right index finger contacts the upper surface of the dysfunctional rib pos terior and lateral to the costotransverse articulation.

2. The physician's left hand guides the patient's head forward and side bends and rotates it away from the side of dysfunction to take the tension off the scalene muscles.

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FIGURE 57.11. Treatment for ribs 2-6, held in i n h a lation. FIGURE 57.12. Treatment for ribs 7-10, held in i nh a lation.

3 . The patient is instructed to inhale and exhale deeply. 4. As the patient exhales, the physician exerts a caudad and for ward pressure on the superior surface of the rib.

6. Sreps four and five are repeated three to seven rimes until maximal motion of the rib has been achieved.

5. The physician resists inhalation motion of the rib.

7. Success of rhe technique is determined by reresting motion of the dysfuncrional rib.

6. Inhalation and exhalation are repeated three to seven times until maximal motion of the dysfunctional rib has been obtained. 7. Success of the technique is determined by retesting motion of the dysfunctional rib.

Rib Dysfunction-Ribs 2-6 Held in Inhalation (Fig. 57. 1 1) Diagnosis Position: Inhalation rib; a left rib moves fully in inhalation; left rib is held in inhalation. Restriction: Restriction of exhalation; rib stops early in ex halation; extent and duration of the exhalation movement are decreased. Type of Musde Energy Respiratory assistance.

Rib Dysfunction-Ribs 7- 1 0 Held in Inhalation (Fig. 57. 12) Diagnosis Position: Inhalation rib; a rib moves fully in inhalation; a rib is held in inhalation. Restriction: Restricrion of exhalarion; rib stops early in exhala rion; extent and durarion of exhalation movement are decreased. Type of Musde Energy Respiratory assistance. Treatment Position Patient: Supine. Physician: Sranding ar the side of the table.

Treatment Position Patient: Supine with the head and shoulders elevated. Physician: Standing at the head of the table.

Procedure 1. The patient's upper body is side-bent to rhe side of dysfuncrion until rension is taken off rhe dysfuncrional rib.

Procedure l. The patient's upper body is bent forward until the tension is taken off the dysfunctional rib.

3. The patient is instrucred to inhale and exhale deeply.

2. The web formed by the physician's thumb and index finger is placed in the intercostal space above the dysfunctional rib on its anterior, superior surface. 3. The patient is instructed to inhale and exhale deeply. 4. On exhalation, the physician exaggerates the pump handle motion of the rib being treated. 5. On inhalation, the physician resists the inhalation motion.

2. The web formed by the physician's thumb and index finger is placed in the lateral aspect of the intercostal space above the dysfunctional rib on its superior surface. 4. On exhalation, the physician exaggerares the bucket handle morion of rhe rib being treated. 5. On inhalation, the physician resisrs motion of the rib. 6. Steps four and five are repeated three to seven rimes until maximal motion of the rib has been achieved. 7. Success of the technique is determined by retesting morion of rhe dysfunctional rib.

892

VI! Osteopathic Considerations in PaLpatory Diag nosis and Manipulative Tr eatment

FIGURE 57.13. Treatment for ribs 1 1 and 12, e l evated.

Rib Dysfunction-Ribs 1 1 and 12 Elevated (Fig. 57. 1 3) Diagnosis Position: Elevated floating rib; a rib moves fully in elevation; a rib is held in elevated. R estric tion: Restriction of depression. Type of Muscle Energy Joint mobilization using muscle force ( quadratus lumborum) and reciprocal inhibition. Treatment Position Patient: Prone. Phy sic ian: Standing at the side of the table on the side opposite the dysfunctional rib. Procedure 1. The heel of the physician's cephalad hand is placed posterior and medial to the angle of the dysfunctional rib and exerts a sustained lateral and caudad pressure.

2. The physician's caudad hand grasps the ipsilateral anterior superior iliac spine and pulls upward toward the ceiling. 3. The patient is instructed to "pull your hip down toward the table." 4. This contraction is held for a full 3 to 5 seconds. 5. Direct the patient to relax, simultaneously ceasing your COUll terforce. 6. Wait 2 seconds for the tissues to relax, and then increase the pressure on the dysfunctional rib. 7. Steps three, four, five, and six are repeated three to five times until maximal motion of the rib has been achieved.

FIGURE 57.14. Treatment for ribs 1 & 2, held in exhalation.

R estriction: Restriction of inhalation; rib stops early in inhala tion; extent and duration of inhalation motion are decreased. Type of Muscle Energy Joint mobilization using muscle force and reciprocal inhibition. Treatment Position Patient: Supine. Physic ian: Standing at the side of the patient opposite the side of the dysfunctional rib. Procedure l. The patient's head is turned about 30 degrees away from the side of the dysfunctional rib.

2. The patient's arm on the side of the dysfunction is placed with the dorsum of the wrist against the forehead. 3. The physician's caudad hand reaches under the patient and grasps the angle of the dysfunctional rib exerting continuous traction in a caudad and lateral direction. 4. The patient is instructed to "lift your head straight up to ward the ceiling." This is done without altering the 30 degree rotation of the head. 5. This contraction is held for a full 3 to 5 seconds. 6. Direct the patient to relax, simultaneously ceasing your counterforce. 7. Wait 2 seconds for the tissues to relax, and then exert increasing caudad and lateral traction with your caudad hand beneath the rib. 8. Steps four, five, six, and seven are repeated three to five times.

8. Success of the technique is determined by retesting motion of the dysfunctional rib.

9. Success of the technique is determined by retesting motion of the dysfunctional rib.

Rib Dysfunction-Ribs One and Two Held in Exhalation (Fig. 57. 1 4)

Rib Dysfunction-Ribs 3, 4, or 5 Held in Exhalation (Fig. 57. 1 5)

Diagnosis Position: Exhalation rib; the rib moves fully in exhalation; the rib is held in exhalation.

Diagnosis Position: Exhalation rib; a rib moves fully in exhalation; a rib is held in exhalation.

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FIGURE 57.16. Treatment for ribs 6-10, held in exhalation. FIGURE 57.15. Treatment for ribs 3-5, held in exhalat i o n .

Restriction: Restriction of inhalation; rib stops early in inhala tion; extent and duration of inhalation motion are decreased. Type of Muscle Energy Joint mobilization using muscle force, reciprocal inhibition. Treatment Position Patient: Supine. Physician: Standing at the side of the patient opposite the side of dysfunction. Procedure 1. The patient's arm on the side of dysfunction is abducted 135 degrees at the shoulder and flexed 90 degrees at the elbow.

2. The physician's caudad hand reaches under the patient and grasps the angle of the dysfunctional rib, exerting continuous traction in a caudad and lateral direction. 3. The physician's cephalad hand restrains the patient's elbow on the side of dysfunction. 4. The patient is instructed to " lift your elbow upward and at tempt to draw it across the body toward your opposite hip." 5. This contraction is held for a full 3 to 5 seconds.

6. Direct the patient to relax, simultaneously ceasing your counterforce. 7. Wait 2 seconds for the tissues to relax, and then exert increased caudad and lateral traction with the caudad hand. 8. Steps four, five, six, and seven are repeated three to five times. 9. Success of the technique is determined by retesting motion of the dysfunctional rib.

Rib Dysfunction-Ribs 6, 7, 8, 9, or 1 0 Held in Exhalation (Fig. 57. 1 6) Diagnosis Position: Exhalation rib; the rib moves fully in exhalation; the rib is held in exhalation.

Res triction: Restriction of inhalation; rib stops early in inhala tion; extent and duration of inhalation motion are decreased. Type of Muscle Energy Joint mobilization using muscle force and reciprocal inhibition. Treatment Position Patient: Supine. Physician: Stands at the side of the patient on the same side as the dysfunctional rib. Procedure 1. The patient's arm on the side of dysfunction is abducted 90 degrees.

2. The physician's caudad hand reaches under the patient and grasps the angle of the dysfunctional rib, exerting continuous traction in a caudad and lateral direction. 3. The physician's lateral thigh contacts the abducted arm at about the level of the elbow.

4. The patient is instructed to "pull your arm straight down toward your hip." 5. This contraction is held for a full 3 to 5 seconds.

6. Direct the patient to relax, simultaneously ceasing your counterforce. 7. Wait 2 seconds for the tissues to relax, and then exert increased caudad and lateral traction with the caudad hand. 8. Steps four, five, six, and seven are repeated three to five times. 9. Success of the technique is determined by retesting motion of the dysfunctional rib.

Rib Dysfunction-Ribs 1 1 and 12 Depressed (Fig. 57. 1 7) Diagnosis Position: Depressed rib; the rib moves fully inferiorly; the rib is held depressed. Restriction: Restriction of elevation.

894

VII. Os teo pathic Co ns ideratio ns in PaLpato ry D iag nos is and ManipuLative Treatment

FIGURE 57.17. Treatment for ribs 11 and 12, d epressed.

Type of Muscle Energy Post-isometric relaxation (quadratus lumborum) . Treatment Position Patient: Prone. Phys ic ian: Standing on the side of the patient opposite the dysfunctional rib. Procedure 1 . Draw the patient's legs approximately 1 5 to 20 degrees away from the side of the dysfunctional rib.

2. The physician places the heel of the cephalad hand inferior and medial to the angle of the dysfunctional rib. 3. The physician's caudad hand grasps the ipsilateral anterior superior iliac spine and lifts toward the ceiling. 4. The patient is instructed to "pull your hip down toward the table." 5. This contraction is held for a full 3 to 5 seconds. 6. Direct the patient to relax, simultaneously ceasing your counterforce. 7. Wait 2 seconds for the tissues to relax, and then exert a cepha lad and lateral pressure with the hand contacting the angle of the rib. 8. Steps four, five, six, and seven are repeated three to five times. 9. Success of the technique is determined by retesting motion of the dysfunctional rib.

Rib Dysfunction-Ribs 2-9 Held Anterior (Fig. 57. 1 8) Diagnosis Pos itio n: Anterior rib; rib held anterior. Res tric tio n: Rib resists moving posteriorly. Type of Muscle Energy Joint mobilization using muscle force.

FIGURE 57.18. Treatment for ribs 2-9, held anterior.

Treatment Position Patient: Seated. Phys ic ian: Standing on the side opposite the dysfunctional rib. Procedure 1 . Place the patient's hand ipsilateral to the dysfunction on the opposite shoulder.

2. Place your anterior hand on the patient's elbow. 3. Place the heel of your posterior hand medial to the angle of the dysfunctional rib and exert a continuous lateral pressure. 4. Use your anterior hand to pull the patient's arm toward you. Raise or lower the arm until your posterior hand feels the forces localize to the dysfunctional rib. 5. Instruct the patient to "pull your elbow away from me." 6. This contraction is held for a full 3 to 5 seconds. 7. Direct the patient to relax, simultaneously ceasing your counterforce.

8. Wait 2 seconds for the tissues to relax, and then increase the lateral pressure against the angle of the dysfunctional rib. 9. Steps five, six, seven, and eight are repeated three to five times. 1 0. Success of the technique is determined by retesting motion of the dysfunctional rib. Innominate Dysfunction

Dysfunction of the innominate bones is due to faulting of the biomechanics of the sacroiliac joint. Due to the irregular sur face of the sacroiliac joints, this necessarily results in a separa tion of the joint surfaces and a drawing taut of the anterior and posterior sacroiliac ligaments. It is this ligamentous tension that maintains the presence of the somatic dysfunction. Muscle energy

57. Mus cle En ergy T ec hn iques

895

4. The patient is instructed w "pull your knee down wward the table."

5. This contraction is maintained for a full 3 to 5 seconds. 6. Direct the patient w relax, simultaneously ceasing your coumerforce. 7. Wait 2 seconds for the tissues w relax, and then further extend the hip until a new restrictive barrier for the innominate is engaged. 8. Steps four, five, six, and seven are repeated three w five times or until a sudden release of the innominate dysfunction is palpated. 9. Effectiveness of the technique is assessed by retesting iliosacral motion.

Innom inate Dysfunction-Anterior Rotation (Fig. 57.20) Diagnosis Pos ition : Innominate rotated anteriorly. Res triction: Innominate restricted in posterior rotation. FIGURE 57.19. Treatment for poste riorly rotated i n n o m i nate.

technique is directed at reswring normal anicular relations across the sacroiliac joim. Pubic symphysis dysfunction is also considered w be innom inate dysfunction, but with the greatest positional diswnion of the innominate bones ( and usually the sympwmawlogy as well) , located at and about the pubic symphysis.

Type of Muscle Energy Joint mobilization using muscle force.

Innom inate Dysfunction-Posterior Rotation (Fig. 57. 1 9) Diagnosis Pos ition : Innominate rotated posteriorly. Res tr iction : Innominate restricted in amerior rotation. Type of Muscle Energy Joint mobilization using muscle force. Treatment Position Patien t: Prone with the knee on the side of the dysfunction flexed 90 degrees. Phys ician : Standing on the side opposite the dysfunction. Procedure 1. Physician's caudad hand grasps the patient's ipsilateral knee just proximal w the patella. The dorsum of the patient's foot rests against the anterior aspect of the physician's shoulder.

2. The heel of the physician's cephalad hand is placed over the posterior superior iliac spine ( PSIS) on the side of dysfunction. 3. The patient's hip is passively extended until forward motion is sensed at the PSIS.

FIGURE 57.20. Treatment for anteriorly rotated i n n o m i nate.

896

VII. Osteopathic Con sideration s in Palp atory D iagn osis an d Man ipulative Treatmen t

Treatment Position Patien t: Supine. Phy sician : Seated on the table on the side of dysfunction. Procedure 1. The patiem's leg on the side of dysfunction is flexed at the hip and the knee, and the foO[ is placed on the physician's shoulder.

2. The physician's hands are placed against the hamstring muscles just proximal to the popliteal region. 3. The patiem is instructed to "push your thigh against my hands." 4. This contraction is held for a full 3 to 5 seconds.

5 . Direct the patiem to relax, simultaneously ceasing your counterForce. 6. Wait 2 seconds For the tissues to relax, and then reposition the innominate into further posterior rotation by further flexing the hip umil the new restrictive barrier is engaged. 7. Steps three, four, five, and six are repeated three to five times or until a sudden release of the innominate dysfuncrion is palpared.

8. EfFectiveness of the technique is assessed by rechecking il iosacral morion.

Pubic S ym physis-Fixed Compression (Adducted Pubic Bones) (Fig. 57. 2 1 ) Diagnosis Position: Pubic bones are compressed medially; there is typically bulging and renderness of rhe symphysial cartilage. Restriction : Normal pubic symphysis motion is resrricred. Type of Muscle Energy Joinr mobilizarion using muscle force. Treatment Position Patien t: Supine wirh hips flexed to 45 degrees, knees flexed 90 degrees, and rhe feer flar on the rable. Phy sician : Standing on eirher side of rhe parient.

FIGURE 57.21. Treatment for adducted pubic bones.

Procedure l. The patiem's knees are separated to allow insertion of rhe physician's forearm ( elbow to heel of hand) between rhem.

2. The patient is instructed to "try to pull your knees together." 3. This comraction is susrained For a Full 3 to 5 seconds. 4. Direct the patiem to relax.

5. Wait 2 seconds for the rissues to relax. There is no need for repositioning in this rechnique. 6. Sreps two, rhree, four, and five are repeated rhree to five times or umil a sudden release of the pubic symphysis is Felt by rhe patient. 7. Success of rhe rechnique is derermined by reexamining the symphysial cartilage.

Pubic S ym physis-Fixed G apping (Abducted Pubic Bones) (Fig. 57.22) Diagnosis This is often suspected based on rhe patiem's history of recem childbirth or surgery performed in rhe lithotomy posirion. Due to rhe fascial srresses placed on the urethra, some parients experience urinary frequency and urgency suggestive of infecrious cysriris; however, laboratory studies do nor supporr this diagnosis. Position : Pubic bones are distracted larerally; rhere is typically a deeper rhan normal sulcus overlying rhe symphysial cartilage, which is extremely tender. Restriction: Normal pubic symphysis motion is resrricted. Type of Muscle Energy Joim mobilization using muscle force. Treatment Position Patien t: Supine with hips flexed to 45 degrees, knees flexed to 90 degrees, and feet flat on rhe table. Phy sician: Sranding on eirher side of the patiem.

FIGURE 57.22. Treatment for abd ucted pubic bones.

57. Mus cle Energy T ech niques

897

Procedure 1 . The patient's knees are separated about 1 8 inches.

2. The lateral aspect of the knee closest to the physician is placed against the physician's abdomen ( often a pillow is used to protect the physician). 3. The physician reaches across to the other knee and grasps the lateral aspect of that knee with both hands. 4. The patient is instructed to "pull your knees apart as hard as you can." 5. This contraction is maintained for a full 3 to 5 seconds. 6. Direct the patient to relax, simultaneously ceasing your counrerforce. 7. Wait 2 seconds for the tissues to relax, and then pull the knees slightly closer together. 8. Steps four, five, six, and seven are repeated three to five times. 9. Success of the technique is determined by reexamining the prominence of the symphysial cartilage.

Sacrum

The diagnosis of sacral dysfunction generally requires just two rypes of information: I.

Th e rela tiv e pos ition of th e tw o sa cra l s ulc i a nd th e tw o infe rior la tera l a ngles (IL As) ( Fig. 57.23). The two sacral sulci are designated as feeling either deep or shallow compared with each other. The inferior lateral angles are designated as being posterior/inferior or anterior/superior relative to each other. For unilateral sacral dysfunction, when the deep sulcus and the posterior/inferior ILA are on opposite sides of the sacrum, you have torsion. When the deep sulcus and the posterior/inferior ILA are on the same side of the sacrum, you have a unilateral sacral flexion ( shear) or extension.

2. A motion tes t. Several different motion tests have been devised over the years to assess unilateral sacroiliac dysfunction.

FIGURE 57.24. Lumbar spring test.

( Fig. 5 7 . 24). In this test, the patient is prone, and a springing force is directed anteriorly into the lumbar spine. Normal spring ( negative spring test) indicates the presence of an anterior torsion or a unilateral flexion. Increased resistance to pressure ( positive spring test) indi cates the presence of eirher a posterior torsion or a unilateral extension. • S ph inx tes t ( Fig 57.25), also called lumbopelvic hyperexten sion, employs observation in changes in asymmetry at the sacral sulci. When going from the prone position to the sphinx position, if the sacral sulci become more symmetric, you have an anterior torsion or a unilateral flexion. If the sacral sulci become more asymmetric, you have a posterior torsion or a unilateral extension. • Seated flexion test ( see Chapter 52). • S ea tedass ess ment oflL A asymmetry ( Fig 57.26 and 57.27). This is performed in a manner similar to a seated flexion test ( see Chapter 5 2 , Special Tests of the Pelvis), but the [ LAs are mon itored. As in the sphinx test, if the asymmetry increases, you

• L umba r sp ring tes t

A

B FIGURE 57.23. Sacral landmarks. A: the sacral sulci and (B) the inferior lateral a n gles.

898

VIi. Ost eopathic Con siderat ion s in PaLpat or y Diagn osis an d Man ipuLat ive Tr eatm ent

FIGURE 57.25. Sphinx test. FIGURE 57.27. Test for inferior lateral angle sym metry-at end of flexion.

have a posterior [Qrsion or unilateral extension. If the asym metry decreases or stays the same, you have an amerior [Qrsion or un ilateral flexion. • Four dig it cont act (Fig. 57.28). Comact the four corners of the sacrum as depicted. Assess motion of the sacrum by direct pressure on the sacrum, moving it about its various axes, or quietly palpate sacral motion while the patient respires.

Sacral Dysfun ction -An terior Torsion (Fig. 57. 29) Diagnosis Ex am pLe: A left on left sacral [Qrsion. Pos it ion : Anterior [Qrsion about a left oblique axis; a L on L sacral [Qrsion (the fi rst L designates the direction of sacral rotation, the second L designates the oblique axis on which this rotation is occurring). Restr ict ion : Posterior rotation about the left oblique axis is restricted. The oblique axes are not free [Q alternate during the gait cycle.

FIGURE 57.26. Test for i nferior lateral a n g l e symmet ry-starting position.

Type of Muscle Energy Complex: the experts are still debating exactly what hap pens during this technique, but it is likely a combination of multiple muscles simultaneously going through post-isometric relaxation. Treatment Position Pat ient: Left lateral modified Sims' position (lying on the side of the axis). Physician : Stands at the side of the table facing the patient. Procedure 1 . The patiem's right shoulder is pressed as close [Q the table as it will go. Post-isometric relaxation technique may be used [Q obtain optimal positioning.

2. The physician's cephalad hand palpates over the right sacral sulcus. 3. The patient's hips and knees are flexed [Q 90 degrees. Both legs are then dropped off the side of the table. A pillow may be necessary [Q cushion the distal thigh against the table edge.

FIGURE 57.28. Four d i g it contact.

57. Muscle Energy T ec hniques

899

FIGURE 57.29. Treatment of anterior sacral tors i o n .

4 . The physician's caudad hand is placed just proximal to the lateral malleolus of the upper leg. 5. The patient is instructed to "lift your legs straight up toward the ceiling."

6. This contraction is held for a full 3 to 5 seconds. 7. Direct the patient to relax, simultaneously ceasing your counterforce. 8. Wait 2 seconds for the tissues to relax, and then press both legs toward the Aoor until a new restrictive barrier is reached. 9. Steps five, six, seven, and eight are repeated three to five times. 1 0. Success of the technique is determined by rechecking the symmetry of the sacral sulci and lLAs, and by retesting sacral motion.

Sacral Dysfunction-Posterior Torsion (Fig. 57.30) Diagnosis Ex ample: a left on right sacral torsion. Position: Posterior torsion about a right oblique axis; a L on R sacral rorsion (the L designates the direction of sacral rota tion, the R designates the oblique axis on which this rotation is occurring). Restriction: Anterior rotation about the right oblique axis is restricted. The oblique axes are not free to alternate during the gait cycle. Type of Muscle Energy Complex: the experts are still debating exactly what happens dur ing this technique, but it is likely a combination of joint mobi lization using muscle force and post-isometric relaxation. Treatment Position Patient: Right lateral recumbent position (lying on the side of the axis). Physic ian: Stands at the side of the table facing the patient. Procedure 1 . The patient's left shoulder is carried posteriorly until the initial restriction is sensed.

FIGURE 57.30. Treatment of posterior sacral torsion.

2 . The physician's cephalad hand palpates over the left sacral sulcus.

3. The patient's hips are Aexed to 45 degrees and the knees to 90 degrees. 4. The patient's upper leg is flexed further at the hip and dropped off the table cephalad to the lower leg. 5. The physician grasps this leg just above the lateral malleolus.

6. The patient is instructed to "lift your ankJe up toward the ceiling as hard as you can." 7. This contraction is maintained for a full 3 to 5 seconds. 8. Direct the patient to relax, simultaneously ceasing your counterforce. 9. Wait 2 seconds for the tissues to relax, and then press the leg further toward the Aoor until a new restrictive barrier is reached. 1 0. Steps six, seven, eight, and n i ne are repeated three ro five times. 1 1 . Success of the technique is determined by rechecking the symmetry of the sacral sulci and lLAs, and by retesting sacroiliac motion.

Sacral Dysfunction-Unilateral Flexed Sacrum (Fig. 57. 3 1) Diagnosis Ex ample: Unilateral flexed sacrum, right. Position: Unilateral flexed sacrum-right; right sacral shear. R estriction: Right sacroiliac joint is restricted in extension.

900

VII Os teopathic Cons iderations in PaLpatory Diag nos is and Manipula tive Treatment

FIGURE 57.31. Treatment of uni lateral flexed sacrum.

Type of MuscIe Energy Respiratory assistance. Treatment Position Patient: Prone. Phys ic ian : Standing beside the patient on the side opposite the side of dysfunction. Procedure 1. The hypothenar side of the heel of the physician's left hand is placed on the right lLA of the sacrum and exerts a steady pressure caudad and toward the (able. It is reinforced with the physician's right hand. 2. The patient is instructed to, "take a deep breath."

3. During inhalation, the physician follows posterior nutation of the sacrum. 4. The patient is instructed to, "exhale slowly." 5. During exhalation, the physician exerts increased pressure against the ILA to prevent rerum of the sacrum toward a flexed position.

6. Steps two, three, four, and five are repeated three to seven times. 7. Success of the technique is determined by rechecking sym metry of the sacral sulci and inferior lateral angles, and by retesting sacral motion.

Sacral Dysfunction-Unilateral Extended Sacrum (Fig. 57. 32) Diagnosis Ex ample: Unilateral extended sacrum-right. Pos ition: Unilateral extended sacrum-right. R es tric tion: Right sacroiliac j oint restricted in flexion. Type of Muscle Energy Respiratory assistance.

FIGURE 57.32. Treatment of u n ilateral extended sacrum.

Treatment Position Patient: Sphinx position (prone with the elbows supporting the upper body). Phys ic ian: Standing at the side of the patient opposite the side of dysfunction. Procedure 1 . The hypothenar side of the heel of the physician's right hand is placed in the region of the right sacral sulcus exerting a steady pressure directed toward the table. It is reinforced by the physician's left hand. 2. The patient is instructed to "inhale and then exhale quickly."

3. During exhalation, the physician follows forward nutation of the sacrum. 4. During inhalation, the physician resists posterior nutation of the sacrum. 5. Steps two, three, and four are repeated three to seven times.

6. Success of the technique is determined by rechecking symme try of the sacral sulci and the ILAs, and by retesting sacroiliac motion.

The Extremities

When muscular restrictions affect the motion of a peripheral joint, the most common method used is a simple range of motion technique combined with post-isometric relaxation. Examples of this are given for the hip girdle. For similar treatment of the shoulder, the reader is referred to the section on Spencer technique in Chapter 5 5 . Muscle energy protocol can readily b e added to many of the stages of this common technique. This same type of thinking can be applied to the elbow, wrist, knee, and ankle, as well as the digits. Representative examples of commonly used techniques are given. On occasion, muscles will be contracted to move articulations. Examples of this type of technique are the elevated proximal clavicle and the posterior and anterior proximal fibula.

901

57. Mus cL e Energy Techniques

FIGURE 57.33. Treatment of hypertonic hamstring m uscle. FIGURE 57.34. Treatment of hypertonic gluteus maxim us muscle.

Hip Girdle Dysfunction-Hamstring Muscles (Fig. 57. 33) Diagnosis Pos ition: The hip joint is held extended by hyperronic hamming muscles. Res triction.' The hip joinr is restricted in flexion by hypenonic hamsrring muscles. Type of Muscle Energy Post-isomerric relaxation. Treatment Position Patient: Supine. Phys ician: Seated on the side of the table on the side of dys function at the level of the patienr's knee. Procedure I . The patienr's hip is flexed ro the initial resistance while keeping the knee in extension.

Hip Girdle Dysfunction-Gluteus Maxim us Muscle (Fig. 57. 34) Diagnosis Pos ition: The hip joinr is held extended by hypertonic gluteal muscles. Res triction: The hip joint is restricted in flexion by hypertonic gluteal muscles. Type of Muscle Energy Post-isometric relaxation. Treatment Position Patient: Supine. Phys ician: Seated on the side of the table on the side of dys function at the level of the patient's knee.

2. The patienr's leg is then placed on rop of the physician's shoulder.

Procedure 1 . The patienr's hip is flexed ro the initial resistance while keeping the knee in a flexed position.

3. The physician's hands are placed on rop of the patienr's thigh ro mainrain the knee in extension throughout the technique.

2. The physician's hands are placed on the posterior thigh just proximal ro the popliteal fossa.

4. The patient is instructed ro "push your leg gently down inro my shoulder. "

3. The patienr is insrructed ro "push your leg gently against my hands."

5. This contraction is held for a full 3 ro 5 seconds.

4. This contl'action is held for a full 3 ro 5 seconds.

6. Direct the patient ro relax, simultaneously ceasing your counterforce.

5 . Direct the patient ro relax, simultaneously ceasing your counterforce.

7. Wait 2 seconds for the tissues ro relax, and then further flex the hip until a new resrrictive barrier is met.

6. Wait 2 seconds for the tissues ro relax, and then further flex the hip unril a new restrictive barrier is met.

8. Steps four, five, six, and seven are repeated three ro five times or unril no additional motion can be gained.

7. Steps four, five, six, and seven are repeated three or until no additional motion can be gained.

9. Effectiveness of the technique is assessed by retesting hip range of motion in flexion with the knee extended.

8 . Effectiveness of the technique is assessed by retesting hip range of motion in flexion with the knee flexed.

ro

five times

902

VII. Os teop athic Co ns ideratio ns in PaLp atory Diag nos is and Manip ula tiv e Treatment

FIGURE 57.36. Treatment of hypertonic h i p abductor muscles. FIGURE 57.35. Treatment of hypertonic h i p add uctor muscles.

Hip Girdle Dysfunction-Abductor Muscles (Fig. 57. 36)

Hip Girdle Dysfunction-Adductor Muscles (Fig. 57. 35)

Diagnosis Pos itio n: The hip joint is held abducted by hypertonic abductor muscles. R es tric tio n: The hip joint is restricted in adduction by hyper tonic abductor muscles.

Diagnosis Pos itio n: The hip joint is held adducted by hypertonic adductor muscles. R es tric tio n: The hip joint is restricted in abduction by hyper tonic adductor muscles.

Type of Muscle Energy Post-isometric relaxation.

Type of Muscle Energy Post-isomeuic relaxation.

Treatment Position Patient: Supine. Phys ic ian: Standing at the end of the table.

Treatment Position Patient: Supine. Phys ic ian: Standing at the side of the patient between the patient's abducted thigh and the table. Procedure 1 . The patient's hip is abducted until initial resistance met.

Procedure 1. The patient's hip is flexed until it can clear the other leg and then adducted until initial resistance is met. 2. The physician's hand is placed on the lateral aspect of the patient's ankle.

3. The patient is insuucted to "pull your leg gently against my hand." IS

2. The physician's cephalad hand is placed on the conualateral anterior superior iliac spine. The physician's caudad hand is placed on the patient's ipsilateral ankle.

3. The patient is insuucted tei "pull your leg gently against my thigh. " 4 . This contraction i s held for a full 3 t o 5 seconds. 5 . Direct the patient to relax, simultaneously ceasing your counterforce.

6. Wait 2 seconds for the tissues to relax, and then further abduct the hip until a new resuictive barrier is met. 7. Steps four, five, six, and seven are repeated three to five times or until no additional motion can be gained. 8. Effectiveness of the technique is assessed by retesting hip range of motion in abduction.

4. This conuaction is held for a full 3 to 5 seconds. 5 . Direct the patient to relax, simultaneously ceasing your counterforce.

6. Wait 2 seconds for the tissues to relax, and then further adduct the hip until a new restrictive barrier is met. 7. Steps four, five, six, and seven are repeated three to five times or until no additional motion can be gained. 8. Effectiveness of the technique is assessed by retesting hip range of motion in adduction.

Hip Girdle Dysfunction-Psoas Muscle (Fig. 57.37) Diagnosis Pos itio n:The hip joint is held flexed by a hypertonic psoas muscle. R es tric tio n: The hip joint is restricted in extension by a hyper tonic psoas muscle.

57. MuscL e Energy T ec hni ques

FIGURE 57.37. Treatment of hypertonic psoas muscle.

903

FIGURE 57.38. Treatment of hypertonic h i p external rotator muscles (piriformis muscle).

Type of Muscle Energy Posr-isomerric relaxarion. Treatment Position Patient: Supine wirh legs exrended off rhe end of rhe rable. Phy sic ian: Sranding ar rhe end of rhe rable. Procedure I . The parienr's hips are Aexed while keeping rhe knees in a Hexed posmon.

2. The parienr's leg on rhe side of dysfuncrion is dropped down off rhe end of rhe rable while rhe patienr holds the conrraJ ate raj hip in a Aexed posirion. 3. The physician's hand is placed on the anrerior thigh j ust prox imal to the knee. 4. The patienr is insrructed co "Iifr your leg gently againsr my hand." 5. This conrracrion is held for a full 3 co 5 seconds.

6. Direct rhe patienr co relax, simulraneously ceasing your counrerforce. 7. Wair 2 seconds for rhe rissues co relax, and rhen furrher extend rhe hip unril a new resrricrive barrier is mer.

Treatment Position Patient: Prone. Phy sician: Sranding at rhe side of rhe rable. Procedure l. The pariem's knee is Aexed co 90 degrees.

2. The patiem's hip is inrernally rorared unril rhe initial resisrance is paJ pared. 3. The physician's hand is placed on rhe medial side of rhe ankle. 4. The parienr is instrucred co "press your leg gently againsr my hand." 5. This conrracrion is held for a full 3 co 5 seconds.

6. Direcr rhe parienr co relax, simulraneously ceasing your counrerforce. 7. Wair 2 seconds for rhe rissues co relax, and rhen furrher inrer nally rorate rhe hip unril a new resrrictive barrier is mer. 8. Sreps four, five, six, and seven are repeared rhree co five rillles or unril no addirional morion can be gained. 9. Effecriveness of the rechnique is assessed by retesting hip range of motion in inrernal rorarion.

8. Sreps four, five, six, and seven are repeared rhree co five rimes or unril no addirional morion can be gained.

9. Effecriveness of rhe rechnique is assessed by reresring hip range of morion in exrension.

Hip Girdle Dysfunction-External Rotator Muscles (Piriform is) (Fig. 57. 38) Diagnosis Position: The hip joinr is held in exrernaJ rorarion. Restriction:The hip joinr is resrricred in internal rotarion. Type of Muscle Energy Posr-isomerric relaxarion.

Hip Girdle Dysfunction-Internal Rotator Muscles (Fig. 57. 39) Diagnosis Position: The hip joim is held in imernal rotation. Restriction: The hip j oinr is restricred in external rotarion. Type of Muscle Energy Posr-isometric relaxation. Treatment Position Patient: Prone. Phy sician: Standing ar rhe side of rhe rable.

904

VIi. Os teop athic Cons iderations in Palp atory Diagnos is and Manip ula tive Treatment

FIGURE 57.39. Treatment of hypertonic h i p internal rotator m uscles.

Procedure 1 . The patient's knee is flexed

(Q

FIGURE 57.40. Treatment of hypertonic rectus femoris muscle.

4. This contraction is held for a full 3

90 degrees.

2. The patient's hip is externally rotated until the initial resistance is palpated.

5. Direct the patient counterforce.

(Q

(Q

5 seconds.

relax, simultaneously ceasing your

3. The physician's hand is placed on the lateral side of the ankle.

6. Wait 2 seconds for the tissues (Q relax, and then further flex the knee until a new restrictive barrier is met.

4. The patient is instructed hand."

7 . Steps four, five, six, and seven are repeated three (Q five times or until no additional motion can be gained.

(Q

"press your leg gently against my

5. This contraction is held for a full 3

6. Direct the patient cou n terforce.

(Q

(Q

5 seconds.

relax, simultaneously ceasing your

7. Wait 2 seconds for the tissues (Q relax, and then further exter nally rotate the hip until a new restrictive barrier is met. 8 . Steps four, five, six, and seven are repeated three or until no additional motion can be gained.

(Q

five times

8. Effectiveness of the technique is assessed by retesting knee range of motion in flexion with the hip in neutral.

Knee-Proxim al Fibula Posterior (Fig. 57. 4 1)

9. Effectiveness of the technique is assessed by retesting hip range of motion in external rotation.

Diagnosis Pos ition: The proximal fibula is posterior. Res triction: The proximal fibula is restricted in anterior glide.

Knee Dysfunction-Rectus Femoris Muscle (Fig. 57.40)


Diagnosis Pos ition: The hip joint is held in flexion with the knee extended. Res triction: W ith the hip held in neutral, the knee is restricted in flexion. Type of Muscle Energy Post-isometric relaxation. Treatment Position Patient: Prone. Phys ician: Standing at the side of the table. Procedure 1 . The patient's knee is flexed until the initial resistance palpated.

IS

2. The physician's hand is placed on the ankle. 3. The patient is instructed hand."

(Q

"press your leg gently against my FIGURE 57.41. Treatment of proximal f i b u l a posterior.

905

57 Muscle E nergy Techniques Treatment Position Patient: Supine with hip flexed 45 degrees and knee flexed 90 degrees. Physician: Standing at the foot of the table facing the patient. Procedure I . The physician's medial hand is placed on the dorsum of the foot with his or her thumb on the lateral aspect and the fingers on the medial aspect.

2. The physician's lateral hand anchors the calcaneus. 3. The ankle is inverted to the initial resistance. 4. The patient is instructed to "push your foot sideways into my thumbs and up into my hand." This eversion/dorsiflexion of the ankle is thought to contract the extensor digitorum longus and the tibialis anterior muscles, drawing the fibula forward. 5. This contraction is held for a full 3 to 5 seconds.

6. Direct the patient to relax, simultaneously ceasing your counterforce. 7. Wait 2 seconds for the tissues to relax, and then further invert the foot until a new restrictive barrier is met. 8. Steps four, five, six, and seven are repeated three to five times or until no additional motion can be gained.

9. Effectiveness of the technique is determined by retesting mo tion at the proximal tibiofibular articulation.

Knee-Proxim al Fibula Anterior (Fig. 57.42) Diagnosis Position:The proximal fibula is anterior. Restric tion: The proximal fibula is restricted in posterior glide. Type of Muscle Energy Joint mobilization using muscle force. Treatment Position Patient: Supine with hip Aexed 45 degrees and knee flexed 90 degrees. Physician: Standing at the foot of the table facing the patient.

FIGURE 57.42. Treatment of proximal f i b u l a anterior.

Procedure l. The physician's medial hand is placed on the dorsum of the foot with thumb on the lateral aspect and the fingers on the medial aspect. 2. The physician's lateral hand anchors the calcaneus.

3. The ankle is inverted to the initial resistance. 4. The patient is instructed to "push your foot sideways into my thumbs and down into my hand." This eversion/plantar flexion of the ankle is thought to contract the fibularis longus and soleus muscles, drawing the fibula backward. 5 . This contraction is held for a full 3 to 5 seconds.

6. Direct the patient to relax, simultaneously ceasing your counterforce. 7. Wait 2 seconds for the tissues to relax, and then further invert the foot until a new restrictive barrier is met. 8 . Steps four, five, six, and seven are repeated three or until no additional motion can be gained.

to

five times

9. Effectiveness of the technique is determined by retesting mo tion at the proximal tibiofibular articulation.

Ankle-Soleus Muscle (Fig. 57. 43) Diagnosis Position: The ankle is held plantar flexed by a hypertonic soleus muscle. Restriction: The ankle is restricted in dorsiflexion by a hyper tonic soleus muscle. Type of Muscle Energy Post-isometric relaxation. Treatment Position Patient: Prone with the knee Aexed 90 degrees. Physician: Standing at the side of the foot of the table. Procedure I . The physician's hand grasps the patient's heel with the wrist and distal forearm contacting the sole of the foot right down to the toes.

FIGURE 57.43. Treatment of hyperto n i c soleus muscle.

906

VIJ. Ost eopathic Cons iderat ions in Palp at ory Diagnos is and Manipulat ive Tr eat ment

2. The sole of the foot is mainrained parallel to the floor as the ankle is dorsi flexed and the knee is flexed. This motion is conrinued unril the initial resistance is met.

2. The shoulder is abducted 90 degrees and then externally ro tated unril initial resistance is met.

3. The patienr is instructed to "push the ball of your foot up inro my arm."

3. The patienr is instructed to "gently press your wrist forward and toward the Aoor." This force would normally inrernally rotate the humerus in a horizonral position.

4. This contraction is held for a full 3 to 5 seconds.

4. This conrraction is held for a full 3 to 5 seconds.

5. Direct the patienr to relax, simultaneously ceasing your counterforce.

5. Direct the patienr to relax, simultaneously ceasing your counrerforce.

6. Wait 2 seconds for the tissues to relax, and then further dor siAex the ankle unril a new restrictive barrier is met.

6. Wait 2 seconds for the tissues to relax, and then further ex ternally rotate the shoulder unril a new restrictive barrier is met.

7. Steps three, four, five, and six are repeated three to five times or until no additional motion can be gained. 8 . Effectiveness of the technique is assessed by retesting ankle range of motion in dorsiflexion.

7. Steps three, four, five, and six are repeated three to five times or unril no further clavicular motion can be gained. 8. Effectiveness of the technique is assessed by retesting clavicular motion.

Clavicle-Anterior Rotation (Fig. 57.44) Diagnosis Pos it ion: The clavicle is rotated anteriorly. Rest rict ion: The clavicle is restricted in posterior rotation. Type of Muscle Energy Post-isometric relaxation.

Clavicle-Superior Sternal End (Fig. 57.45) Diagnosis Pos it ion:The proximal clavicle is displaced medially and cephalad. Rest rict ion: The proximal clavicle is restricted in motion later ally and caudad.

Treatment Position Pat ient : Seated. Phys ician: Standing behind the patient.


Procedure 1. The physician grasps the patienr's wrist.

Treatment Position Pat ient : Supine with shoulder abducted 45 degrees. Phys ician: Standing at the side of the table. Procedure 1 . The physician grasps the extended wrist, externally rotates the arm, and gently presses it down toward the floor until initial resIstance IS met. 2. The physician's other hand palpates the sternal end of the clavicle.

FIGURE 57.44. Treatment of anteriorly rotated clavicle.

FIGURE 57.45. Treatment of s u perior disp lacement of the proximal clavicle.

57. Mus cle E nergy T ech niques 3. The patient is instructed to "lift your arm up toward the ceiling." 4. The pectoralis muscles pull the clavicle laterally and inferior. 5. This contraction is held for a full 3 to 5 seconds.

6. Direct the patient to relax, simultaneously ceasing your counterforce. 7. Wait 2 seconds for the tissues to relax, and then press the patient's arm further toward the floor. 8. Steps three, four, five, and six are repeated three to five times or until no additional sternoclavicular motion is gained. 9. Effectiveness of the technique is assessed by retesting stern oclavicular motion.

907

2 . Ruddy TJ. Osteopathic rhythmic resistive duction therapy. Ln: Barnes MW, ed. Yearbook ofthe Academy ofApplied Osteopathy. Indianapolis, IN: American Academy of Osteopathy; 1 96 1 : 5 8. 3. Guyer AF. Proprioceptive neuromuscular facilitation for vertebral joint conditions. In: Grieve GP, ed. Modern Manual Therapy ofthe Vertebral

Column. New York, NY: Churchill Livingstone; 1 986:626. 4. Lewit K, Simons DG. Myofascial pain: relief by post-isometric relax ation. Arch Phys Med Rehabil. 1 984;6 5 : 4 5 3--456. 5 . Travell JG, Simons DG. Myofoscial Pain and Dysfonction: The Trigger

Point Manual, vol. 2. Baltimore, M D : Will iams & Wilkins; 1 992: 1 O. 6. Mitchell Jr FL, Moran PS, Pruzzo NA. An Evaluation and Treatment

Manual of Osteopathic Muscle Energy Procedures. Valley Park, M O : Mitchell, Moran, a n d Pruzzo; 1 979. 7. Mitchell Jr FL. The Muscle Energy Manual. East Lansing, M l : MET Press; 1 999. 8. Goodridge, J P. Muscle energy technique: definition, explanation, merh ods of procedures. JAm Osteopath Assoc. 1 98 1 ; 8 1 :249-254. 9. M i tchell J r FL, Moran PS, Pruzzo NA. An Evaluation and Treatment

REFERENCES

Manual of Osteopathic Manipulative Procedure. 2nd ed. Kansas Ci ty, MO: Institute for Continuing Educarion in Osteopathic Principles, I nc; 1 973:325.

I . Mitchell Sr FL. Structural pelvic function. In: Barnes MW, ed. Year

1 0. Jull GA,Janda V Muscles and motor control in low back pain; assessment

book of the Academy ofApplied Osteopathy. I ndianapolis, I N : American

and management. In: Twomaey LT, Taylor J R, eds. Physical Therapy for

Academy of Osteoparhy; 1 9 58:79.

the Low Back. New York, NY: Churchill Livingstone; 1 987:272.

FASCIAL-LIGAMENTOUS RELEASE: INDIRECT APPROACH ANTHONY G. eHILA

PHILOSOPHY OF MANIPULATION

KEY CONCEPTS • Relevance of osteopathic philosophy co the technique of

fascial-ligamemous release • Location and function of fascia (super ficial, subserous, and

deep), aponeurosis, and tendon • Indirect techniques of functional release and strain/

• • •

• • • •

counterstrain as manipulative models, and how they are incorporated imo the technique of fascial-ligamentous release Basic procedures involved in fascial-ligamencous release Hysteresis and creep, how they allow for relaxation of tissues, and why the relaxation may be temporary How fascial-ligamentous release allows for sustained relaxation and resolution of chronic dysfunction via cemral nervous system desensitization Supine treatmem model Three componems of the doctor-patiem relationship in making a diagnosis Benefits of using a fulcrum in treatmem Positioning for the following areas: sacrum and pelvis, sacrum, iliosacrurn, lower lumbar, abdominal fascia, upper lumbar, psoas muscle, liver, lower extremiry (abduction phase, adduction phase, and foot), rib cage, lower and upper thorax, cervical, upper extremiry (scapula, axilla, thoracic apertures, clavicle, radius, ulna, hand, and fingers), occipiwatlantal joim and basilar axes of the skull

Classic osteopathic thought has assigned importance co the role of the connective tissue system of the body in health and dis ease. In his writings, A.T. Still emphasized the connective tissue system in the diagnosis and treatmem of dysfunction. Although manipulative approaches based on fascial-ligamemous consider ations have enjoyed a reawakening in recent years, they are in fact representative of early osteopathic methods. This chapter offers a synthesis of the thoughts of various represemative osteopathic au thors on this sub ject. Other sources provide further detail about fascial-Iigamentous release (I -8).

A philosophy of manipulation is central co, and not synonymous with, the practice of osteopathy. Osteopathic theory holds that when the anacomic-physiologic tendency of a human being is coward a state of health, all functions of the body have an opti mal performance capaciry. Still made reference co a philosophy of manipulation that was based on absolute knowledge of form and function proceeding from a perfect image of the normal ar ticulations. In Still's view, the adjustment of tissues of the body according co form, function, and image was the basis of treatment. Still indicated equally clearly that diseases could be regarded as ef fects occurring in regions of the body when optimal performance capaciry became compromised.

CONNECTIVE TISSUE CONTINUITY

Fascia of the human body can be described as a sheet of fibrous tissue that envelops the body beneath the skin; it also encloses muscles and groups of muscles, separating their several layers or groups. An aponeurosis is a fibrous sheet or expanded tendon that gives attachmem co muscular fibers and serves as the means of origin or insertion of a Hat muscle. Ir sometimes performs the office of a fascia for other muscles. A tendon is a fibrous cord or band that connects a muscle co bone or some other structures. Ir consists of fascicles of densely arranged collagenous fibers, tendon cells, and a minimum of ground substance. In addition co extensive attachment for muscles, the fascia of the human body is provided with sensory nerve endings and is thought co be elastic as well as contractile. Fascia supports and stabilizes, helping co maimain balance. It assists in the production and comrol of motion and the interrelation of motion of related parts. Many of the body's fascial specializations have postural functions in which stress bands can be demonstrated. Finally, the dura mater is a special connective tissue surrounding the central nervous system. Bony anchors for this tissue exist in the skull and at the sacrum. Fascia in the human body is described as being superficial, deep, or subserous. The superficial and deep layers are found ev erywhere in the body as complete ensheathments. The subserous layer lies innermost on the deep layer anywhere there is a body

58. FasciaL-Ligamentous ReLease: Indirect Approach caviry. The deep layer of fascia is the most complicated of the three, being two-layered with intervening septa. Clinically, it is possible to conceptualize such wrapping as be ' ing a big bandage of the body. Such an analogy is implied in osteopathic literature. One can find reference to the idea that the body retains form even if everything except the connective tissue framework is removed. If this is so, then it is also reasonable that form permits the consideration of motion. The continuiry of this arrangement and considerations of structural-functional interre lationships make it possible to discuss biomechanical attributes of fascia in relation to manipulative treatment. MANIPULATIVE MODELS

The study of the application of force in osteopathic manipu lative treatment (OMT) has led to the development of'several manipulative models. In particular, those who seek to reduce the possibiliry of microtrauma to tissues and joints have built on considerations of fascial distribution and specialization. This is especially so in those models which require refinement of palpa tory skills to appreciate subtleties of stress patterns and motion characteristics. The corrective forces underlying these models are generally approaches in which the dysfunctional component of resistance to motion is carried to a point of simultaneous balance and de creased tension. The focus of procedures in such models is on the qualiry of movement, particularly on initiation of motion. Emphasis is reduced on the range of motion and the end point of motion. The correct gauging of force and velociry provides in finite variation in the delivery of technique. Control minimizes force. The effective physician should be able to vary the applica tions of force during a single manipulative treatment or over time for continuing manipulative management. Appropriate use of a fulcrum and leverage can refine the physician's diagnostic touch and treatment effectiveness. The emphases peculiar to the various manipulative models can be selectively used in preparing the individual patient's ma nipulative prescription. Sequencing the diagnosis and treatment allows the physician to improve the qualiry of office records. The level of the patient's response to manipulative treatment can be better documented. Longitudinal assessment of the patient's progress is facilitated. In general, such models are hypothesized to reduce the flow of abnormal afferent impulses into the central nervous system by reprogramming for more normal function. The following three paragraphs illustrate the variable dynamic of fascial-ligamentous release in relation to the functional release and strain and counterstrain approaches. Functional Release

In functional release, the manipulative procedure is guided by palpation at the dysfunctional segment (spinal or appendicular) for continuous feedback information about the patient's physi ologic response to motion. Operator-induced motion compares relative degrees of compliance or resistance of component parts. It does so in opposing directions. The motions introduced are those that lead to an increased sense of compliance (decreased resistance) of component parts.

909

Strain and Counterstrain

In strain and counterstrain, passive movement away from the area of resistance to motion is induced toward and into planes of increased motion, always searching for the position of greatest comfort. The body is folded around the tender point. A position of mild but asymptomatic strain is induced, which is thought to produce the most efficient reflex release of joint dysfunction within a prescribed period of time.

Fascial-Ligamentous Release

Elements of each of the preceding models are incorporated when using fascial-ligamentous release. The patient provides breath as sistance andlor muscular assistance in the corrective procedure. The establishment of a fulcrum is sought within the physician's body to match or balance the fulcrum within the patient's body; this facilitates a continuum of reflex release from within the pa tient's body. Once local and regional dysfunction have been ad dressed by the establishment of an appropriate fulcrum, expand ing leverage is achieved through torsion and traction applied to the extremities. It is the ongoing analysis of dysfunction within this continuum that makes possible the integration of multiple manipulative approaches through variable applications of force.

TREATMENT CONSIDERATIONS

In performing manipulative procedures, the body responds com prehensively to an externally applied force. From the moment of contact with the skin, avenues for the implement ation of vari ations of force are provided by palpatory clues. In the sense of a body covering, the skin may be regarded as a mass adrenergic medium that is useful in the facilitation and amplification of pro prioceptive interchange between unique persons, the patient and the physician. Osteopathic diagnosis and treatment does not concern itself simply with the performance of a single manual procedure. The particular treatment, as well as the construction of a management program, often requires variation in technical approaches. Visual ization and synthesis of messages received through the fingers are the basis for clinical behavior. Conceptualization of anatomic physiologic dysfunction peculiar to a given patient is the key to maximizing manipulative responses. The sustained effective response following treatment is contingent on selective and con trolled variation of force from an appropriate fulcrum. When these conditions are met, inherent neuroregulatory mechanisms acting in accordance with the capaciry of the patient will facilitate the resolurion of dysfunction. Generally speaking, the body's connective tissues are under some degree of load and extension. The increase and subsequent reversal of extension produces a degree of tissue response less than the relatively unloaded state. This phenomenon is referred to as hysteresis. It implies the occurrence of some flow and dissipation of energy throughour the loaded tissue. Hysteresis occurs less with successive cycles of extension, indicating stabilization of response. Connective tissues under sustained load will extend in re sponse to the load. In biomechanical terms, this continued

910


extension is referred to as creep. An imposed constant load will result in relaxation, as the extension remains constant. In either situation, the tissue displays less subsequent resistance to exten sion than in the original state. Behaviors of connective tissues depend on previous mechan ical history. Extension effects revert to their preextension re sponses. This observation may be useful in appreciating recur rence of dysfunctional complaints. The principle of timed release of tissues associated with the fascial-ligamentous release model of manipulative treatment considers these factors. The sequential and expanding progression of this approach permits the patient to tolerate central nervous system modulation. The lowering of afferent inputs is gradually facilitated. If the patient's capacity to respond is appropriate, the model seeks to ensure the significant reduction or elimination of sensitization. This view is attuned to the idea that central nervous system conditioning over time may be the vehicle for the retention as well as the reduction of dysfunctional states. The physician's role is that of a facilitator. By appropriate facilitation, the physician is able to observe the capacity for change while the patient is enabled to expand the power of the change. The standard for the successful outcome of this interchange is the motivation of the patient.

SUPINE TREATMENT Observation and Palpation

With the patient lying in the supine position, observational and systemic palpatory findings help to establish a diagnosis related to the mechanical forces associated with body position. With the head unsupported and the legs fully extended, note the in creased mechanical stresses impacting the cervical and lumbar lor dotic curves. Compromised respiratory-circulatory effectiveness is the result of generalized fascial-ligamentous tension through out the body. For that reason the character of respiration pro vides information about such tension. Observe four factors about respiration: 1. Type ofrespiration: diaphragmatic, costal, or mixed 2. Abdominal wall motion: visible to the level of the umbilicus;

visible to the level of the symphysis pubes

With respect to the last of these aspects, OMT must allow the physiologic function within to manifest its own potency rather than use blind external force and overpower its assistance. This is accomplished through the use of a fulcrum, which is the support or point of support on which a lever turns in raising or moving something. The establishment of an appropriate fulcrum facilitates di agnostic touch. The placing of the hands and fingers on the tissues under examination is done with the idea that the fin gers can mold themselves to the patient's body. The initiation of the pattern within the area of complaint is realized by a slight compression at the fulcrum points. The application of the prin ciple of the fulcrum is as varied as the list of complaints brought to the physician's office. The use of this method is not a time consuming process. Mechanisms already in action are used. It is necessary only to contact them and to sense them speaking for themselves. There are no techniques. The point or points are listening posts. Let the tissues tell the story; be quiet and listen. Biokinetic (dysfunctional) energies or forces are always at work in all physiologic and pathologic processes. With the appropriate use of diagnostic touch, the biodynamic (healing) intrinsic force within is allowed to manifest itself. The findings noted on observation and palpation contribute to the evaluation that governs the administration of OMT. The clinical diagnosis and the tolerance of the patient govern the ap plication of forces in OMT. Any sequence for treatment adopted by a physician should have two intentions: 1. The alleviation or elimination of effects of disease processes that have occurred or are occurring in the various regions of the body 2. The restoration of the patient's ability to resume command of

the clinical situation Positions for diagnostic touch of various areas of the body using the principle of fulcrum are outlined below. Lower Body

The patient's knees are flexed, and the feet placed flat on the table. Lateralization of the feet, with inversion of the toes, helps to stabilize the pelvis.

3. Rate: slow, rapid; documented before and after treatment

4. Duration ofcycle: inspiration and expiration equal, inspiration shorter in duration than expiration, inspiration longer in du ration than expiration, dilation of the nares during respiration

Diagnostic Touch

Diagnosis is an important component in patient care. There are three central elements in an encounter between a physician and a patient: 1. The patient's ideas and beliefs of what the problem could be

Sacrum' and Pelvis 1. Mold with the patient's sacrum with one hand (Fig. 58.1). 2. Place the fingertips of this hand at the level of the spinous process of the fifth lumbar segment (L5). The o'pposite arm

and hand bridge the anterior superior iliac spine (ASIS) on each side of the pelvis (Fig. 58.2). 3. The fulcrum is established by the elbow, which is leaning on

the treatment table. Sacrum, lIiosacrum, Lower Lumbar

2. The physician's concept of what the problem could be

1. Mold with the patient's sacrum with one hand (Fig. 58.3).

3. That which the anatomic-physiologic wholeness of the pa

2. Place the opposite hand under the iliosacral articulation. The

tient's body knows the problem to be

fingertips of this hand contact the spinous process of the lower

58. Fascial-Ligamentous Release: Indirect Approach

FIGURE 58.1. Sacrum and pelvis. One hand molds with the sacrum.

lumbar segments (L3, L4, L5). Both elbows establish the ful crum: one leaning on the treatment table (sacrum), the other leaning on the physician's knee (iliosacrum; lower lumbar).

Abdominal Fascial Tension

Mold with the sacrum with one hand. The opposite hand ac complishes multiple assessments: the abdominal quadrants, costal margins, and linea alba; tension of the inguinal ligaments; and shear dysfunctions at the pubic symphysis. Both elbows establish the fulcrum: one leaning on the treatment table (sacrum), and the other being the elbow of the exploring arm (abdomen). Upper Lumbar, Psoas Muscle

Place one hand under the upper lumbar area (Fig. 58.4). The opposite arm and hand bridge the flexed knees. The fulcrum is established by the elbow on the knee (upper lumbar area). Liver

Place one hand under the lower ribs beneath the liver. Place the opposite hand over the anterior surface of the liver. The fulcrum is established by the elbow on the knee (lower ribs).

FIGURE 58.2. Sacrum and pelvis. Bridge anterior superior iliac spine.

911

FIGURE 58.3. Sacrum, iliosacrum, lower lumbar.

Lower Extremity

Selectively employ torsion (rotation) and traction in two phases to release muscular, fascial, ligamentous, and articular dysfunction. The fulcrum is established by the elbows of the physician's arms in supporting the motions of the patient's foot, lower leg, and knee. Abduction Phase (Lower Leg) Invert the plantar surface of the foot (Fig. 58.5). Introduce torsion between the ankle and the knee. Advance the effect of torsion by slowly moving the knee across the lower abdomen, resulting in progressive abduction of the lower leg. The torsion will be felt in the lateral malleolar area, the medial compartmental area of the knee, the tensor fascia lata area, and the trochanter area. Upon completion of this phase, gradually extend the lower extremity and slowly return it to the tabletop. Adduction Phase (Lower Leg) Evert the plantar surface of the foot ( Fig. 58.6). Introduce torsion between the ankle and the knee. Steadily advance the effect of torsion by slowly moving the knee away from the lower abdomen, resulting in progressive adduction of the lower leg. The torsion will be felt in the medial malleolar area, the lateral compart mental area of the knee, the medial thigh area, and the inguinal

FIGURE 58.4. Upper lumbar, psoas muscle.

912


FIGURE 58.5. Lower extremity. abduction phase. FIGURE 58.7. Foot.

area. Upon completion of this phase, gradually extend the lower exrremiry and slowly rerum it ro the tablerop.

Upper Body

Rib Cage

Foot Note tenderness ro palpation in the plantar myofascial tissues. Give particular attention ro such findings along the medial lon girudinal arch. The conrour of the foot can be analogized ro the spinal complex: The calcaneus represents the sacrum The tarsal bones represent the lumbar region The tarsometatarsal area represents the thoracolumbar junction The metatarsal area represents the thoracic region The metatarsophalangeal area represents the cervicothoracic junction The phalangeal area represents the cervical region Tender points can be analogized ro the ipsilateral spinal level, including paraspinal tissues

1. Place one hand beneath the rib cage, with the fingertips just beyond the spinous processes of the associated thoracic verte brae (Fig. 58.8). 2. Place the other hand on the anterior ends of the ribs. The fulcrum is established by the elbow on the knee. Lower Thorax

Place both hands beneath the patient at the level of the 12th thoracic segment (TI2) ( Fig. 58.9). This area corresponds ro the level of the insertion of the trapezium muscles bilaterally. The fulcrum is established bilaterally by the elbows resting on the tablerop. Upper Thorax

Treatment is by increased plantar flexion of the foot about the point of greatest tenderness ( Fig. 58.7) Perform articularory release of the small joints of the roes in sequence, from the great roe ro the small roe.

The patient's head rests on a pillow. One hand and arm contact the upper thoracic spinous processes, with the fingers spread slightly to contact the ribs on each side (Fig. 58.10). Place the opposite

FIGURE 58.6. Lower extremity. adduction phase.

FIGURE 58.8. Rib cage.

58. FasciaL-Ligamentous ReLease: Indirect Approach

FIGURE 58.9. Lower thorax.

hand on rhe srernum. The fulcrum is esrablished by rhe elbow on rhe rable[Op, benearh rhe parienr's head. Cervical Area

Borh hands bridge rhe enrire cervical area from the base of the skull [0 rhe upper thorax (Fig. 58.1 1). The fulcrum is established bilarerally by the elbows and forearms resting on the table[Op. Upper Extremity

Scapulofascial Release Accomplish rhis by exploring ease and resistance [0 morion in several planes: cephalad, caudad, medially, laterally, clockwise, and counterclockwise (Fig. 58. 12). Both hands are used [0 grasp the scapula completely, both medially and larerally. Axillary Release Accomplish this by manual decongesrion of rhe posrerior axillary tissues and the pec[Oral tissues. Expansion of the Inferior Thoracic Aperture Accomplish this by supporting the elbow region with one hand and the wrist region with the other hand. For this and all sub sequenr procedures, rhe fulcrum is esrablished by rhe elbows of the physician's body in support of rhe motions of the parienr's

FIGURE 58.11. Cervical area.

upper extremity. Bring rhe extended upper extremity of the pa tienr closer [0 the side of rhe body. Sustained supination as the upper extremity is carried [Oward the posterior thorax facilitates release of the thoracolumbar junction. Sustained pronation as rhe upper extremity is carried [Oward the xiphoid process facilitates musculofascial release along the costal margin. The cumulative effect of these forces conrributes [0 ligamen[Ous articular release of the elbow region. Clavicular and Glenohumeral Release Accomplish rhis by placing rhe exrended upper extremity in a neu tral position, with respecr [0 rhe side of the body, and abducting [0 the poinr where a continuum exisrs between the upper extrem ity and the position of the clavicle. Sustained pronation as the upper extremity is carried [Oward rhe manubrial region facilitates release of the manubrial area and the sternoclavicular articulation. Sustained supination as the upper extremity is carried [Oward the posterior thorax facilitates release of rhe acromioclavicular artic ulation and the glenohumeral area. Radioulnar, Wrist, Hand, and Fingers Release Accomplish this by sustained alternaring supination and prona tion. This facilitates the release of fascial ligamenrous tension along the course of the interosseous membrane [0 the flexor reti naculum (Fig. 58.13).

.; / ( FIGURE 58.10. Upper thorax.

913

,a

1.

t.

t

\

\..

FIGURE 58.12. Upper extremity, scapulofascial release.

914


FIGURE 58.13. Upper extremity, radioulnar.

The addition of alternating flexion and extension of the wrist facilitates the release of articular dysfunctions of the carpal bones ( Fig. 58.14). Fascial ligamentous release of the palmar area pre cedes articulatory release of the smalJ joints of the fingers and thumb. The progress of the sequence is from the smalJ finger to the thumb ( Fig. 58.15). Expansion of the Superior Thoracic Aperture Accomplish this by grasping the deep webbing between the in dex finger and thumb of the patient's extended upper extremity. Sustained alternating supination and pronation facilitates the re lease of congestion in this area and contributes to release of the cervicothoracic junction.

Cranium

Occipitoatlantal Articulation l. One hand contacts the posterior tubercle of the atlas

( Fig. 58. 16). 2. The opposite hand contacts the vertex of the patient's head.

FIGURE 58.14. Upper extremity, wrist.

FIGURE 58.15. Upper extremity, hand and fingers.

The fulcrum is established by the placement of the elbow on the tabletop.

Basilar Axes of the Skull

The patient's head rests on the interlaced or overlapped fingers of the physician. The physician's thumbs extend above the ears toward the forepart of the head. The fulcrum is established by the placement of the elbows on the tabletop.

CONCLUSION

Osteopathic treatment does not concern itself simply with the performance of a single manual procedure. The particular treat ment requires variation in technical approaches. Visualization and synthesis of messages received through the fingers are the ba sis for a keen clinical behavior. Conceptualization of anatomic physiologic dysfunction peculiar to a given patient is the key to maximizing manipulative responses. The sustained effec tive response following treatment is contingent upon selective and controlled variation of force from an appropriate fulcrum. When these conditions are met, inherent mechanisms acting in

FIGURE 58.16. Occipitoatlantal articulation.

58. Fascial-Ligamentous Release: Indirect Approach accordance with the capacity of the patient will lead to a state of health.

REFERENCES 1. Becker RE. Diagnostic touch: its principles and application. In: Barnes MW, ed. Academy of Applied Osteopathy Yearbooks. Indianapolis, IN: American Academy of Osteopathy; Part I. 1963:32-40. PartS II and III.

1964:153-166. Part IV 1965:165-177. 2. Becker RF. The meaning of fascia and fascial continuity. Osteopath Ann. 1975;3(6):186/35. 3. Cathie AG. F ascia of the body in relation to function and manipulative

915

therapy. In Barnes MW; ed. Academy of Applied Osteopathy Yearbook. Indianapolis, IN: American Academy of Osteopathy, 1960:74. 4. Greenman PE. Principles ofManual Medicine, 2nd ed. Baltimore, MD: W illiams & Wilkins; 1996. 5. Hubbard RP. Mechanical behavior of connective tissue. In: Greenman PE, ed. Concepts and Mechanisms ofNeuromuscular Functions. New York,

NY: Springer-Verlag; 1984:47-54. 6. Jones LH. Strain and Counterstrain. Colorado Springs, CO: The American Academy of Osteopathy; 1981. 7. Lippincott HA. The osteopathic technic of Wm. G. Sutherland D.O. In: Northup TC, ed. Academy ofApplied Osteopathy Yearbook. Indianapolis, IN: American Academy of Osteopathy; 1949: 124.

8. Zink JG, Lawson WE. An osteopathic structural examination and func tional interpretation of the soma. Osteopath Ann. 1979;7(12):433-440.

BALANCED LIGAMENTOUS TENSION TECHNIQUES JANE E. CARREIRO

KEY CONCEPTS

Understand the principles of balanced ligamentous and balanced membranous articulatory mechanisms • Understand the principles of diagnosis and treatment of balanced ligamentous and balanced membranous articulatory mechanisms as described by William Sutherland, DO • The concept of using the inherent forces within the body as activating forces for manipulative treatment

•

INTRODUCTION

Balanced ligamentous and balanced membranous tension tech niques were first described by William G. Sutherland, DO. Dr. Sutherland graduated from the American School of Osteopa thy and was a student of Andrew Taylor Still, M D. Dr. Sutherland described balanced ligamentous tension technique (BLT) as an approach to diagnosis and treatment of the living human body. His model was initially presented to a small group of students between 1942 and 1944, and then subsequently published as the "Osteopathic Technique of Wm. G. Sutherland" in the 1949 Year Book o/the Academy 0/Applied Osteopathy (1). Ligamentous Articular Mechanisms

The principles ofBLT are formulated around an understanding of ligamentous articular mechanisms. Ligaments regulate and guide the movement in all the articulatory mechanisms of the body. In most joints they act as checks to the voluntary actions of muscles. The clearest example of this idea occurs in the wrist. There are no muscular forces acting directly upon the carpal bones yet we can Rex, extend, circumduct, and move our wrists in all sorts of con figurations. Each of these movements occurs as a result of small rotations, twistings, and turnings of the carpal bones. The fl exor and extensor carpi ulnaris and radialis, as well as some of the mus cles of the digits will initiate motion; the mechanics of carpal bone movement, however, are governed by the nonelastic properties and position of the carpal ligaments. The placement of the carpal

ligaments creates various fulcrums and checks within which the complex movements of the carpal bones occur (2-4). For exam ple, the carpi radialis muscles move the proximal phalanx of the thumb toward the radial side of the forearm. As the phalanx ap proximates the radius, the trapezium, trapezoid, and scaphoid ac commodate this change in spatial relations by moving toward the midline of the wrist. The positions of the other carpal bones will adjust accordingly. None of the carpal bones are directed by mus cular efforts, rather they respond to distal muscular forces. This complicated movement is orchestrated and guided by the small ligaments lying between and around the carpal bones. All move ments of the wrist are accomplished through a similar mechanism. Consequently, the carpal ligaments can be viewed as levers and pulleys and straps guiding the bones and the articular relation ships. Dr. Sutherland described this arrangement as a ligamen tOus articular mechanism. Furthermore while the positions of the carpal bones may change, the tensions on the carpal ligaments do not. In other words, when the wrist is fl exed, the dorsal ligaments are not stretched, nor do the palmar ligaments go slack. As long as the wrist is moved within its physiologic range of motion, the tensions within the carpal ligaments remain balanced. Sutherland called this a balanced ligamentous articular mechanism. Other obvious examples of ligamentous articular mechanisms are the forearm (radial and ulnar intraosseous membrane), the tibia and fibula (again via the intraosseous membrane), and the foot.* While the range of motion is much less than the wrist, the ligaments of the foot are responsible for creating a system that is capable of weightbearing and mobility. Movements of the forefoot and hind foot are dictated by the ligamentous ar rangement. The sacroiliac (SI) joint is yet another example of a ligamentous articular mechanism. Designed for weightbear ing and mobility, the SI joints must also be able to accommo date large changes in size (e.g., during labor and delivery), while maintaining stability. The ligaments of the S1 and lumbosacral areas function with a reciprocal tension mechanism, responding to the moment-tO-moment changes induced by gait (5-7). Ac cording to Sutherland's model, all of the joints in the body are

'Dr. Sutherland also considered the internal dura as the intraarticular liga ments of (he cranium and referred to the principles of balanced membranous rension to describe the mechanics in this area.

59. Balanced Ligamentous Tension Techniques balanced ligamentous articular mechanisms. The ligaments pro vide proprioceptive information that guides the muscle response for positioning the joint, and the ligaments themselves guide the moti�n of the articular components.

91 7

Sutherland coined the terms "reciprocal tension ligaments" and "reciprocal tension mechanism" to describe the tole of ligaments in joints (8). According to Sutherland's model, throughout the physiologic range of motion of any given joint, the associated lig aments maintain a constant level of tension. They do not stretch, nor do they become lax. The motion mechanics between the bones .of a joint are a result of a change in the shape of the joint space, not because one set of ligaments becomes taut while an other becomes slack. Think of the wrist moving in flexion and extensien. As the wrist meves inte flexien there is a displacement .of the distal row of carpal benes toward the dersal surface.of the arm. During extension these same benes meve toward the palmar surface. Accempanying these mevements are rotatiens ef individ ual bones. The sum total .of these mevements acts to maintain the tensien of the carpal ligaments at a consistent level. This is a key concept in Dr. Sutherland's approach. The type .of metion which may occur at any given articula tion is determined by the shape .of the jeint surfaces, the pesitien of the ligaments, and the forces of the muscles acting upen the jeint. Ligaments do net stretch and contract as muscles de; cen sequently, the tensien in a ligament has very little variatien. The tension distributed throughout the ligaments.of any given jeint is balanced. In nermal mevements, as the jeint changes positien, the relationships between the joint's ligaments also change, but the total tension within the ligamenteus articular mechanism dees net. The distribution .of tensien between the ligaments is altered, hewever, when the jeint is affected by injury, inflamma tien, andler mechanical ferces. This is what happens in sematic dysfunction. The distributien and vector .of tensien within any given ligament will change according to the pesitien .of strain in the jeint. However, the shared tensien within the ligamen tous articular mechanism of any given joint remains censtant as leng as the ligament is net damaged. This has been called a re ciprocal tension mechanism. Of ceurse, the balance within the ligamenteus articular mechanism can be strained if the jeint is inappropriately meved beyond its physielegic range of metien. In the fermer case, it is the balance.of tensien, which is distorted. In the latter case, the fibers of the ligament are subjected to mi crescepic tears and stretch. While this (the latter case) will mest assuredly result in a strain to the balance .of the articular liga ments, the ligaments de net need to be disrupted fer the balance to be distorted. The distortion in balance is a mechanical strain, which may er may net involve an anatomical.one. In any sematic dysfunction, there is always a strain in the balanced ligamentous articular mechanism.

recemmended using the inherent ferces within the bedy such as respiratien, fluid mechanics, and pestural changes to cerrect the strain. In the spine, vertebral balanced ligamentous articular strains can be cerrected using a variety.of manipulative techniques such as high velecityllew amplitude (HVLA), muscle energy, ceun terstrain, and se ferth, which indirectly address the liganlentous cemponent through muscles.or benes. H ewever, when the prin ciples .of BLT are used in manipulative treatment, fulcrums and levers are applied directly to direct changes to the ligamentous articular strains. These principles can be used to make cerrec tiens in all ligamentous and membraneus articulatory mecha nisms. In general, the technique cembines a fulcrum introduced by the physician with an activating ferce provided by the patient. The physielegic mevements and ferces are generated in the bedy threugh pesitien and respiratien. The bedy is always in metien. The physielegic metien .of res piratien, fluid pressure changes, and pestural adjustments .occur on a mement-to-mement basis. These metiens, hewever sub tle they may appear, affect rhe entire musculeskeletal system. During deep inspiratien the diaphragm centracts, increasing in traabdeminal pressure. The abdeminal muscles alse centract, in creasing tensien en the theracelumbar fascia. The theracelumbar fascia is firmly attached to the supraspineus and interspineus liga ments. When the abdeminal muscles are tensed, a pesterier ferce is placed en these ligaments through the theracolumbar fascia, resulting in a flattening .of the lumbar lerdesis. As the ribs ele vate with inspiratien the theracic kyphesis .opens and flattens. The scalene muscles centract as well. Their anterior attachment to the cervical vertebrae acts to flex the cervical spine. Thus the "simple" act of respiratien results in a respense througheut the bedy (Fig. 59.1). This is an example.of an inherent ferce, a phys ielegic ferce acting within the bedy. The inherent ferces within the bedy can be used as activating ferces to assist the physician in the manipulative procedure. This is a very safe and effective methed.of treatment. The same principles that are used to successfully execute a bal anced ligamentous manual eperatien are used fer all osteopathic manual procedures. The physician must skillfully pesition the jeint so that all ferces within the articular mechanism converge en .one specific peint. This peint becemes the fulcrum around which the shift.or change will.occur. When performing an H VLA manual eperatien, the physician needs to place the jeint se that all ferces cenverge. The mere skilled the.operator, tlle more spe cific the cenvergence and the less ferce needed to cerrect the dysfunctien. Very skilled physicians will merely ask the patient to exhale, .or will flex the patient's head to articulate the jeint. Te be successful with balanced ligamenteus and balanced mem branous techniques, the physician must balance all ferces within the ligamenteus structures.of the jeint se that a fulcrum is estab lished. The inherent ferces within the bedy can then be used to cerrect the strain.

APP LICATION OF THE PRINCIP LES

PRINCIPLES OF DIAGNOSIS

Within mest articulatory mechanisms.of the body, there are tis sues unde� veluntary and involuntary centrol. Dr. Sutherland

A strain in the balanced ligamentous articular mechanism of a joint creates an alteration in the permitted metien .of that jeint.

Reciprocal Tension

918

VII

Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment Assessing the motion mechanics at a joint requires gentle tac tile discrimination. Large motions are not necessary, nor are they useful when working with the ligamentous components. Patients may be examined sitting, supine, or prone. The supine position is most effective and is the position that will be used to illus trate the point. With the patient supine and the physician sitting at the patient's side, the physician gently slides their hands under the thorax, placing the fingerpads on the spinous processes of the midthoracic vertebrae. Do not lift your fingers up into the spine; rather allow the respiratory motion of the patient's thoracic cage to move your fingers. Observe the flexion/extension movement of these vertebrae during inhalation and exhalation. Is there any lat eral movement occurring? The physician can apply a gentle pres sure on the spinous processes, using them as handles, to encourage the vertebrae into flexion and extension with the appropriate res piratory cycle. The physician may also apply a gentle pressure to encourage the vertebrae into right and left rotation. (Remember that the spinous process will move to the left when the vertebra moves to the right.) With attentive observation, the physician will be able to diagnose the positional strain within the joint. Principles of Treatment

Inhalation

Exhalation

FIGURE 59.1. Schematic diagram depicting alterations in spinal curves with respiration.

This includes the normal motion accompanying respiration and postural changes. Consequently, by observing the motion of a given joint during respiration or active motion, the observer can ascertain the position of the articular surfaces. This observation is usually performed through palpation. The physician uses in voluntary motion to determine the degree of restriction and the specifics of dysfunction. For example, we know that the thoracic kyphosis flattens slightly during inspiration. We can say that the upper thoracic vertebrae move toward extension (or backward bending) and the lower thoracic vertebrae move toward flexion as the anterior concavity straightens. Thus, if T3 is in a flexed lesion position (i.e., does not want to move into extension), what will happen to T3 during inspiration? If we palpate T2, T3, and T4 during inspiration, will there be equal excursion? What will happen during exhalation? Suppose during exhalation T3 rotated toward the left and side bent toward the left, what would this tell us? If the ligaments on the left side of the joint are under more tension than the ligaments on the right side of the joint, the ver tebrae will resist rotation to the right. If the ligaments that restrict extension are tighter than the ligaments that restrict flexion, the vertebrae will move into flexion more easily. Thus, T3 would resist motion during inspiration and move toward the direction of ease (i.e., exhalation/flexion with rotation and side bending toward the left). We could describe the position of T3 as flexed, rotated, and side bent left. A strain in the balance of a ligamentous or membranous articular mechanism will produce exaggerated motion toward the position of the strain and restricted motion toward the neutral position. While this motion is readily apparent with respiration, gentle motion testing may also be employed.

The first and most important step in treatment is establishing BLT in the articular mechanism so that the body's inherent forces can resolve the strain. The point of BLT is the point in the range of motion ofan articulation where the ligaments and membranes are

poised between the normal tension present throughout the free range of motion and the increased tension preceding the strain ... which occurs as a joint is carried beyond its normal physiology (5). All tensions within the ligaments are reduced to the absolute minimum. As a joint reaches the extremes of its range of motion, the tensions within its ligaments increase; as the joint moves to ward neutral, the tensions decrease so that in the neutral position the ligaments have the minimal amount of tension (Fig. 59.2A). When a joint is strained and normal motion restric�ed, the po sition of minimal tension within the joint is no longer its phys iologic neutral (Fig. 59.2B). Consequently, the point of balance for the ligaments will change in relation to the strain that is present. This new point of balanced tension exists somewhere between the tension created by the strain and the physiologic neutral of the joint. We can look at this from a linear model (Fig. 59.2C). When the articular mechanism is held at the pre cise (new) neutral position, all ligaments will be under the least possible strain. The physiologic forces within the body then be come the activating forces to resolve the dysfunction. Initially the physician can learn to establish a neutral in a strained articular mechanism by assessing the degree of permit ted motion in all planes. This is done by gently encouraging the joint first in one direction and then another. For example, to assess the degree of permitted motion in T3 extended and rotated right, the physician would encourage flexion then extension. Next, the physician would assess rotation right then rotation left by apply ing a slow discriminating pressure to the spinous process. There will be a difference in the freedom ofrotation in one direction as contrasted with another. The physician will easily discern it point in the motion of the joint where the tension in the articular mech anism is poised between the increased tension felt as the extremes of range of motion are approached. This is the point of BLT. The

59. Balanced Ligamentous Tension Techniques

919

FIGURE 59.2. A: Schematic diagram depicting ligamentous tension in a normal joint. B: Schematic diagram depicting ligamentous tension in a normal joint. C: Linear model rep resen�ing the point of balanced ligamentous tension.

A

�

B

.-.

________________________

Normal range of motion

X range of motion with strain pattern

)(

c

physician will hold this position while the activating forces wirhin the body, such as breathing, resolve rhe strain. When the strain correcrs, rhe physician will feel a shifr or change in rhe tension in rhe joint such rhat rhe neurral creared is no longer the point of minimal rension. In orher words, the physician will often feel an increase in rension as rhe joint spontaneously moves toward irs physiologic neutral. To establish rhe point of BLT, the physician will need to assess the rension within the ligan1ents in all directions of motion. It is the most neutral position possible under the influence of all the factors responsible for the existing strain pattern. Thus, the balance point will change according to the pattern of the strain.

Diagnosis The physician will evaluate and treat the pelvis by using the patient's legs as long levers. The patient sits squarely on their ischial tuberosities facing the physician. The physician grasps the patient's ankles under the calcaneus and lifts the lower leg until the entire leg is almost straight, taking care not to shift the patient's center of gravity (Fig. 59.3A-C). Using the leg as a long lever, the physician motion tests the 51 joint by compressing one leg and distracting the other in an attempt to turn or pivot the innominate on the ischial tuberosity. The tissue resistance is noted. Then the procedure is repeated with the other leg. The side of greater ease is noted (Fig. 59.3D).

SPECIFIC TECHNIQUE APPROACHES

Treatment

Remember the degree of motion required is very small. Be precise.

The legs are used as levers to bring the pelvis to a point of bal ance (i.e., rhe position of ease as determined by the previous test). Leg lengths are noted. (Typically, rhe long leg will be on the same side as the increased resistance.) The physician then asks the patient to turn away from rhe long leg while main taining the position of the pelvis through the legs. The patient turns until the tension in the involved ligamentous structures feels balanced. (This usually occurs in the range of 45 degrees

Pelvis: The Differential Technique

The goal of treatment is to normalize movement within the pelvic mechanism, including the 51 joints and hips. This approach ad dresses the iliosacral and 51 components. It provides a general approach to the area.

VII

920


B

A

c

FIGURE 59.3. A: Position of patient and physician for differential tech B, (, D: Schematic diagrams depicting vector of applied forces.

nique.

of rotation.) The physician then holds that posItIOn of the pelvis by using the leverage of the legs, as the patient turns back to neutral. The physician may then retest using the same procedure.

Innominates

This technique may be used on all innominate lesions, upslips, downslips, and anterior and posterior rotations.

D

Diagnosis and Treatment Standing flexion test may be used to determine which side will be treated. Most people will treat both sides, as compensatory changes will occur in the "nonlesioned" side. The exact innomi nate diagnosis is made during the treatment. The patient is asked to stand sideways with the side to be treated facing the physician. The physician grasps the innominate bone at the anterior superior iliac spine (ASIS) and under the ischial tuberosiry (Fig. 59.4A). The patient then unloads the SI joint by crossing the leg on the


921

A

B FIGURE 59.4. A: Position of patient and physician for the standing innominate technique. B: Close-up of hand placement.

affected side over the contralateral leg (Fig. 59.4B) . Once the 51 joint is unloaded, the physician attempts to establish BLT at the SI joint. The physician then asks the patient to bend the con tralateral leg, slowly lowering the patient's pelvis toward the floor. During this maneuver the physician supports and fine-tunes the point of balance as follows: 1. If the physician feels theA5IS lowering into their hand first, then the patient has an anterior rotation and the physician will resist the movement of the ASIS as the patient continues bending his or her knee until the innominate engages. The patient is then instructed to slowly straighten the knee while the physician stabilizes the innominate. 2. If the physician feels the ischial tuberosity lower into their hand first, men me patient has a posterior rotation. The physician will resist this movement as me patient continues bending the knee until the physician feels me innominate engage. The patient is then instructed to slowly straighten the knee while the physician stabilizes the innominate. 3. If, upon beginning to bend the knee, the physician im mediately feels both ASIS and ischial tuberosity lower into their hand, then the patient has a downslipped innominate. The ASIS and ischial tuberosity are resisted as the patient continues bend ing the knee until the innominate engages. The patient is then instructed to slowly straighten the knee while the physician sta bilizes the innominate.

4. If the physician does not feel an immediate pressure in their hands as the patient lowers the pelvis, then the patient has an upslipped innominate. The physician has the patient bend me knee until the pelvis has dropped a few inches. Then physician then asks the patient to slowly straighten the knee while the physician resists the upward movement of the innominate. In all cases, once the patient has straightened the knee, the physician continues to stabilize the innominate until full weight bearing is reestablished. Hip Capsule

Diagnosis Active range of motion is assessed with the patient standing facing the physician, and the physician slowly moving the patient's foot into internal and external rotation. Restriction of active motion is noted by assessing movement at me pelvis. The treatment is per formed with the patient sitting facing the physician. The leg to be treated is crossed so that the ankle rests over the contralateral knee.

Treatment for Externally Rotated Legs (Fig. 59. SA) The physician places one hand upon the medial aspect of the femur near the femoral neck to externally rotate the femur. The other hand grasps the patient's knee. The physician establishes a

922

VII.


B

A FIGURE 59.5. A: Position for treatment of externally rotated hip. B: Hand position for treatment of

internally rotated hip. Note: Patient's hands should be placed on the knee similar to (A).

point of balance between the femoral head and the acetabulum. The patient also places his or her hands upon his or her knee. The patient holds the knee down and laterally while rotating the body away from the leg and backward.

Treatment for Internally Rotated Legs (Fig. 59.58) In this instance, the physician's handhold is more proximal so that there is less torque at the acetabulum. The physician establishes a point of balance between the femoral head and the acetabulum. The patient draws the knee medially and upward while rotating forward and toward the affected side.

Costovertebral Arches/Twelfth Rib There are two lumbocostal arches or arcuate ligaments, one me dial and one lateral. The lateral ligament is a thickened band in the fascia that covers the quadratus lumborum muscle. It spans from the front of the transverse process of the first lumbar verte bra to the lower margin of the 12th rib near its midpoint. The medial arcuate ligament is a tendinous arch in the fascia over the psoas muscle. It is continuous with the lateral crus of the di aphragm and attaches to the transverse process of the first lumbar vertebra. Displacement of the 12th rib inferiorly will stretch the lateral arcuate ligament and compress the quadratus beneath it. This may also irritate the iliohypogastric and ilioinguinal nerves. When irritated, the patient may complain of pain in the lateral buttocks, pain in the groin or inguinal area, or pain in the medial thigh or scrotum.

The Sacral Ala Technique This technique addresses the prevertebral and presacral fasciae, the obturator fascia, sacral nutation, and restricted SI joints. The patient sits on a table facing the physician who is positioned slightly lower. The physician's knees are placed outside the pa tient's, thereby internally rotating and adducting the patient's legs. This maneuver acts to spring open the innominates poste riorly, which decompresses the SI joint. The patient his or her places their hands on the physician's shoulders. The physician places their thumbs along the iliac crest at the junction between the rectus abdominus and abdominal oblique muscles. The pa tient is asked to breathe slowly and deeply, with each exhalation the physician moves his or her thumbs posteriorly along the iliac crest and deeper into the pelvic basin toward the anterior aspect of the sacral ala. The patient may slump forward to further reduce the tension in the anterior tissues (Fig. 59.6). This procedure is continued until the physician's thumbs are deep enough into the tissues that they can act as fulcrums for establishing BLT in the involved tissues. At this point the patient is instructed to sit up slowly starting at the sacrum and curling up through the lumbar and thoracic spines to the cervical area. The patient is instructed to inhale while doing this.

FIGURE 59.6. Patient and physician position for sacral alar technique.


923

B

A FIGURE 59.7. A: Patient and physician position for costovertebral arches ligaments and 12th rib technique. B: Close-up of hand position.

Diagnosis The tip of the 12th rib is palpated for motion with respiration, as described previously (during exhalation it should rise). Typi cally, it is found quite posterior and angled more inferiorly than laterally.

held during inhalation and advanced during exhalation until the thumb meets the resistance of the ligament. Once this position has been reached, balanced tension is established berween the ligament and the rib. The thumb is then drawn laterally with a rolling motion as the patient inhales. Motion of the 12th rib is then rechecked.

Treatment Treatment is directed at the arcuate ligament. (The right side is used as an example in Fig. 59.7 A and B.) The patient is seated with the affected side facing the physician. The physician places the left thumb just lateral to the erector spinae muscle mass under the 12th rib. The patient bends the trunk over the physician's thumb, which gradually and gently advances upward and posteriorly each time the patient exhales. The position is

Alternative Treatment Alternate treatment is directed at the 12th rib. Diagnosis is per formed the same way. The patient is supine and the physician sits on the affected side. The physician places one hand under the back and establishes a firm contact on the tip of the 12th rib. The other hand is placed beneath the contact hand and is llsed to lift the rib anteriorly (Fig. 59.8 A and B). A steady lateral traction

B

A FIGURE 59.S. A: Patient and physician position for alternate approach, to the 12th rib. B: Close-up of hand position.

924

VJI.


is then placed upon the rib at a veccor of 90 degrees from the spine co establish BLT, which integrates the arciculation berween the rib and the vercebra through the arcuate ligaments and the coscovertebral ligaments. The patient breathes slowly and deeply as the physician continues co traction the rib and takes up any slack. This position is held until the rib is felt co slip superiorly with exhalation.

Thorax

Diagnosis This technique is especially effective in patients with chronic degenerative processes in the vercebral column. Patients may be examined sitting, supine, or prone. The supine position is most effective. With the patient supine and the physician sitting at his or her side, the physician gently slides his or her hands under the thorax, placing the fingerpads on the spinous processes of the midthoracic vercebrae (Fig. 59.9). Do not lift yourfingers up into the spine; rather allow the respiracory motion of the patient's thoracic cage co move your fingers. Observe the Aexion/extension movement of these vercebrae during inhalation and exhalation. Is there any lateral movement occurring? The physician can apply a gentle pressure on the spinous processes, using them as handles, co encourage the vercebrae inco Aexion and extension with the appropriate respiracory cycle. The physician may also apply a gentle pressure to encourage the vercebrae into right and left rotation. (Remember that the spinous process will move to the left when the vertebra rotates to the right.)

Treatment

The physician uses the spinous process co direct the vertebra inco a position of balance in relation co the vertebra below. Side bend ing, rotation, Aexion, and extension can be gently introduced through the spinous process. Postural cooperation may be used to augment positioning as follows:

1. Side bending right in the lower thoracic spine or thora columbar junction would be augmented by asking the patient to dorsiflex the ipsilateral foot. Above T6, side bending right would be augmented by asking the patient co elevate the left shoulder coward the ear or side bend the head co the right. 2. Flexion above T8 is augmented by asking the patient co exhale; extension is augmented by asking the patient co inhale. Below T8, inhalation will exaggerate flexion and exhalation will exaggerate extension. This is based on the fact that the spinal curves relax during inhalation. (If in doubt, motion test by asking the patient co inhale and exhale.) Once a point of balance is established, the position is held through a few respiracory cycles until there is a change in the point of balance and the tension in the ligaments. Ribs

Diagnosis Rib restrictions can be diagnosed by palpating rib excursion through a cycle of respiration. It is important to remember that when a vertebral lesion occurs the rib is usually affected.

Treatment (Figs. 59.1 OA and B) The patient is supine with the physician sitting beside the affected side. One hand is placed under the back to contact the rib to be treated. The other hand is placed under the back such that a finger contacts the transverse process of each vertebra attached to the rib. The rib is gently tractioned anterolaterally while the physician uses the spinous processes co establish balance berween the vertebra-rib w1it. The vertebral rib unit includes the rib and both involved vertebrae. Embryologically the rib is an extension of the articular disc, consequently the entire unit needs to be brought co a point of balance. Once found, the position of balance is held through a series of respiratory cycles until a change in tension is felt. Postural and respiratory cooperation may be used.

B

A FIGURE 59.9. A: Patient and physician position for treatment of thoracic vertebra. B: Hand position demonstrated on thoracic spine model.

59. BaLanced Ligamentous Tension Techniques

B

A

c

Alternate Treatment (Fig. 59.1 0C) The patient is sitting with the affected side toward the physician. The physician grasps the shaft of the rib using one hand anteriorly and one hand posteriorly. The physician stabilizes the rib as the patient slowly rotates his or her body toward the affected side. The physician monitors the rib for movement. Once a point of balance has been reached, the patient holds that position and inhales and holds the breath. The physician monitors for a change in tension. The second rib is done using one hand under the axilla.

925

FIGURE 59.10. A: Patient and physician position for supine approach to the ribs. B: Hand position demonstrated on thoracic spine model. e: Patient and physician position for sitting approach to the ribs.

First Rib

Diagnosis Diagnosis is made by assessing mechanics during deep respiration. The elevated first rib is treated. The physician's thumb is placed lateral to the trapezius muscle and advanced medially along the rib with each inhalation until contact is made with the posterior surface of the rib (Fig. 59.11). The physician should attempt to work the thumb under the trapezius as this is the most effective position. The patient is instructed to slowly turn the neck toward

926

VII.

Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment for movement of the scapula. The physician places the other hand on top of the scapula, grasping the spine of the scapula with the fingers (Fig. 59.12B). An inferior traction is placed on the scapula to achieve balance between the serratus anterior, rhomboids, and teres muscles. The physician holds this position until a relaxation of the serratus anterior is achieved. Clavicle

The physician assesses the position of the clavicle by compar ing the proximal ends at the sternoclavicular joints. The inferior clavicle is treated first.

Treatment (Fig. 59.1 3)

FIGURE 59.11. Patient and physician position for treatment of the first rib.

the affected side as the physician resists movement of the rib to establish a point of balance at the costovertebral articulation. The patient then inhales deeply and holds the breath until a change in tension is noted. Scapulothoracic Joint

In this technique, the serratus anterior, rhomboid, and teres major muscles are viewed as the functional ligaments of the joint.

Diagnosis The physician assesses position of scapula on thorax (i.e., scapu lothoracic joint). A hypertonic serratus anterior will produce el evation and lateral displacement of scapula.

Treatment The physician stands on the side of the shoulder to be treated, placing the pad of the thumb on the ribs at the midaxillary line as superior as possible. The physician then slides the thumb pos terior along the patient's ribs until it is under the scapula with the pad of the thumb on the thoracic cage and thumbnail against the scapula (Fig. 59.12A). The physician asks the patient to lean toward him or her so that the thumb slides further under the scapula until the resistance of the serratus anterior is reached. The thumb will act as a fulcrum

The fulcrum for superior-inferior movement of the clavicle is the costoclavicular ligament, located approximately I-inch lateral to the sternoclavicular joint. To treat the clavicle, the patient sits facing the physician. The physician contacts the distal end of the clavicle with one hand, resting the fingers across the acromio clavicular joint (A-C) and the pad of the thumb under the distal clavicle. The other thumb is placed under the proximal end of the clavicle, just lateral to the sternoclavicular joint. The patient is asked to lean forward onto the physician's thumbs. The physician applies a gentle pressure to the shoulder at the acromial end until a subtle disengagement or "give" is felt at the A-C joint. The patient is then asked to carry the contralateral shoulder posteriorly, thereby disengaging the sternal end. These two movements are performed to establish a balance in the lig aments at the articulation. This position is held as the patient breathes until a slight "shift" in the clavicle is felt. The patient is then asked to slowly carry the contralateral shoulder forward, and then sit upright. The operator maintains contact with the clavicle until the patient is upright and all weight is removed from the thumbs. The other clavicle is then treated. Humerus/Glenohumeral Joint

Freedom of rotation of the humerus in the glenoid cavity is tested with the arm at an angle of 45 to 90 degrees laterally from the body, and the elbow flexed. Comparison of the motion on the two sides is made by carrying the hand laterally and upward to test external rotation of the humerus, and medially and downward for internal rotation. Restricted motion in one direction indicates a lesion in the opposite position (Fig. 59.14). Correction is made with the patient seated. The physician stands on the side of lesion, facing the patient. The physician's hand, which is toward the back of the patient, palpates the shoul der joint. The other hand is placed under the axilla, against the ribs and as close to the head of the humerus as possible. This hand acts as a fulcrum for disengagement of the humeral head (Fig. 59.15). The patient reaches the hand of the involved side across the chest to the distal third of the opposite clavicle and holds that shoulder. If the patient elevates the elbow, the in ternal rotation lesion is exaggerated. If the patient lowers the elbow, external rotation is exaggerated. The physician directs the elbow to the degree necessary to arrive at the point of bal anced tension. The patient is instructed to move the uninvolved


927

FIGURE 59.12. A: Schematic diagram of hand place ment for scapula technique. B: Patient and physician position for scapula technique.

B

A

shoulder posteriorly, carrying with it the hand of the lesioned side. This draws the lower end of the humerus across the chest in order that the leverage over the fulcrum provided by the physician's hand disengages the head of the humerus. BLT is then established by gently internally or externally rotating the humerus. This position is held until there is a change in tissue tension. Respiratory cooperation may be employed to correct the lesion.

The Sacroiliac Joint

The 51 joint is a ligamentous mechanism that can be assessed and treated using the same principles that are used in the spine. To assess mechanics at the 51 joint, the physician sits at the side of the supine patient. One hand is placed under the pelvis so that the fingerpads lie along tlle medial aspect of the 51 joint. (It is easiest to use the left hand to assess the right 51 joint.) The other hand is placed on the innominate over the A5I5 (Fig. 59.16 A and B). While monitoring the 51 joint posteriorly, the innominate is gen tly totated anteriorly and posteriorly by applying pressure to the A5I5. The tension in the articular mechanism of the 51 joint is assessed. Then the joint is placed in a position of BLT using the innominate position to establish the neutral. Decompression of the joint is sometimes needed to facilitate the neutral position. This is accomplished by applying an anterior pressure on the sacrum with the posterior hand. Once the point ofBLT is found, it is held until the patient's inherent forces correct the strain.

As with treatment of the spine, respiration may also be used to augment the neutral position.

The Lower Cervical Spine

To assess and treat the T lIC7 articular mechanism, the physician sits at the head of the supine patient and cradles the neck between the hands. The physician places the pads of the index or middle fingers along the articular pillars of the lower cervical vertebrae. The left middle finger is placed under the left articular pillar ofC7 and the right under the right transverse process of Tl (Fig. 59.17 A and B). The physician slowly applies a gentle anterior pressure to the left articular pillar of C7 to encourage C7 to rotate to the right while stabilizing Tl with the other hand. The hands are then switched so that the left rests on the transverse ptocess of TI while the right fingerpad contacts the articular pillar of C7. A slow, gentle, anterior pressure is applied to C7 to encourage it to rotate toward the left while Tl is stabilized from below. The physician compares the tension created within the articular mechanism during the cwo procedures. If there is greater tension created when C7 is encouraged into right rotation, then the ligaments that limit right rotation are restricted. Left rotation would be "easier" and we could say that C7 was rotated left. The physician would then assess freedom of motion with respiration. To correct the strain the physician positions the hands to en courage C7 into the direction of ease. IfC7 was rotated to the left,

928

VI!


FIGURE 59.13. Patient and physician position for clavicle technique.

FIGURE 59.14. Position for assessment of rotator cuff.

the pad of the right middle finger would be placed on the right articular pillar ofC7 and the pad of the left on the transverse pro cess of Tl . The physician then applies a gentle anterior pressure to the right articular pillar encouraging C7 to rotate toward the left, paying close attention ro the changing ligamentous tension between the two vertebrae. The articular mechanism is only rotated

such as the O-A release may relieve suboccipital soft tissue conges tion, a more specific approach to the O-A mechanism is needed to "address" the ligamentous component. BLT can be established between the occiput and atlas through subtle, gentle guiding forces. The physician cradles the occiput in one hand so that the pad of the middle finger slides inferi orly toward the opisthion. The index and ring fingers are placed slightly lateral [0 the midline, approximating the plane of the

to the point where the tension within the ligaments is felt to be in a point ofbalance-a neutral point. The physician then holds the joint in this position of BLT while the patient quietly breathes. The patient's breathing is the activating force and it will correct the strain. The remainder of the cervical spine can be treated in the same manner. The physician can "walk the fi ngers" up on the articular processes assessing the mechanics of each vertebra and treating the findings. The occipital-atlantal (O-A) joint is treated with a different approach and is discussed subsequently. Occasionally, the physician needs to employ respiratory co operation from the patient. In this situation, the physician will ask the patient to inhale and hold his or her breath or exhale and hold his or her breath, in order to fine-tune the point of BLT. The Upper Cervical Spine

The O-A joint is a ligamentous articular mechanism. The pro prioceptive role of the short muscles and ligaments of this area is particularly important to balance and posture. While techniques

FIGURE 59.15. Patient and physician position for treatment of the glenohumeral joint.


929

FIGURE 59.16. A: Photograph of patient and physician position for treat ment of the sacroiliac joint. B: Schematic diagram of hand p lacement.

A

B

FIGURE 59.17. A: Patient and physician position for treatment of the cervical spine. B: Schematic diagram of hand p lacement.

A

B

930

VII.


FIGURE 59.19. Schematic of hand placement for treatment of the atlantal-axial joint.

FIGURE 59.18. Schematic diagram for treatment of the occipital atlantal joint.

occipital condyles. The other hand is placed under the upper cervical complex with the pad of the middle finger just above the spinous process of C2 (Fig. 59.18). The head must rest, re laxed upon the physician's hands. The physician then asks the patienr to dorsiflex the feet. The physician will feel a change in the tension under their hands. The patienr is then asked to tuck the chin toward the chest all the while keeping his or her head in the physician's hand unril BLT is established between the occiput and atlas. The physician will feel their finger, which is above C2, slide superiorly and come in contact with the tubercle of C 1. This finger is creating an anrerior vector stabilizing C1 as the patient flexes the occiput. The physician monitors the resis tance in the tissues by comparing the tension berween the hands. The physician may further augmenr the procedure by asking the patient to hold his or her breath in either inhalation or exhala tion. The release is often felt just as the patienr can no longer hold his or her breathing.

respiratory cooperation may be used to augment the point of bal ance. The A-A joinr is often treated after rebalancing of the O-A joinr.

ACKNOWLEDGMENTS

In the production of this manuscript the author is indebted to Anne Wales, DO, for supervision and guidance; Michael Burruano, DO, Andrew Goldman, DO, and Hugh Ettlinger, DO, for critical reading; and osteopathic manipulative medicine predoctoral fellows Lynette Bassett, Derek Libby, and Kim Corneal for technical assistance.

REFE RENCES 1 . Lippincott HA. The osteopathic technique ofWm. G. Sutherland, D.O. In: Academy ofApplied Osteopathy, 1 949 Yearbook. Academy of Applied Osteopathy; 1 949. 2. Nordin M, Frankel VH. Basic Biomechanics ofthe Musculoskeletal System. Philadelphia, PA: Lea & Febiger, 1 989. 3. Norkin CC, Levangie Pc. Joint Structure and Function. Philadelphia,

Atlantal-Axial

According to Dr. Sutherland's model, the occiput, atlas, and axis act as a unit of function. Assessmenr and treatment of atlanral axial (A-A) strains are done using the same principles as the lower cervical spine. However, the hand position is quite differenr. The physician places the hands in the position assumed for treatmenr of the O-A, but the pad of the finger of the lower hand main tains conract with C2, while the upper hand stabilizes Cl . If the physician's hands are large enough, they may be able to con tact each of the articular pillars of C2 (Fig. 59.19). A point of BLT is established berween Cl and C2. This position is held as the patient goes through several respiratory cycles. Positional and

PA: FA Davis Co; 1 992. 4. Steinberg BG, Plancher KD. Clinical anatomy of the wrist and elbow.

Clin Sports Med. 1 99 5 ; 1 4:299. 5 . Magoun HIS. Osteopathy in the Cranial Field, 3rd ed. Kirksville, MO: The Journal Priming Company; 1 976. 6. V1eeming A, Snijders q , Stoeckart R, Mens JMA. A new light on low back pain: the seiAocking mechanism of the sacroiliac joints and its im plication for sitcing, standing and walking, In: Vleeming A, Mooney V, Snijders q, Dorman T, eds. The Integrated Function ofthe Lumbar

Spine and Sacroiliac Joints. Rotterdam: European Conference Organiza tion; 1 99 5 .

7. Snijders q, Vleeming A, Stoeckart R . Transfer o f the lumbarsacral load to iliac bones and legs. Clin Biomech 1 993;8:285. 8. Sutherland WG. Teachings in the Science of Osteopathy. Porrland, OR: Rudra Press; 1 990.

INTEGRATED NEUROMUSCULOSKELETAL RELEASE AND MYOFASCIAL RELEASE ROBERT C. WARD

KEY CONCEPTS • • • • • • • •

The meaning of the term myofascial release (MF R) The meaning of the term integrated neuromuscwoskeletal release (INR) A theoretic basis for using M F R and INR concepts Some of the science that supports I NRlMFR ideas How the neuromusculoskeletal system responds to mechanical forces How integrated peripheral and central neuroreflexive activities influence myofascial functions General INR and M F R applications To gain an understanding of and apply general M F R and (INR) techniques

Integrated neuromuscular and myofascial release approaches and treatment processes are used to diagnose and modifY altered re flex and mechanical patterns anywhere in the body. Applying this form of treatment depends on one's ability to palpate and interac tively respond to shifting reflex and mechanical changes as they occur. Recognition of active and passive elements influencing both local and general myofascial and skeletal patterns are im portant elements in the process. The key to clinical success is the systematic development and application of the MAN acronym Mechanics, Anatomic relationships, and interdependent Neural influences. As V iidik writes: The structure of most biological materials (tissues) is to some extent influenced or modified by the in vivo generated mechanical forces which act upon them under physiologic (and pathophysiologic) con ditions. The mechanic.,j properties of all materials, living tissues as well as dead are dependent on their structural configurations from the molecular level to the macroscopic

(1).

A significant integrated neuromusculoskeletal release (INR)/ myofascial release (M FR) concept acknowledges that all human activities are mechanical at many levels-macroscopic to micro scopic. In the course of these activities, behavioral patterns both affect and are affected by myriad neuroreflexive and neurovascular activities. Inevitably, both fixed and temporary three-dimensional

patterns arise from a variety of factors such as genetics and age; behavioral characteristics, such as elation and depression; and lifestyle factors, such as good health, effects of accidents, nutri tion, drug use, and physical fitness. The clinical challenge is to assess and appropriately treat interdependent "MAN" factors to the extent possible. INR and M F R i deas have been a part ofAmerican osteopathic thinking fro m early in the profession's h istory. Until recently, they were commonly referred to as isometric and isotonic methods, fascial release, and functional techniques. Oral tradit ions over four or five generations suggest that A.T. Still used reflex-based stretch and relaxation procedures without referring to them as such. Pictures of Still performing one or rwo procedures sug gest that he used both functional indirect and articulation meth ods. Both are described elsewhere in this text (see Chapter 70, "Still Techniques"). Unfortunately, his descriptions lack detail, but Still's writing heavily emphasizes both funct ional anatomy and related mechanics (2) . This author has been using combinations of isometric, iso tonic, functional indirect, and MFR concepts since the early 1950s. At that time, Wilbur Cole and Esther Smoot intro duced these procedures to osteopathic medical students attending the Kansas City (Missouri) College of Osteopathy and Surgery. Dr. Cole taught preclinical osteopathic manipulative treatment (OMT) skills, neuroanatomy, and clinical neurology. He was also a neuroanatomy researcher and published rwo early papers con cerning motor end plates on striated muscles (3,4) . D r. Smoot, with a full-time practice in the Osteopathic Hospital of Kansas C ity, said she learned her methods from several osteopathic pi oneers, but she never specifically described her experiences or teachers. Along with Still and Smoot, W illiam Neidner, who prac ticed in both Massachusetts and Michigan, was an early pro ponent of fascial rwist maneuvers but wrote little about his work (EL. Mitchell, Sr. , personal communication, 1 970; R. H ruby, personal communication, 1 9 89). No doubt there were others.

DEFINITION

INR and M F R techniques are combined procedures (5) de signed to stretch and reflexively release patterned soft tissue and

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joint-related restrictions. Both direct and indirect methods are used interactively. (See "osteopathic manipulative treatment" and its methods in the Glossary at the end of t his text.)

The definitions of many common patterns, provided by the American Academy of Orthopedic Surgeons' Glossary, follow (7) .

Definitions Motion segment:

GOAL

Stress: Three-dimensional neuromusculoskeletal movement patterns are determined by every aspect of b iology and behavior. Because of this, a fundamental treatment goal is to interactively assess and modify maladaptive patterns within the ability of the patient to adapt . The process is more effective when the operator uses simultaneously applied, two-handed palpation, much like play ing a two-handed musical instrument. By searching out tight and loose end-feels (described in the Glossary), patterned soft tissue and joint-related movements are assessed and treated simultaneously. As both static and dynamic movement barriers are encountered, they are released by sequen tially loading areas of tightness using combined compression, traction, and twist ing maneuvers. (Static barrier is defined as any soft tissue or bony impediment to passively induced motion by an operator. Dynamic barrier is defined as any soft tissue or bony impediment to inherent tissue motion.) Reflexively modulated releases, occurring as varieties of direct and indirect maneuvers, st ress and strain the neuromusculoskele tal networks from the skin to t he deepest spinal joints and their attachments. A working knowledge of musculoskeletal mechan ics is essential (see C hapters 44 to 53). Additional discussion of neutral and non neutral spinal mechanics including vertebral dysfunctions can be found in Greenman's text (6). By integrati ng patient-assisted release-enhancing maneuvers, the treat ment process is accelerated. FUNCTIONAL ANATOMY AND CLINICAL PROBLEM SOLVING The Tight-Loose Concept

Tight-loose patterns involve not only the bony skeleton, but also superficial and deep soft tissue structures of all types. Looking for three-dimensionally related t ightness and looseness is essential to the process. For example, patterned three-dimensional changes can be sensed as large or small areas of myofascial and bony positional asymmetry that are tight and loose relative to one another. Assessing tightness and looseness between and among layers of tissue is often helpful. Some examples: One shoulder commonly tight and the other loose Tight left hip and sacroiliac mechanics, loose right Tight left cervicothoracic junction, loose right Tight right sternocleidomastoid, loose right scalenes Tight right sternocleidomastoid, tight left scalenes Tight lumbodorsal fasciae, loose second layer muscles, tight third and Fourth layer muscles

MECHANICS AND FORCES

Patterns can be mechanically assessed by noting effects of multi directional Forces on both local and distant joints and soft tissues.

Strain: Stiffness: Compliance: Creep:

Viscoelastic material:

A vertebra, its disc, and associated ligaments. Force normalized over the area on which it acts. Normal stress is perpendicular to the cross-section, and sheer sr ress is parallel to it. C hange in shape as a result of stress. The ratio of a load to the deformation (strain) it causes (the "tight" concept). The inverse of stiffness (the "loose" concept). The continued deformation (i ncreasing strain) of a viscoelastic material under constant load over time. Direct MFR methods create creep by using combinations of r raction, compression, and twist. Any material that deforms in relat ion to t he rate of loading and deformation.

Force Effects

All tissues exhibit nonlinear, srress-strain responses that are func tions of their densities and viscosities. For example, tendons de form at different rates than muscle fibers, ligaments, and bone. Many mechanical components of the body are composed of water-absorbing collagen and supporting ground substances. Chemically, they include glycoproteins, glycosaminoglycans, and other low-molecular-weight material. It is on this background that mechanical forces exert their effects ( 1 ). I nevitably, a number of mechanical principles interdepen dently affect neurologic and anatomic functions. Palpatory diag nosis and man ipulative r reatment apply many of these concepts. Examples are: Wolff's Law, Hooke's Law, and Newton's Third Law:

Wolff's Law:

Hooke's Law:

Newton's Third Law:

states that bones tend to deform along the lines of force placed upon them. This is also true for soft tissues (8). states that any srrain (deformation) placed on an elastic body is in proportion to the stress (force) placed upon it (8). states that when two bodies interact, the force exerted by the first on the second is equal in magnitude and opposite in direction to the force exerted by the second on the first (8).

Passive and Active Patterns

Mechanical patterns are both passive and active. Passive external factors such as body conformation are easily recognizable. Passive internal factors, such as asymmetric srruc tural supports, muscle inhibition, and bony asymmetries, are less evident.

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JV, Nyberg R. Rational Manual Therapies. Baltimore, MD: Wi l l iams & W i l ki ns; 1993:230.) FIGURE 60.1. Fascia in gross dissection. (From Basmajian

Active patterns, that is, those arising from neurally medi ated activities, are superimposed on the passive system. Examples include: • • • • • •

Sitting Standing Walking Sleeping Working Sporting activities

Figures 60. 1 to 60.4 demonstrate a 1 987 soft tissue dissec tion done by Frank George, DO, in the anatomy laboratories of Michigan State University. From this work, we learned that fas cia and muscle are anatomically inseparable. Earlier authors like Cathie (9) and Becker ( 1 0) suggested that fasciae move inde pendently. George's work suggests that fasciae probably move in response to complex muscle activities acting on not only bones and joints but also ligaments, tendons, and fasciae. This view is reinforced by other research highlighting the im portance of fascia in maintaining general proprioception. Since proprioception is ultimately controlled by inte rdependent neural and muscular elements, after joint and muscle spindle activity is accounted for, 75% of remaining proprioception occurs in fascial

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FIGURE 60.3. S h a rp d issection difficulties resu lting from muscle a n d

fascia b e i n g inseparable. (From Basmajian JV, Nyberg R. Rational ual Therapies. Ba ltimore, MD: W i l l iams & W i l kins; 1993:231.)

Man

sheaths ( 1 1 ) . Such responses were actually demonstrated in the 1 960s by Earl ( 1 2) and Wilson ( 1 3) in their work with muscles under stretch.

Palpation to Develop Haptic Skills

Palpation is the key to successful use of any manipulative method. Some untrained observers occasionally suggest that the ability to palpate is inborn and difficult to teach. This may be true in a few instances, but all health care professionals are regularly challenged to develop palpation skills when performing physical examinations and myriad medical and surgical procedures. Haptic neuroscience analyzes both sensory and motor aspects of hand activities. Palpatory diagnosis, technically, is a high-level haptic skill. In an almost lite ral sense, skilled palpating hands learn to "see" anatomic and mechanical detail, much like a blind person senses the environment. As improvements appear, appreciation for seem ingly obscure, but important, subtleties e me rge. Sensing Positional and Movement-Related Asymmetries

One key to success is the ability to identify tethering effects that persistently c reate and maintain pathologic asymmetries. Tight

ness suggests tethering, whife looseness suggests joint and/or soft tissue

FIGURE 60.2. Closer view of fascia i n gross dissection. (From Basmajian

JV, Nyberg R. Rational Manual Therapies. Baltimore, MD: Wi l l iams & W i l kins; 1993:230.)

FIGURE 60.4. Position for thoraco l umbar release: head to most com forta ble side with arms off table.

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laxity with or without neural inhibition. Sometimes tethering re lates directly to changes in coupled vertebral motions and altered joint play; the motion segment is altered. Knowing the difference berween neutral and nonneutral vertebral mechanics is essential (see Chapters 4 1 , 43- 50, 52). Both local soft tissue and neu toreflexive and neurocirculatory changes, such as viscerosomatic reflex changes, are common contributors to tethering. Tethering arises from many sources: The spine, with altered coupled vertebral motions from any source T he synovial joints and their influences on joint play Altered soft tissue mechanics (remembering that all tissues and their inherent motions are intrinsically asymmetric) Asymmetric neural inpurs arising from: Multiple levels of the central nervous system , including cranial nerves, brainstem, midbrain, thalamus, and cortex Limbic system and reticular activating system Primary spinal cord sources Peripheral nervous system sources at any level Viscerosomatic reflexes Somato-somatic reflexes Neurohumoral activities of all kinds Lowered reflex thresholds from sites of disease, IOJury, and degeneration Biobehavioral and sociocultural factors are common sources of "tethering" and somatic dysfunction Awareness of individual beliefs, perceptions, biases, and expec tations in relat ion to expected outcome is an essential requirement for both clinician and patient. Importantly, patients commonly seek ptofessional help when environmental stressors trigger un desirable symptoms. Difficulty coping with overwhelming events is a common presentation in any neutomusculoskeletal practice. Medicalization of nondisease-related problems is frequent. Un witting encouragement of dependent and co-dependent behav iors, including requests for manip ulative treatments, is common under these conditions. Monitoring Inherent Tissue Motion

Inherent tissue motions are palpably evident, asymmetrically pat terned, neuroreflexive activities in the soft tissues. T hey con stantly move, often at variable rates. Palpation that focuses on these motions should readily identify patterns of shifting asym metric tightness and looseness. Asymmetrically perceived end feels are commonly referred to as direct and indirect barriers. As a rule, inherent movements are easier in some directions, less so in others. Myofascially, shifting tightness and looseness identifies unevenly distributed direct and indirect barriers. Many are in dependent of joint mechanics. Others are tightly linked to joint mechanisms.

affect the opposite lower limb, lower costal cage and trunk rota tors, the opposite shoulder, the cervical spine, and cranial base. In some cases, it is likely that successful treatments link as yet unclear intrinsic body movements of both the patient and operator at some level. How this occurs is unknown, but it is likely that both conscious and subconscious brain-mediated factors are at play. Experienced practitioners and patients often comment that a treatment went especially well or not as well on a particular day. Some research indirectly suggests how this occurs. In 1989, Grinberg-Zylerbaum and Ramos reported on their stuclies of nontouching, silent communication berween rwo or more individuals. E lectroencephalography ( E E G) was used as a means for studying silent communication patterns berween rwo individuals. Partners who reported feeli ngs of being blended with one another altered their EEG patterns to the point of being virtually identical (14). This author and others have repeatedly identified similar blending effects during MFR and craniosacral treatment encoun ters. Whether these experiences are in any way similar to the Grinberg-Zylerbaum and Ramos work has not been investigated. Other hypotheses and experiments point out subtle cranial bone movement changes that may be involved. In one instance, Norton hypothesized a model for quantitatively assessing pressure variations in soft tissues of both the subject and examiner. His study is completely theoretical, however, and lacks experimental data ( 1 5) . Adams and colleagues, on the other hand, made parietal bone movement measurements in cats that suggest the presence of neurally generated waveforms that create 1 - or 2-JLm movements across the parietal suture ( 1 6). Individual abilities to palpate these subtle changes have been carried out in a number of experiments (17,18). Tight-Loose Concept Exercise {Figs. 60.86 and 60.87}

A simple laboratory exercise readily demonstrates the tight-loose concept. With the patient lying supine, the operator grasps the patient's wrists. By slowly raising the upper limb toward full over head extension, one gets a sense of shifting three-dimensional tightness or looseness that begins at the wrists and eventually in volves the whole of the patient's body. By carefully attending to both the quality and amplitude of these passively induced op erator forces, clearly defined mechanically asymmetric sites of tightness and looseness become apparent. As each limb is moved separately and together, tight-loose rela tionships vary considerably and their end-feels are different . Some are abrupt , almost like hitting a wall. Others are soft,. like either falling into or fluffing a pillow. Importantly, these asymmet ric shifts rarely follow classic anatomic patterns. With practice, vari able tensions and loads are readily sensed from the hands and wrists distally into the lumbodorsal fascia and pelvis. Pain at Loose Sites

TREATMENT SKILLS

Treatment skills improve as one learns to apply well-directed forces interactively against direct and indirect barriers. A common example occurs when restrictions involving one side of the pelvis

Painful sensations are common at loose sites, particularly in chronic cases. Typically, there is little muscle spasm or' tight ening. Under these conditions, associated muscles are commonly weak and inhibited. Some practitioners refer to these sites as hy permo bile, implying that ligamentous laxity and joint instability

60.

are the fundamental problems. An alternative idea concludes that loose, painful muscles are weak and inhibited over large, often ill-defined areas, including ver tebral mechanics. F� om a clinical perspective, whole body effects are the r ule rather than an exception. Loosened sites are often vulnerable to injury under relatively trivial circumstances. Repeated ankle and lumbosacral sprains, as well as neck and shoulder problems ar ising from altered lumbopelvic and lower limb mechanics, are common examples. CLINICAL ASSESSMENT

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groups. The pattern often changes when the head is sequen tially changed from left to center to r ight. A com mon prone wraparound patter n is as follows: Tight poster ior left hip, sacroiliac joint, lumbar erector spinae, and lower costal cage Loose poster iorly on the r ight Tight anterior and r ight lateral costal cage Tight r ight upper anterior costal cage Tight left thoracic inlet, poster iorly Tight r ight scalenes, and cervical flexors Tight left craniocervical attachments, including sternocleido mastoid, jaw, and facial mechanics

Tightness and looseness should be evaluated from a patterned three-dimensional context that includes: Skeletal and soft tissue configurations Upper and lower motor neuron influences Effects of mechanical modeling and remodeling of bones, joints, and soft tissues Effects of general skeletal factors Injury history Effects of repetitive daily activities Psychoemotional states Limiting psychosocial and socioeconomic factors Locating direct and indirect barr iers is a useful method for understanding tightness, looseness, and tether ing effects. Tightness ofany kind suggests tethering and direct barriers. It also implies the presence of direct barriers and "bind" (see Glossary at the end of this text) . Some are of bony origin, but many are not. Whether these tethers and areas of bind should be removed requires careful assessment. One form of tether ing is acute muscle spasm, which is almost always self-limited. Another relates to generally tight muscles, which are not always sources of pain and altered function. Stress ful lifesryles and personaliry issues are common in this group. Tr ue spastici ry, centrally mediated neural tethering, arises from upper motor neuron pathologies. Cerebral palsy, central spinal stenosis, strokes, and effects of head injur ies are common examples. Scar tissue implies the presence of passive mechanical tether ing that may actually stabilize an otherwise unstable site. Acute localized muscle tension and tethering generally im ply peripheral neural involvement. A history of direct trauma is common for this group.

Looseness generally occurs in association with indirect barriers, neural inhibition, and painful sites. Since inhibition often accom panies neural injury and Waller ian degeneration, pain reports and muscle weaknesses are a common theme with this group. THREE-DIMENSIONAL PATTERNS

Three-dimensional vertical, horizontal, and wraparound patter ns are the rule and can be identified with some practice. Looking for three-dimensionally related areas of tightness and looseness is the key. For example, in the ptone position, r ight hip extension should create left lumbar, latissimus dorsi, and shoulder movements, and vice versa. Well-conditioned individuals will extend the hip with minimum use of contralateral back extensors and shoulder

TREATMENT GOALS

The general goal is to release tightness and restore three dimensionally patterned functional symmetry to the extent pos sible without aggravating hyper mobiliry. As forces against direct and indirect barriers are sequentially applied, an experienced op erator can effic iently treat the w hole body in a reasonably short time. Direct and Indirect Techniques

Simultaneous direct and indirect two-handed techniques are used. With practice, direct and indirect maneuvers can be ap plied simultaneously, w ith one hand per for ming direct release while the other per for ms i ndirect release. Release-Enhancing Maneuvers and Integrated Neuromuscular Release Processes

Star ting from the skin and working inward, varieties of traction, twist, shear, and compression are applied three-dimensionally while inherent tissue and joint motions are simultaneously mon itored for shifting tightness and looseness. Inherent tissue move ments have been described as "wormlike" activities beneath the palpating hands and fingers. The clinical assumption is that these perceived activities are neuroreflexive responses to the externally applied forces. Direct Myofascial Release

Direct M F R maneuvers strain (defor m) areas of tightness. By holding firmly against the soft tissue resistance (i.e . , the direct myofascial barriers) releases are tr iggered. By making tightness even tighter, releases occur rather quickly, often in multiple di rections at the same time. W he n this happens, the tissues often feel as though they are quivering in multiple directions at the same time. Indirect Myofascial Release

For every area of perceived tightness, there are one or more areas of three-dimensionally related looseness. Commonly, the looseness is i n exactly the opposite direction from the tightness. This m irroring concept is similar to those identified using func tional indirect methods descr ibed in Chapters 6 1 , 64, and 70.

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Exper ienced operators locate these interdependent relationships quite readily, finding it easier to follow gently behind releases as they occur. Integrated Neuromuscular Release

Patient assistance with release-enhancing maneuvers helps speed the treatment process. A few enhancers are listed below: 1 . Breath holding dur ing phases of inhalation and exhalation changes. The goal is to alter both intrathoracic and intraabdomi nal pressures using costodiaphragmatic, shoulder girdle, and lum bopelvic interactions. 2. Prone and supine simulated swimming and pendulum ar m swing maneuvers use the arms as direct and indirect barriers are released. 3. Right, center, and leftward head turning in any body po sition is often helpful. 4. Isometric limb and neck movements against the table or chair create post-isometric muscle relaxations at various sites. For example, in the prone position, stubborn lumbopelvic problems often persist until proximal thoracolumbar and iliopsoas attach ments are stressed by alternately forcing the knees, thighs, and iliopsoas hip flexors against the table. This can be easily done both prone and supine. 5. For reasons as yet unclear, varieties of patient-invoked cra nial nerve activities, such as eye, tongue, j aw, and oropharyngeal isometric and kinetic movements are also helpful. Apparently, progressively engaged cranial nerve activities create central and peripherally mediated neural activities that alter abnormal pat ter ns as external forces are applied. It is also probable that dis traction plays a role, similar to the Jendrassik maneuver used to enhance the patellar jerk reflex.

POSTTREATMENT EVALUATION

Posttreatment evaluation is essential for a number of reasons: 1 . To know whether appropriate and helpful changes have oc curred 2. To help the patient understand what to expect from the treat ment 3. To help design an appropriate individualized exercise program 4. To help develop an appropriate phar macologic program, should it be necessary 5 . To identify and accurately record changes for the medical record

occurs only once, but those with rheumatologic disorders such as lupus erythematosus and fibromyalgia can experience repeated flare-ups.

ROLE OF EXERCISE IN MAINTAINING CHANGES

It is essential that a simple, time-efficient exercise program be worked out. The program should stretch areas of tightness without aggravating pain or instability. Restor ing adequate pro prioception by using one-leg standing activities is essential for long-term success. Looseness, or areas of inhibited individual and patterned muscle activities, requires strengthening and ton ing. For example, identification ofweak, inhibited muscle groups, such as altered gluteus maximus and hamstring firing sequences, helps develop a clear rehabilitation focus. In this example, back pain patients often fail to fire one or both gluteus maxim us mus cles dur ing prone straight leg hip extensions.

CONCLUSION

This section introduces a few basic myofascial and integrated neuromusculoskeletal release concepts. Keys to diagnostic and treatment successes lie in the ability to sor t out interdependent mechanical, anatomic, and neurologic problems contributing to altered three-dimensional movement patter ns. Hallmarks for identifying these patter ns lie in the ability to assess and treat inter active areas oftightness, looseness, and tether ing. A well-designed, individualized, easy-to-follow exercise program is essential for long-term success. The following sections of this chapter present a few useful tech niques.

INTEGRATED NEUROMUSCULOSKELETAL TECHNIQUES FOR SPECIFIC AREAS

There are many ways to approach neuromusculoskeletal problems manually. For the sake of practicality, descr iptions are limited to a few methods used with relative ease that have stood the test of time. Those familiar with muscle energy terminology can record and monitor I N RlMFR processes by superimposing fu nctional anatomy descriptors. For example, bony positional changes, such as unilateral left sacral flexion (also called sacral shear), left on r ight sacral torsion, and L4 nonneutral extension-rotation-side bending left, easily combine with these methods.

Lumbosacral Spine and Pelvis POSTTREATMENT DISCOMFORT

Patients commonly exper ience a temporary worsening of discom fort following the fir st treatment or two. This possibility should be identified before the patient leaves the office. The phenomenon is similar to postexercise muscle soreness, but does not occur with everyone. Older age groups and general deconditioning are common contributors to the problem. Usually the experience

The general goal is to three-dimensionally balance lumbopelvic mechanics, keeping in mind that the costal cage and lower limbs play major roles in the process.

Thoracolumbar Release

Figures 60.4 ro 60. 1 1) illustrate this process.

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FIGURE 60.5. Position for thoracolumbar release: head to most com forta ble side with arms on table.

FIGURE 60.8. Hands placed at thoracolumbar junction, with head in

midline.

FIGURE 60.6. Position for thoracolumbar release: head comfortable, feet and arms off table.

FIGURE 60.9. Head midl ine.

FIGURE 60.7. Operator stands beside patient's h i p, with head to side.

FIGURE 60.10. Head right.

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VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment blanching, the site of major soft tissue tension commonly be comes reddened and warmer, the so-called "blush phenomenon" (Fig. 60. 1 1). 10. Typical releases occur three-dimensionally w ith sustained traction and twist, and they can occur singly or in multiples. The latter often creates a wormlike sensation under the palpating hands. As multiple releases continue, so-called unwinding phe nomena often occur, as shifting patterns of tightness and looseness alter three-dimensional relationships. With practice, one learns to feel deeply into the areas surrounding facet joints. Symmet ric segmental movements to passive three-dimensional stressing suggest that the procedure is complete. Treatment is complete when repetitive stressing of selected sites no longer creates release act ivity.

FIGURE 60.11. Blush sign. After blanching. areas receiving major

stressing commo n l y become reddened and wa rmer.

Objective To balance the thoracolumbar j unction three-dimensionally in relation to lumbopelvic, thoracocostal, and diaphragmatic me chanics.

Review Review cervical, trapezius, shoulder girdle, and costal cage anatomy for their three-dimensional perspectives and f unctional relationships to the area.

Procedure

Prone t. The patient's feet should be off the end of the table to minimize lower limb stresses in relation to the pelvis and low back ( Figs. 60.4 to 60.7). 2. Initially, the patient's head should be turned to the most comfortable side. Holding it exclusively in the midline, as many wish to do, often obscures tight-loose effects at the thoracolumbar junction. 3. The hands and arms are comfortably placed either over the sides of the table, or on the table beside the hips and thighs. 4. Stand beside the patient's hip, facing cephalad (Fig. 60.6) . 5. Place your hands at the thoracolumbar junction, cover ing posteroinferior rib, trunk rotator, and diaphragmatic sites (Figs. 60.7 to 60. 1 1 ) . 6. Place hands widely open with the thumbs pointed cephalad along either side of the spinous processes while the remainder of each hand spreads over the posteroinferior costodiaphragmatic and upper lumbar areas. 7. Identify superficial and deep t ightness and looseness pat terns three-dimensionally. 8 . Firmly separate the thumbs across the midline as the left hand creates clockwise and the right hand creates counterclock wise traction. The hands should not slide on the skin. 9. As the skin is stretched between the thumbs, it will ini tially blanch. As compression, tract ion, and twist are maintained, tissues begin to relax both reAexively and mechanically in accor dance with principles discussed earlier in this chapter. After initial

Combined Sacroiliac, Sacral Base, and Lumbopelvic Releases

This process is shown in Figs. 60.12 to 60. 1 9 .

Objective The goal is to establish symmetric sacral nutation and counternu tation movements in relation to the innominates, lumbar spine, and lower limbs. Nutation is anterior nodding (Aexion) of the sacral base in relation to the lumbar lordosis; counternutation is posterior nodding (extension) of the sacral base in relation to the lumbar lordosis.

Review Review three-dimensional anatomy of the sacroiliac joint, sacral base, and lumbopelvic mechanics, including proximal and distal erector spinae and iliopsoas relationships, quadratus lumborum, multifidus, and deep layer, hip rotator, and pelvic diaphragm rela tionships. Also be aware of congenital anomalies, and iliolumbar innominate-sacral base inAuences.

Diagnosis With practice, sacral torsions, Aexions (in some cases called sacral shears), and innominate positions become readily apparent. In nominate positions are commonly referred to as "anterior," "pos terior," or "shear." Most typically, they are diagnosed using muscle e nergy nomenclature.

Procedure

Prone 1. The feet should be off the end of the table to minimize lower limb stresses in relation to the pelvis and low back. 2. The head should be turned to the most comfortable side. Holding it in the midline, as many wish to do, often obscures t ight-loose effects in the thoracolumbar regions. 3. The hands and arms are comfortably placed either over the sides of the table, or on the table beside the hips and thighs. 4. Stand at the patient's left shoulder facing caudad. 5. Place your proximal left hand longitudinally over the thora columbar j unction, w ith the long finger covering the upper lumbar spinous processes. For best results, place the metatar sophalangeal joint of the long finger precisely at the TI2-U junction (Fig. 60. 1 2).

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FIGURE 60.12. Position for combined sacroil iac, sacral base, and l u mbopelvic releases.

6. The distal right hand covers the sacrum between the two in nominates with the index finger overlying the right sacroiliac joint and inferior lateral angle while the ring finger covers the left. The long finger will fall naturally over the sacral spines and sacral hiatus (Fig. 60. 1 3) . 7. Evaluate patterns o f tightness and looseness: a. Proximally and distally, by distracting the sacrum and lumbar spine in the long axis of the spine (Fig. 60. 1 5) . b . Circumferentially, by transversely translating each hand in opposite directions across the lumbopelvic system (Figs. 60. 1 6 to 60.19). 8. Induce lumbosacral distraction by assertively moving the left

hand proximally up and over the thoracic curve while forcing the right hand distally up and over the natural curve of the sacrum (Fig. 60. 1 5) . Importantly, one must respect both the sacral base angle and the natural configuration of the sacral curve. Some are in a more or less straight-line relationship with the back, while others are acutely angled, demonstrating more or less perpendicular relationships with the spine and pelvis. 9. Both heavy-handed and, in some cases, light-handed loads mechanically induce reflexively controlled inherent tissue and sacral movements. Learning both methods takes some practice.

FIGURE 60.13. PQsition for combined sacroil iac, sacral base, and l u mbopelvic releases.

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FIGURE 60.14.

1 0 . As loading develops, var ieties of three-dimensional tight ness and looseness become apparenr. Sacral torsions, fle xions (shears), innomi nate changes, and sacroiliac joint factors, such as close and loose packing, are noted. 1 1 . By using combinations of distraction and compression (Figs. 60. 1 4 and 60. 1 5) while monitoring inherent tissue movements, sacroiliac positional and movement changes commonly give way and become more symmetr ic. 1 2 . As the lumbopelvic complex passively drifts right and left, it often helps to change the hands per pendicular to [he spine to induce further movement in a crosswise fashion (Figs. 60.1S and 60. 1 9) .

1 3 . Treatment is complete when sacroiliac joint and general lum bar movements are as symmetric as can reasonably be ex pected. Focused Prone Sacral Base Release: Two-Handed Technique

This ptocess is shown in Figs. 60.20 and 60.2 1 .

Objective The goal is to three-dimensionally balance the sacral base in rela tion to L4-5 mechanics, the iliolumbar ligament, and positional innomi nate asymmetr ies.

From shoulder

FIGURE 60.15.

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FIGURE 60.16.

Review

3.

Review lumbopelvic anatomy, L4- 5 mechanics in relation to the sacrum and pelvis, iliolumbar ligament, and innominate, hip rotator, and pelvic diaphragm relationships, including distal iliopsoas and piriformis muscle influences.

4. If right-handed, stand at the patient's left shoulder, facing caudad.

Diagnosis See "Sacroiliac Release: Supine" later in this chapte r.

Procedure

Prone 1. The feet should be off the end of the table to minimize lower limb stresses in relation to the pelvis and low back. 2. The head should be turned to the most comfortable side.

The hands and arms are comfortably placed eithe r ove r the sides of the table or on the table beside the hips and thighs.

5. Place one hand either horizontally, or transverse to the sacrum, contacting the posterior superior iliac spines and medial gluteus maximus attachments bilaterally.. 6. Place the other hand over the bottom hand along the long axis of the sacrum berween the rwo innomi nates, with the index finger overlying one sacroiliac joint and inferior lateral angle as the ring finger covers the other. By using this hand placement, the long finger falls naturally over the sacral spi nes and sacral hiatus.

FIGURE 60. 17.

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VI!. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment

FIGURE 60.18.

7. Evaluate patterns of tightness and looseness by rocking the sacrum in multiple planes: a. Proximally and distally, by distracting the sacrum and lumbar spine at the sacral base along the long axis of the spine. b. Circumferentially, by transversely translating each hand across the pelvis in opposite directions. 8. Using a rocking nutation-counternutation gapping motion, induce lumbosacral joint distraction (Fig. 60.2 1 ) . Be sure to create the motion by moving the distal hand caudally as well as up and over the natural curve of the sacrum. ' See step no. 8 under " Sacroiliac, Sacral Base, and Lumbopelvic Releases Combined Technique" earlier in the chapter.) Some sacrums

are in a more or less straight-line relationship with the spine. Others are sometimes acutely angled with the plane of the sacral base virtually perpendicular to the flow of the operator imposed forces. 9. Both light- and heavy-handed force can be used, depending on your skill. A key to success is the ability to monitor, induce, and enhance both inherent tissue and craniosacral activi ties. 1 0. As both static and dynamic loading is applied, inherent tissue movement-related tightness and looseness usually becomes apparent. Static forces load the system against di rect and indirect barriers without superimposing oscillat ing movements. Dynamic forces load the system with subtle

FIGURE 60.19.

60.


943

Sacrotuberous Ligament Release

Objective The goal is to balance three-dimensional sacrotuberous and sacrospinous ligamenr factors affecting lumbopelvic, lowe r limb, and pelvic diaphragm mechanics.

Review Review functional anatomy of pelvic diaph ragm, ligaments of the sacrum, sacrotuberous-sacrospinous ligament relation ships, pelvic diaphragm, and proximal adductor-hamstring relationships.

Procedure

Prone 1. The patient's feet should be off the end of the table to min

FIGURE 60.20.

imize lower limb stresses in relation to the pelvis and lower li mb.

operator-induced forces thar: a. Follow along behind inhere nr tissue and craniosacral movements b. Systematically seek out three-dimensional shifts of direct and indirect barriers as releases occur 1 1 . Success is more apt to occur when special arrenrion is given to the sacral base in relation to L4-5 mechanics, iliolumbar ligamenr anomalies, degenerative changes, and nonneurral verrebral mechan ics. (See entries for E Rs and FSR in the Glossary.) 1 2 . Treatmenr is complete when L5 and sacral base mechanics and associated inhere nr motions are as symmetric as can reasonably be expected.

2. The patienr's head should be turned to the most comfortable side. 3. The hands and arms are comfortably placed either over the sides of the table, or on the table beside the hips and thighs. 4. Stand beside the patienr's left knee, facing cephalad. 5. IdenrifY inferior and posterior sacral sur faces near the apex ( Figs. 60 .22 and 60.23). 6. IdenrifY the medial surface of the sacral tuberosity where the sacrotuberous-sacrospinous system attaches (Figs. 60.24 and 60.25). 7. With a firm grasp on each buttock, place the th umbs halfway between the sacral apex and each sacral tuberosity, pressing firmly anreriorly and superiorly toward the symphysis pubis ( Figs. 60.26 and 60.27). 8. By shifting the system three-dimensionally, identifY tightness and looseness: areas of direct and indirect barriers.

FIGURE 60.21. Using a rocking motion, distraction.

induce l u m bosacral joint FIGURE 60.22. Inferior sacral s u rface.

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VI!. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment

FIGURE 60.23. Posterior sacral su rface.

FIGURE 60.26. Place thu mbs h a lfway between the sacral apex and each sacra I t uberosity.

9. This is accomplished by firmly pressing anteriorly and supe riorly into the pelvic diaphragm and its attachments while turning the thumbs systematically against either tightness or looseness. Tightness and looseness in both the ligaments and pelvic diaphragm should become quickly apparent (Fig. 60.28) . Hint: Think of turning a steering wheel with the thumbs. 1 0. Using each hand interactively, sequentially induce forces against tightness and looseness, stressing both direct and in direct barriers until releases occur. 1 1 . Treatment is complete when sacrotuberous-pelvic di aphragm mechanics and related inherent motions are as sym metric as can reasonably be expected.

FIGURE 60.24. Med i a l s u rface of the sacral tu berosity.

FIGURE 60.25. Med i a l surface of the sacral t uberosity.

FIGURE 60.27. Place t h u m bs h alfway between the sacral apex and each sacral tu berosity.

60.

FIGURE 60.28. Press anteriorly and superiorly w h i l e t u r n i n g t h u m bs systematica l ly agai nst either tightness or looseness.

Supine Releases

Even after prone maneuvers are successful, lumbopelvic mechan ics commonly remain asymmetric during supine assessment. A.s a result, one should learn to release the lumbopelvic, diaphragm, trunk rotator, pelvis, and hip rotator mechanics from this posi tion. Primary focus is on the sacrum, pelvis, trunk rotators, and thoracolumbar junction. Pubic Symphysis Release


945

FIGURE 60.29. Assess for symphyseal shear and positional asymmetry.

(Figs. 60.29 and 60.30) . Some prefer visual analysis, while oth ers prefer a combination of palpation and vision. Tightness and looseness in the rectus sheath often identifY the most problematic site. Sometimes tightness will be on the inferior side, sometimes the superior. Usually there are strong correlations w ith innomi nate positioning, but there are enough exceptions that one must be alert. 4. Place the thenar eminences on either side of the symphysis pubis, thumbs pointed superiorly and anteriorly. Proximal adduc tor and iliacus tendon attachments should be palpably evident under the thenar muscles (Figs. 60.3 1 and 60.32).

Objective The goal is to restore symmetry to the pubic symphysis.

Review Review the functional three-dimensional relationships among the proximal thigh adductors, anterior and posterior innominates and their asymmetries, as well as changes involving the rectus sheath and transverses abdominis muscles, w here they attach to the pubic symphysis.

Procedure

Supine 1 . The patient lies supine with heels on the table and the arms comfortably at the sides or on the abdomen. Short-armed individuals should keep the arms on the table to avoid stressing shoulder and thoracolumbar systems. This more or less assures that unusual mechanical stresses transmitted through the Achilles tendons and ankles will be neutralized. For those w ith significant kyphosis, it is helpful to use a large pillow to minimize cervical and thoracolumbar problems. 2. Facing cephalad, the practitioner sits or stands beside the patient's right thigh, near the knee. 3. First, assess for symphyseal shear and positional asymmetry

FIGURE 60.30. Assess for symphyseal shear a n d positional asymmetry.

946

VII.


FIGURE 60.33.

FIGURE 60.31. Symphysis release. Thenar e m i nences are placed on

either side of symphysis pubis. t h u m bs pointed superiorly and anteriorly.

5. Induce fi rm, slow forces that either exaggerate (indirecr bar riers) or decrease (di rect barriers) symphysis asymmetry. Direct rocking back and forth, similar to an articular maneuver, is often effective. Hold agai nst the barriers until releases occur. Mild oscil lations usually become evident as the rectus fasciae, boay pelvis, pelvic diaphragm, trunk rotators, and thigh adductors become more symmetric.

Anterior Pelvic-Innominate Release

This process is shown in Figs.60.33 to 60.38.

2. Review anterior proximal and distal il iopsoas, diaphragm, and pelvic diaphragm elements, including piriformis and quadra tus femoris relationships. Remember that distal il iopsoas re lationships can be evaluated as they pass beneath the inguinal ligaments on their way to proximal attachments on the lesser rrochanters of the femurs. 3. Review lateral hip abductor and knee relationships in rela tion to gluteus medius and mini mus, gluteus maximus, tensor fasciae larae relationships with trunk rotators, and quadratus lumborum. 4. Review lower limb mechanics of all types and their potent effects on innominate asymmetries.

. Procedure Objective

Supine

The goal is to reduce functional obliquity berween the rwo in nominates in relation to one another.

1 . The patient lies supine with heels on the table, arms com fonably at the sides. This basically assures that unusual mechan ical stresses transmitted through the Achilles tendons and ankles will be neutralized. For those with significant kyphosis, it is help ful to use a large pillow to minimize cervical and thoracolumbar problems. 2. Face cephalad, standing beside the patient's right thigh. 3. Place the palms across the anterior superior iliac spines, being sure to cover the inguinal ligament medially. Include the

Review 1 . Review posterior and lateral functional relationships among distal erector spinae groups, gluteus maximus, quadratus lum borum, trunk rotators, lumbodorsal fascia, latissimus dorsi, serratus posterior inferior, diaphragm, and lower rib cage.

FIGURE 60.32. Thenar emi nences are p l aced on either side of symph ysis pubis, t h u m bs pointed superiorly and anteriorly.

FIGURE 60.34.

60.

Neuromusculoskeletal and Myofoscial ReLease

FIGURE 60.37.

FIGURE 60.35.

iliopsoas muscles as they pass beneath the ligament toward their attachments on the lesser trochanter of the femur (Figs. 60.33 and 60.34). 4. Assess pelvic obliquity both positionally and function ally. Usually the right innominate is more anterior and resists practitioner-imposed posterior displacements. Commonly, the left innominate is positionally more posterior. Typically, this po sitioning resists operator-induced anterior displacements (i.e., di rect barriers are apparent). Conversely, operator-induced poste rior displacements assess indirect barriers (Figs. 60.35 and 60.36) . 5. Barriers can be stressed both directly and indirectly at the same time by holding one innominate in each hand and three-dimensionally exaggerating pelvic obliquity (Figs. 60.37 and 60.38). As both direct and indirect barriers are approached, a sense of increasing tension occurs. Shifting direct barriers seem to firmly disrupt passively induced shifts, while indirect barriers impose a softer, pillowlike palpatory sensation. 6. Hold against the imposed barriers until release{s) occurs. Usually there are several release sequences, so you must be alert. 7. Remember to assess sequential changes involving both the bony pelvis and ilioinguinal sites. 8. Treatment is complete when positional and tight-loose barrier-related asymmetries are resolved.

FIGURE 60.36.

947

Sacroiliac Release: Supine

This process is shown in Figs. 60.39 to 60.46.

Objective The goal is to create both positional and movement symmetry by creating nutation and counternutation in the sacroiliac system, with particular attention to sacral base asymmetries and associated iliolumbar ligament, L4 and L 5 relationships.

Review Review functional relationships throughout the pelvis, and sacrum, including L4-5 elements and erector spinae inA uences through the four layers of back muscles. In addition, review pos terior sacral relationships in relation to the gluteus maximus sys tem and hip rotators, including distal iliopsoas and piriformis quadratus femoris elements. Be aware of relative sacral position ing between the ilia and in relation to both L5-S 1 factors as well as pelvic diaphragm mechanics.

Procedure

Supine 1 . The patient lies supine wi til heels on the table, arms comfort ably at the sides. This basically assures that unusual mechanical stresses transmitted through the Achilles tendons and ankles

FIGURE 60.38.

948


FIGURE 60.39. Hand position for sacroil iac release.

will be neutralized. For those patients with significant kypho sis, it is helpful to use a large pillow to minimize cervical and thoracolumbar problems. 2. Sit beside the patient's right knee. 3.

Resting comfortably on the right forearm, place the right hand behind the sacrum so that each sacroiliac joint is covered by an index and ring finger. The apex should easily cover the metatarsophalangeal joints. Notably, some practitioners pre fer to place the whole sacrum in the palm. As a practical matter, this positioning is not really necessary because sacral move ments are readily palpated with either method (Fig. 60.39).

4. For recording purposes, use muscle energy terminology to identify sacral flexions and torsions. [dentify the following:

a. Three-dimensionally related positional and movement asymmetries in relation to the innominates. b. General tight-loose active and passive movement asymme tries. c. Sacral n utation and counternutation capabilities as side bending, and axial twisting movements are induced. d. Positional and movement asymmetries in relation to the pelvic diaphragm and lower limb. e. Sacral movements associated craniosacral rhythms. 5. Using distraction, compression, and twisting movements, simultaneously stress direct and indirect barriers (Figs. 60.40 to 60.46) . Sustained forces of this type create both mechanical and neurologic releases.

FIGURE 60.40. Hand position for sacro i l iac release.

60.

NeuromuscuLoskeLetaL and MyofosciaL ReLease

949

FIGURE 60.4 1 .

6. After general myofascial and sacral balancing have occurred, monitor sacral nutation and counternutation (craniosacral flexion and extension) until the rhythm is smooth and symmetric. Thoracic Cage and Diaphragm

Objective The goal is to three-dimensionally balance the thoracic cage and related spinal mechanics in relation to the upper limbs, di aphragm, trunk rotators, and lumbopelvic mechanisms.

Review Important three dimensionally related functional relationships involve: 1 . The shoulder girdle anatomy and innervations 2. Scapulothoracic, omohyoid, costal cage, diaphragm, and trunk rotator interactions 3.

Erector spinae elements

4. Cervical-mediated phrenic nerve activities

5 . Multiple, autonomically mediated viscerosomatic and soma tovisceral reflex factors

FIGURE 60.42.

950


FIGURE 60.43.

6. Cardiopulmonary, upper gastrointestinal, renal, and splenic elements are considered along with lumbopelvic influences, such as proximal iliopsoas, quadratus lumborum, and rectus abdominis organization and function

Procedure

Prone This technique is virtually identical to the prone, basic, thora columbar junction release described previously. The only dif ference is the movement of the practitioner's hands cephalad between the scapulae. The major differences between the two are tight-loose functional relationships associated with trapez ius, rhomboids, subscapularis, iliocostalis, and thoracic attach-

ments of posterior and lateral cervical muscles. It is impor tant to remember that primary cervical mechanisms commonly create significant sites of somatic dysfunction into the mid dle thoracic spine by way of the splenius cervicis muscles. It is also important to remember that shoulder girdle and costal cage mechanisms are primarily innervated through cervical and brachial plexus mechanisms, as well as local spinal and autonomic components.

Thoracic Cage, Spine, Diaphragm, and Lower Costal Cage: Supine

This process is shown in Figs. 60.47 to 60. 53.

FIGURE 60.44.

60.


951

FIGURE 60.45.

Objective The goal is to three-dimensionally balance scapulothoracic, tho racic spine, and costodiaphragmatic relationships.

Review See preceding "Prone" procedure.

Procedure

Supine 1 . The patient lies supine with heels on the table, arms comfort ably at the sides. This basically assures that unusual mechanical stresses transmitted through the Achilles tendons and ankles will be neutralized. For those patients with significant kypho sis, it is helpful to use a large pillow to minimize cervical and thoracolumbar problems. 2. Sit at the head of the table.

3. Resting your elbows on the table, reach under the patient and place the hands fi rmly against inferior costothoracic attach ments on either side of the thoracic spine. Be sure to maintain whole hand contact across and along the erector spi nae as well as around the costal cage (Figs. 60.47 and 60.48) . 4. Both positional and movement-related tight-loose asymme tries will become apparent. 5. Focus on the following: a. Diaphragmatic asymmetries that become apparent as the patient slowly but deeply inhales and exhales (Fig. 60.49) b. Upper limb asymmetries which occur as the patient actively moves the upper limbs in a variety of directions (Figs. 60. 50 to 60.53) c. Repeat the procedure by passively moving each arm and shoulder with one hand remaining behind the patient. d. Thoracolumbar j unction asymmetries are assessed by hav ing the patient move the lower limbs in a variety of di rec tions; focus on the proximal iliopsoas as well more distal, lumbopelvic relationships as they respond to active patient movements. 6. As inherent tissue movements become apparent, gently, but firmly, lift the thoracolumbar attachments anteriorly and lat erally. Shifting sites of tightness and looseness are balanced against each other until inherent movements become qui etly symmetric. Sometimes considerable traction and twist are needed to release asymmetrically tight areas.

FIGURE 60.46.

7. As tightness releases, varieties of release-enhancing activities are helpful. Examples are: a. Three-dimensional upper and lower limb movements b. Breath holding at neutral, during moderate and deep in halation, and then during moderate and deep exhalation, that can be combined with three-dimensional upper and lower limb movements.

952


FIGURE 60.47.

8 . Treatment is complete when thoracocostal movements are as functionally symmetric as can be expected. Craniocervical Spine

Seated Position

This procedure is shown in Figs. 60.54 to 60. 57.

Goal The goal is to increase cranial, craniocervical spine, upper ribs, upper thoracic spine, and shoulder girdle ranges of motion.

Review

3. Three-dimensional costosternal, costovertebral, and cervico costal relationships including scalene, crapezius, omohyoid, rotator cuff, scapulocostal, and anterior chest wall factors such as pectoralis major and minor influences on cervical mechanics.

4. Functional neurologic relationships, including cranial nerve innervations to the neck and shoulder girdle, as well as auto nomic and phrenic nerve/diaphragmatic elements. 5. Remember that intrinsic cardiopulmonary as well as many other medical problems have significant and long-lasting cer vical consequences.

Review the following: 1 . Craniosacral concepts. 2. Craniocervical functional anatomy including scalene, trapez ius, anterior and posterior cervical influences.

Procedure

Note: Palpably apparent tissue and movement-related differences at the same sites during passive and active movements are com mon with this procedure. Patient Seated 1 . The patient sits with relaxed posture. 2. Stand behind the patient. 3. With each hand, assess lateral, thoracic inlet and poste rior cervicothoracic mechanisms for tightness and looseness (Fig. 60. 54) . 4. Combinations of active and passive operator- and patient induced neck movements usually improve treatment quality (Figs. 60. 5 5 and 60.56). 5 . Commonly tightness occurs in upper and middle thoracic sites where cervical muscles attach to the upper and middle back. For example, trapezius, splenius cervicis, levator scapu lae, and semispinalis capitis often exhibit tightness as low as T6-7.

FIGURE 60.48.

6. Tight-loose asymmecries involving deep cervical rotators and side-benders, as well as sternocleidomastoids and scalenes factors, are common.

60.

NeuromuscuLoskeLetaL and MyofasciaL ReLease

953

FIGURE 60.49.

7. Plac(; the hands around lateral and posterior cervicothoracic attachments. Be prepared to move anteriorly and laterally as releases get under way. Cranial nerve and upper limb inte grated release-enhancing maneuvers are particularly helpful (Fig. 63.57). Mild head nodding and rotations are often powerful release inducers.

8. Simultaneous bilateral, anterior, inferior, and circumferen tial twist and stress are induced across and around the cervi cothoracic j unction. Three-dimensionally related direct and indirect barriers quickly appear. 9. Generally, releases begin fairly quickly. Once underway, inherent tissue movements are followed until three dimensional symmetry occurs.

1 0 . It is particularly important to assess changes that combine varieties of active and passive head, cervical spine, upper limb, and respiratory efforts. 1 1 . Treatment is complete when three-dimensional symmetry has been established in relation to active and passive cervi co thoracic, upper limb, respiratory, and costal cage mecha nisms. Patient Supine

This process is shown in Figs. 60.58 to 60.64. The goal is to establish three-dimensional movement symmetry i n the cervical spine from basiocciput to upper thoracic influences. Particular

FIGURE 60.50.

954

VII

Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment stresses transmitted through the Achilles tendons and ankles will be neutralized. For those patients with significant kypho sis, it is helpful co use a large pillow co minimize cervical and thoracolumbar problems. 2 . Sit at the patient's head. 3. Two hand positions, among many possibilities, are particularly useful: a. One hand overlapping the other-this permits carefully controlled and focused, twist, traction, and side-bending maneuvers. The maneuvers are used both separately and with patient cooperation (Figs. 60. 6 1 and 60.62) . b. By grasping the basiocciput with the palms of each hand, the fingers are left free co sort out both superficial and deep mechanisms (Figs. 60.63 and 60.64).

FIGURE 60.51.

emphasis is placed on restoration of adequate side bending and rotation, both generally and in relation to single segment mobil ity. This tech nique is usually more effective after lower cervical, cervicothoracic junction, and upper thoracic, upper limb factors have been released beforehand (Figs. 60. 5 8 to 60.60). Note: To protect the vertebral arteries, take particular caution co avoid simultaneous side-bending and extension maneuvers.

While importantfor aLI age groups, most injuries have occurred under age 35. Review See preced ing "Seated" description.

Procedure 1 . The patient lies supine with heels on the table, arms comfort ably at the sides. This basically assures that unusual mechanical

4. From either hand position, traction , turning, and side bending maneuvers assess myofascial and joint-related tight ness and looseness. a. Pay particular attention CO tightness, remembering that loose joints with surrounding inhibited muscle groups are common sources of pain and disability. I n more acute situa tions, on the other hand, loose joints are usually associated with tight muscles as they work co protect and stabil ize the system. The opposite findings are also common, such as tight joints with accompanying inhibition of overlying muscles. b. Facet joints are often tight on one side, loose on the other. Side-co-side motion testing wi th only a Ii ttle rotation will determine which facets are failing co effectively open or close (see Chapter 59) c. The procedure's focus is co carefully, but persistently, ap ply well-focused stress against tight sites with and without patient assistance. d. I N R cranial nerve and upper limb activities such as finger tapping and hand rolling are commonly helpful. They also save the practitioner time.

FIGURE 60.52.

60.

NeuromuscuLoskeLetaL and MyofasciaL ReLease

955

FIGURE 60.53.

5. Linking subtle translatory maneuvers (e.g., combinations of distraction and extension with flexion, extension, side bending, and rotation) is usually helpful. In particular: a. Release deep upper cervical muscles by combining cra nial nerve (CN) activities with occipitoatlantal nutation and counternutation. Remember that sternocleidomastoid (SCM) , trapezius (CN XI), and scalene mechanics are easily accessible primary neck stabilizers that are often asymmet ric in relation to each other. For example, the left SCM mechanism is typically tighter than the right from origin to insertion. Commonly, the underlying scalene system is looser (i.e., tightness and looseness occur among ipsilat-

eral layers as well as from side-to-side, front-to-back, and circumferen tially) . In the process: 6. Atlantoaxial joints and surrounding attachments are carefully rotated against tightness. 7. Middle and lower cervical attachments and coupled joint movements are stressed using translatory movements with combinations of side bending, flexion, and extension rhat avoids a lot of rotation. (Remember the vertebral arteries!) 8. Treatment is complete when symmetric movements are re stored to facet joints and surrounding soft tissues within the ability of the patient to adapt.

Left anterior inferior medial

FIGURE 60.54.

956


FIGURE 60.57. FIGURE 60.55.

Lower Limb

Trea[menr proced ures for [he lower limb are shown in Figs. 60.65 ro 60.68. Goal The goal is w release each lower limb from lumbopelvic and hip rorawr anachmenrs w [he foo[ and ankle.

Review Review [he following:

FIGURE 60.58.

FIGURE 60.56.

FIGURE 60.59.

60.

NeuromuscuLoskeLetaL and MyofasciaL Release

951

FIGURE 60.62. FIGURE 60.60.

1 . Functional neurology of the lower limb, including pelvic gir dle, low back, rrunk rotarors, and lumbodorsal fascia, latis simus dorsi, scapulocostal stabilizers in relation ro the low back, brachial plexus influences through shoulder girdle struc rures, 'IS well as djaphragmatic-phrenic influence. Remember that the limbs are precisely represented in cerebellopontine functions as well as in multiple areas of the homunculus and precentral gyrus, among many. 2. Functional neuromuscular anatomy of the foot, ankle, knee, and their myofascial elements. 3. Functional neuromuscular anatomy of the hips and upper leg. 4. Circularory anaromy of both the lumbopelvic system and lower limbs. 5 . The effects of common medical problems, such as arthritis, diabetes, and effects of trauma and surgery.

Smokjng-related circulatory problems, arthritis, and diabetes are among the most common sources of lower limb dysfunctions. Note 2: Proprioceptive instability on one leg is a common sig nal of unilateral muscle weakness and neural inhibition anywhere

Note

1:

from the low back ro the plantar surface of the ipsi lateral foot. Pain is a common presenting complaint. Procedure Supine 1 . To begin, the heels should be on the table with knees ex tended to m inimize lower limb stresses. The head and neck should be comfortable with minimal stress on the spine and pelvis. Note: Remember to check for leg length inequalities and al tered hip mechanics both prone and supine. It is common ro find differences supine, prone, and seated. Pelvic obliquities are common when these inconsistencies occur.

2. The hands and arms are comfortably placed either on the abdomen or at the sides. 3. Sit or stand beside the patient. 4 . Grasp distal fem ur and distal patellar/proximal tibial attach ments (Fig. 60.65). 5. Using firm, passive, circumferential movements, assess each fully extended knee for three-dimensional tightness and loose ness (Figs. 60.65 ro 60.68) . Particular care is taken in assessing

FIGURE 60.6 1 .

958


FIGURE 60.63.

FIGURE 60.65.

medial hamstring as well as lateral hamstring/iliotibial band/proximal fibular head tight-loose relationships. Note: Myofascially, this is a fairly ambiguous area to assess and treat, so one must subjectively rely on tight-loose end-feels. Remember that both lumbopelvic and foot-ankle mechanics significantly influence the system. 6. Assess hip function in the same way, with the leg in full exten sion and then with varieties of flexion, internal and external rotation, abduction, and adduction.

7. Passively twist the knee in opposite directions (axial twist), being sure that the hand and fingers are firmly in contact with areas of maximum tightness. Usually maximum tightness is in two places: a. Laterally around distal iliotibial band attachments and proximal fibular head b. Medially and posteriorly near and around distal hamstring arrachments. 8. Asymptomatic lateral knee/fibular head problems (tightness) in response to medial complaints where the knee is generally

FIGURE 60.64.

FIGURE 60.66.

FIGURE 60.67.

60.


959

FIGURE 60.68.

more mobile are common. Distal tensor fasciae latae problems are also common in this group in conjunction with ipsilateral gluteus medius weakness. A positive standing Trendelenburg test is the most common signal of gluteus medius weakening. a. Remember that proximal sacroiliac joint and sacrotub erous-sacrospinous ligamentous factors are also common sources of distal difficulties, and vice versa. Alternative Treatment

The process for alternative treatment is shown in Figs. 60.69 to 60.76. After assessing and releasing compromised knee mechan ics, one commonly encounters proximal hip rotator, abductor, and adductor problems.

FIGURE 60.70.

loose elements by carrying the extended limb into varieties of rotation, abduction, and adduction. This can also be done with both limbs simultaneously. b. Hold against either the direct or indirect barrier, while fo cusing attention on associated tight-loose relationships. Note: It helps to remember that si tes oflooseness commonly signal neural inhibition, along with the possibility of ab solute or relative hypermobility. Also, they often correlate with pain reporrs. c. Releases occur as twist, traction, compression, and shear

1 . With knee fully extended, lift each leg off the table, creating slight hip Aexion. a. Simultaneously focus on both single and bilateral tight loose hip rotator-lumbopelvic factors. Search out tight-

FIGURE 60.69.

FIGURE 60.71.


960

FIGURE 60.72.

against direct and indirect barriers and are used interac tively. Compression is often surprisingly useful. Unwinding Maneuvers

The process for unwi nding maneuvers is shown in Figs. 60.69 to 60.76.

Background Unwinding methods refer to operator-induced spontaneous bending and rwisting maneuvers affecting both upper and lower limbs. Their osteopathic origins are unclear. These procedures

FIGURE 60.73.

FIGURE 60.74.

have been described for decades by many osteopathic practition ers. At times, the patient's whole body takes parr. Single and multiple operators sometimes participate together.

Goal From the foot of the table, long lever unwinding maneuvers re lease the whole lower limb, including the foot and ankle, in rela tion to the lumbar spine and pelvis. With practice, one can learn to work through the whole body from the foot of the table. Both rapid and slow-moving releases become apparent as operator skill Improves.

FIGURE 60.75.

60.

FIGURE 60.76.


FIGURE 60.78.

Procedure Combinations of traction, compression, rwisting, and bending are used to sequentially follow shifting release activities. Some times the limb(s) move rapidly, sometimes slowly. As treatment progresses, seemingly chaotic random movements are apt to oc cur. Then, suddenly, they stop temporarily as a "still point" oc curs, similar to entering the eye of a hurricane. The process then starts again. Presumably, these seemingly random movements re flect a variety of interacting electromechanical events affecting central, peripheral, autonomic, and even psychologic functions. Amid much speculation, satisfactory sciel1[ific descriptions for the events are lacking. Foot and Ankle

Treatment of the foot and ankle (Figs. 60.77 to 60.80) is virtually identical to knee approaches. For example, lateral ankle looseness is commonly associated with medial foot tightness involving the

FIGURE 60.77.

FIGURE 60.79.

FIGURE 60.80.

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VII Osteopathic Considerations in PaLpatory Diagnosis and ManipuLative Treatment

deltoid ligament. Whether reLease of the tightness is helpfuL is a

matter ofcLinicaLjudgment, because pLantar surface, heeL, and tarsaL metatarsal factors play such important roLes. Upper Limb and Shoulder

Rotator Cuff and Partially Frozen Shoulder Dysfunctions

Goal The goal of this treatment is to three-di mensionally balance cer vical, shoulder, scapulocostal, anterior chest wall, rotator cuff glenohumeral, upper arm, elbow, wrist, and hand inA uences. Review Review the following: 1 . Functional neurology of the neck in relation to the upper limb, including brachial plexus and cervical autonomic elements, as well as cranial nerve sensory and motor functions.

FIGURE 60.82.

2. Rotator cuff, glenohumeral, elbow, wrist inAuences. 3.

Craniocervical spine relationships with particular reference to large and small muscle inAuences from basiocciput to upper thoracic and related scapulothoracic, scapulocostal inAuences.

Procedure The procedure is carried out with the patient prone, with their arm and shoulder off table (Figs. 60. 8 1 to 60.85). Most of the time this position is used to deal directly with compromised shoulder and scapulocostal mechanics (see also "Spencer Techniques," Chapter 5 5) . Direct myofascial stress ing occurs across and around the rotator cuff, acromioclavic ular joint, distal glenohumeral attachments, and inferior sub scapularis, latissimus dorsi, infraspinatus, teres major and mi nor attachments.

1 . The patient's feet should be off the end of the table to min imize lower limb stresses in relation to the pelvis and lower limb. 2. The patient's head should be turned to the most comfortable side. Note the effect of head turning on tigh tness and loose ness across the shoulder in question. Proximal and superior

FIGURE 60.81.

FIGURE 60.83.

FIGURE 60.84.

60.


FIGURE 60.85.

cervical attachments are often comprom ised and need to be released along with the shoulder. Note: Keeping the head in the midline readily neutralizes craniocervical asymmetries, but also reduces the chance that significant tight-loose asymmetries will be missed. 3. The patient's hands and arms are comfortably placed either over the sides of the table or on the table beside the hips and thighs. I f the hands are over the sides of the table, be sure to note any asymmetric scapulocostal effects (see "Note" above) . 4. The operator sits on a rolling stool that allows movement in response to shifting sites of tightness and looseness. 5. Holding the affected arm between the knees allows the op erator use of the rolling stool to guide movements as specific stressing against tight barriers occurs. 6. Initially, place both hands firmly around the glenohumeral attachments immediately lateral to the acromioclavicular joint. The fingers of one hand firmly contact pectoralis ma jor attachments anteriorly, while the other hand contacts teres/infraspinatus attachments posteriorly (Figs. 60. 8 1 to 60.83) .

FIGURE 60.86.

Supine

This process is shown in Figs. 60.86 and 60.87. Goal The goal is to generally mobilize the shoulder and its relationships with the cervical spine and thorax. Review Same as prone.

1 . This positioning is less helpful for frozen shoulder situations than prone or side-lying. 2. This position is usually more helpful for lower craniocervical upper thoracic components affected by the shoulder problem. Mobilizing C6-8 costovertebral mechanics as well as first, sec ond, and third rib mechanics are particular keys to success.

7. Assess tightness and looseness by three-dimensionally stress ing the system using distraction, compression, twist, and shear (Figs. 60.84 and 60. 8 5 ) . 8. Direct and fi r m stressing against tightness gets the process under way. For example, approximately 5 to 1 5 pounds of load are common before initial releases begin. 9. Pay particular attention to posterior and inferior gleno humeral restrictions close to the scapula.

1 0. Long-term problems usually require firmly held movements that assertively stretch the area without interfering with neu rocirculatory functions. 1 1 . A well-organized home exercise and/or physical therapy pro gram is usually needed to maintain improvement. 1 2. Side-lying techniques using a similar approach are also helpful.

963

FIGURE 60.87.

964

VII.


FIGURE 60.88. FIGURE 60.89. Forearm-el bow-wrist release, d i rect techniq ue, trans verse approach.

Procedure 1 . The patient is supine with heels on the table, arms comfort ably at the sides. This basically assures that unusual mechanical stresses rransmined through the Achilles tendons and ankles will be neutralized. For those patients with significant kypho sis, it is helpful ro use a large pillow ro minimize cervical and thoracolumbar problems.

2. Stand at either me side or head of the table. Choice of position is dictated by scapulocostal-glenohumeral ranges of motion, as well as inAuenriai tight-loose facrors. Note: In addition ro primary joint involvement, compromised glenohumeral functions commonly involve pecroralis major mechanics near anachments at me intertubercular groove of the humerus. They also commonly affect posterolateral teres and infraspinarus elements. 3. Grasp the patienr's wrists. 4. Progressively apply distraction, compression, and rwist ro as sess end-feels, potential ranges of motion, and barrier-related properties (Figs. 60.87 and 60.88). 5 . Use alternating direct and indirect barrier stresses ro trigger an unwinding process (see discussion on page 96 1 ) . As soft tissue and joinr barriers release, overall ranges of motion com monly improve. This is particularly true when intrinsic joint mechanics are minimally compromised (i.e., degenerative and calcification changes are minimal ) .

tions were so marked, she could open her mouth about 1 . 5 cm rather than the expected 4 ro 5 cm. Facial expressions were mask like and almost immobile. There was also anterior abdominal wall involvement. Swallowing was an increasing problem because of the myofascial changes. Fortunately, visceral involvement was minimal. Raynaud phenomenon was severe, with marked flexion contractures of the palmar fasciae and finger flexors. The patient had previously been placed on penicillamine and had physical therapy without substanrial success. After working with her for several visits, it was clear that stan dard osteopathic manipulative approaches were not helpful. Hav ing had considerable experience with muscle energy techniques as well as fascial rwisting maneuvers advocated by Ruddy in the early 20th century (see Chapter 57) and Neidner, the patient was asked if assertive rwisting movements of the forearms, elbows, wrists, and hands could be performed. She readily agreed, and, ro everyone's surprise, the skin and underlying tissues gave way under the firmly assertive rorsional and compressive loads. From this beginning, a series of assertive, very direcr release maneuvers were designed ro resrore soft tissue resilience anywhere

Forearm, Elbow, and Wrist Release

Direct Technique, Transverse Approach

This technique is shown in Figs. 60.88 ro 60.9 l . The goal is ro generally release the forearm, elbow, and wrist by transversely straining direct myofascial barriers along the forearm, elbow, and wrist in a stepwise fashion. Historical note: This is the first direct M F R technique de veloped for this system of rreatment. In 1 976, it came about accidentally while rreating a patient with a particularly difficult case of scleroderma. The patient's skin was generally thickened by pannus (inAammarory granulation tissue) that had severely restricted most available myofascial and joint movemenrs about the head, neck, face, chest wall, and upper limbs. Facial resrric-

FIGURE 60.90. Forearm-el bow-wrist release, d i rect technique, trans verse approach.

60.

NeuromuscuLoskeLetaL and MyofasciaL Release

FIGURE 60.91. Forearm-el bow-wrist release. d i rect technique. trans

FIGURE 60.92.

verse approach.

on the body. In this particular instance, family members were taught the maneuvers. They turned out to be of great help, and after about 1 8 months, most of the patient's flexibility was re stored. This included the upper limbs, facial muscles, and craJl iomandibular mechanics. At the time of this writing, she was carrying on a normal lifestyle with minimal need for further attention. Review Review the following: I.

Upper limb functional anatomy, including kinesiologic, scapulohumeral, scapulocostal, and craniocervical relation ships.

Wrist-Forearm-Elbow

Direct Technique: Long-Axis Approach

This technique is shown in Figs. 60.92 to 60.95. Goal The general goal is to release forearm flexors and extensors in relation to distal wrist and hand mechanics, as well as proximal lateral and medial elbow to shoulder mechanics. As the release process unwinds the system, special attention is paid to sequential releases affecting both superficial and deep myofascial and joint mechanics.

2. Upper limb functional neurology, including cervical innerva tions, autollomic elements.

Review Review the following:

3. Upper limb myofascial and ligamentous anatomy, including ulnar nerve-elbow relatiollships, retinaculum of the wrist, and carpal runnel and transverse carpal ligament influences.

1 . Upper limb functional anatomy

Procedure 1 . The patient is seated, standing, supine, or prone. Stand or sit comfortably for easy access to the forearm.

2. Upper limb functional neurology, including central, periph eral, and autonomic influences 3. Cervical spine anatomy and its relationships with shoulder and arm functions

2. With a light hold on the skin, place the hands transversely across the forearm or wrist, with the knuckles of each index finger touching one another (Figs. 60.88 and 60.89) . 3. Induce deformation against the direct barrier by twisting the skin and underlying soft tissues in opposite directions. Then twist in the opposite directions (Figs. 60.90 and 60.9 1 ) . 4 . When barriers are encountered, hold firmly until they give way under the load. Sometimes considerable force is needed to create a release, sometimes nor. 5. Treatment is complete when as much free and easy inherent soft tissue motion occurs as can be reasonably expected.

Note: What the release event represents is unknown. Func tionally, the phenomenon presumably represents a combination of viscoelastic rebound and a combination of peripheral and cen trally controlled neurovascular changes.

965

FIGURE 60.93.

966


FIGURE 60.94. Wrist-forearm-el bow, approach.

d i rect

technique,

long-axis

Procedure 1 . The patient is standing, seated, or supine.

2. Firmly grasp the thenar eminence with four fingers as shown in Fig. 60.92. The index and long fingers should contact the area of the rransverse carpal ligament. 3. Place the grasping thumb on the extensor surface of the hand and wrist pointing proximally along the long axis of forearm as demonstrated in Figs. 60.93. Figure 60.96 shows an alternative hand position.

FIGURE 60.96. Wrist-forearm-el bow, approach.

d i rect

technique,

involving the whole limb. At other times they are rapid, even jerky, like a spring suddenly and rapidly uncoiling. 8. Treatment is complete when as much soft tissue motion occurs as can be reasonably expected.

4. With the other hand, firmly grasp the patient's forearm at elbow. 5. With elbow firmly held, turn the wrist until a tight barrier is noted at either side of the elbow, or within the mechanics of the wrist and hand. (Fig. 60.94 shows twist in one direction, Fig. 60.95 twists in opposite direction.)

Carpal and Palmar Tunnel Release

Direct Technique, Transverse Approach

This technique is shown in Figs 60.97 ro 60. 1 0 1 .

6. Hold the tightness firmly for a few seconds until mechanical release is induced. At this point, the limb can be safely re leased and retested for soft tissue resilience and joint ranges of motion. 7. An alternative option is ro continue holding firmly ro induce unwinding. Sometimes the movements are slow and arclike,

60.95. Wrist-forea rm-el bow, approach.

FIGURE

d i rect

technique,

long-axis

long-axis

FIGURE 60.97. Wrist-carpal tun nel release.

60.

NeuromuscuLoskeLetaL and MyofosciaL ReLease

967

FIGURE 60.98.

Goal The goal is to restore freedom of movement within the carpal and palmar tunnels by simultaneously releasing the soft tissues of the wrist, the carpal bones, and the palmar-carpal tunnel, and the transverse carpal ligament. Review Review the following:

1 . Functional anatomy of the hand, wrist, and elbow

FIGURE 60.100. Wrist-carpal t u n n e l release.

4. The distal hand thumb points along the long axis of forearm as described above (Fig. 60.98 ) . 5 . With the proximal hand, grasp the wrist with specific atten tion to carpal-metacarpal and palmar tunnel-carpal tunnel tight-loose relationships.

2. Functional neurology of the hand, wrist, and elbow

6. Twist in supination until the myofascial barrier separates and opens the carpal tunnel (Fig. 60.99).

Procedure I . The patient is seated, standing, or supine.

7. Then twist in pronation to further release the radiocarpal attachments (Fig. 60. 97) .

2. Stand comfortably in front or beside the patient. 3. With the distal hand, grasp the thenar, palmar tunnel trans verse carpal ligamentous attachments (Fig. 60.97).

8. Hold firmly against the tightness for a few seconds until release occurs. 9. A second option is to continue holding firmly to see what happens as unwinding occurs. 1 0. Treatment is complete when as much soft tissue motion oc curs as can be reasonably expected.

FIGURE 60.99. Wrist-ca rpal tunnel release

FIGURE 60.101.

968


CQNCLUSION

These rudimentary M F R and I N R techniques can help ease any number of neuromusculoskeletal problems. Having stood rhe rest of time, they are easily learned and can be applied with relative ease.

7. Woo S-L, An K-N, Arnoczky SF, et al. Anatomy, biology, and biome

chanics of tendon, ligament, and rotation. In: Simon SR, ed. Ortho

pedic Basic Science. American Academy of Orthopedic Surgeons; 1 994: 45-88.

8. The New Lexicon W0bsters Dictionary ofthe English Language. New York, NY: Lexicon Publications; 1 988.

9. Cathie AG. The fascia of the body in relation to fi.lnction and ma nipulative therapy. In:

The American Academy of Osteopathy Year

book. Indianapolis, IN: American Academy of Osteopathy; 1 974:

REFERENCES 1 . Viidik A. Interdependenc e. berween structure and function in collage

nous tissues. In: Viidik A, Vuust J , eds. Biology of Collagen. New York,

NY: Academic Press; 1 987:257.

2. Still AT. Philosophy of Osteopathy. Kirksville, MO: Journal Priming Co; 1 899.

8 1 -87.

1 0 . Becker RF. The meaning oHa cial and fascial continuity. Osteopath Ann. 1 975;3 :8-32.

1 1 . Bonica ]J. The Management of Pain, 2nd ed. Philadelphia, PA: Lea & Febiger; 1 990:66.

1 2. Earl E. The dual sensory role of muscle spindles. Phys Therj. 1 965;45:4. 1 3. Wilson YJ.

Inhibition

1 966;5 : 1 02- 1 08.

in the central

nervous system.

Sci Am.

3. Cole WV. Some histological aspects of the motor end plate. j Osteopath.

1 4 . Grinberg-Zylerbaum J , RanlOs J . Interpersonal communication: an ex

4. Cole wv. A gold chloride method for motor end plates. Stain Technol.

1 5 . Norton IN. A tissue pressure model for the palpatory perception of the

5 . The G lossary Review Commirree o f rhe Educational Council o n Osteo path,c Principles. Glossary of osteopathic terminology. I n : Allen TW,

1 6. Adams TA, Heisey RC, Briner BA. Parietal bone mobility in the anes

5 1 :7: 1 820:44.

1 946;2 1 :2325 .

perimental approach. lnt j Net/rosci. 1 989;36:41-52.

cranial rhythmic impulse. jA OA. 1 99 1 ; 1 0: 975-994. thetized cat. jAOA. 1 992;5:599-622.

ed. A OA Yearbook and Directory of Osteopathic Physicians. Chicago, IL:

1 7. Upledger JE. Reproducibility of craniosacral examination findi ngs: a

6. Greenman PE. Principles ofManual Medicine, 2nd ed, Baltimore, MD:

1 8 . Upledger JE, Karni Z. Mechanoelectric parrerns during cran iosacral

American Osteopathic Association, 1 996. Williams & Wilkins; 1 996:65-73

statistical analysis. jAOA. 1 977;6:746.

osteopathic diagnosis and treatment. jAOA. 1 978; 1 1 :782-79 1 .

FUNCTIONAL TECHNIQUE: AN INDIRECT METHOD WILLIAM L. JOHNSTON

KEY CONCEPTS • • • • • • • • • • •

•

History of indirect methods Historic principles behind functional technique Motion-function test pattern Palpable motor dysfunction: descriptive research Functional technique as a distinctive i ndirect method Diagnosis in a functional approach, including tissue compression and motion testing stages Criteria for j udgment during functional procedures Functional guidelines for application of an indirect manipulative method "Response information" guides functional technique Conceptual basis of functional technique Practical application of functional technique for the body, including thoracic, lumbar, and sacral regions, cervical region , costal region, thoracic cage, i n nominate, and appendicular regions Spinal motion dysfunction: regarding the differential i n palpatory diagnosis for reflex manifestations o f somatic and visceral inputs

HISTORICAL PERSPECTIVES

To engage the term fonctional technique, one needs to sense the stimulus driving its initial development in the early 1950s. Within the osteopathic discipline, there was a growing recog nition that motor fonction had a broader conceptual framework than just bony relationships, with their structural configuration relatively confined to joints, and to concepts for motion of one bone on the bone below. To open up this conceptual model, it was necessary to give i ncreasing attention to the physiologic aspects and clinical manifestations of motor control. Fot a mobile sys tem, specific directions of regional motion tests were becoming effective in delineating positive diagnostic signs of dysfunctional behaviors, both regional and segmental. Withi n these broader functional parameters, motion tests would supply promising tools for application in clinical practice and osteopathic research.

To engage the term indirect as a method of manipulation, one needs to refer back to the early 1900s. [n the history of os teopathy, information derived from palpatory examination had led to the development of a classification for methods of ma nipulation . Development of the terms direct and indirect gave recognition to the specific d irections of motion forces used in osteopathic manipulative procedures. A brief look at 100 years of professional history indicates a significant struggle regard ing the issue of terminology. The controversy involves two areas: 1. Verbalizing palpatory findings i n the musculoskeletal system, and 2. Conceptualizing models for palpable findings, for example: the use of bony malposition at a joint, to depict a local area of segmental dysfunction (referred to in the past as a lesion , the Still lesion, o r osteopathic lesion). Difficulties with terminology create problems for communi cation about the clinical signs of m usculoskeletal dysfunctions. To describe a direct manipulative technique for segmental dys function, initial concepts of somatic dysfunction focused on joint restriction and direct forces to encounter and overcome restric tion; this fit the layperson's concept of "putting the bone back in place." Other techniques did not directly encounter the restric tion yet still overcame restricted movement. Such manipulative procedures did not fit the concept of the direct method. They did use motion and maneuvers in the opposite direction of the restriction effectively, however, and were given the term indirect. Owing to the fact that they seem to defy positional relationships and joint concepts, i ndirect methods are often set aside. Since they do not fit with those earlier models of thought, they con tinue to present a special challenge for instructio n . Several early osteopathic practitioners expressed these issues. Edythe F. Ashmore, a faculty member at the American College of Osteopathy in Kirksville, Missouri, wrote the first textbook on the mechanics of osteopathy in 1915. She stated: There are two methods commonly employed by osteopathists in the correction of lesions the older of which is the traction method, the


970

later the direct method or thrust.' Those who employ the traction

the point ofbalanced tension. When the tension is properly balanced,

method secure the relaxation of the tissues about the articulation by

the respiratory or muscular cooperation of the patient is employed

what has been termed exaggeration of the lesion, a motion in the

to overcome the resistance of the defense mechanism of the body to

direction of the forcible movement which produced the lesion, as

the release of the lesion

if its purpose were to increase the deformity. The exaggeration is held, traction made upon the joint, replacement initiated and then completed by reversal of the forces.! The direct method consists in the application of a precisely di rected force toward a bony prominence during the process of putting the articulation or lesion through the spinal movement which is the reversal of that which produced the lesion. 'The term "direct" is preferred for the reason that the imitators of osteopathy have given the word "thrust" an objectionable meaning of harshness.

! This method is the more difficult of the rwo and for the instruction of students does not find favor with the author

(l).

Ashmore's footnotes about terminology and instructional prob lems are particularly illuminating. The limited concepts implied by the expressions "exaggerating the lesion" and "reversal of that [movement] which produced the lesion remained in use for many years. The direction of restricted movement was even then be coming a determ inant for methods of manipulative technique and their classification as direct and indirect. Carl P. McConnell, DO, was another osteopathic pioneer who actively contribu ted to osteopathic literature ftom 1905 to 1938. He commented: "

So, striving to get the bones in normal position, per se, or perhaps to keep them in position, is simply hopeless. In this regard, the bony item is simply an idol, and a similar idol could be made of the muscles, and so forth

(2).

McConnell also wrote: Precision of merhod follows definiteness of diagnosis. It is evident that there are many ways of applying the same mechanical principles. But ease and effectiveness should be the goal of operative activity. In adjusting lesions it is obvious that a method which retraces the path of the lesion with a minimum of irritarion is highly desirable

(3).

McConnell's orientation was still on "the path of the lesion, " but this was tempered by a growing discomfort with using bony posi tion or any single anacomic structure as the key co conceptualizing abour areas of musculoskeletal dysfunction. By 1923, in Principles and Practice of Osteopathy, c. Harrison Downing (4) went a step further in describing restriction at a le sioned segment. He referred to the fact that, when testing a phys iologic motion, the lesioned segment becomes more restricted going in one direction. He added that the restriction decreases i n the opposite direction , and "apparently disappears. " Keeping his motion testing procedure as a frame of reference, Downing pro vided palpacory information about the restriction decreasing i n a direction opposite t o the direction of restricted motion. These new facts sometimes supported the concepts centered on the joint and bony description of malposition, and sometimes did not. By 1 949, Howard A. Lippincott reported on the osteopathic technique of William G. Sutherland as follows: The articulation is carried in the direction ofthe lesion, exaggerating the lesion position as far as is necessary to cause the tension of the

(5).

This described an i ndirect method of treatment, but the anacomic construct was more "ligamentous. "The "point ofbalanced tension" (also referred to as "the point of balanced ligamentous tension") became the significant phrase used co describe techniques where the physician palpated throughout the procedure and continually adjusted treatment co the changing tissue tensions. Descriptive terminology still relied mainly on a positional orientation co ex press this important feedback of palpable information during motion. " Balance and hold" became another phrase CO describe i ndirect techniques, but this phrase fails co point out the con tinued balancing carried out by the physician in response co the tissues changing. In the early 1940s at the Chicago College of Osteopathy, in direct diagnostic skills were a part of students' formal training. This involved instructing students regarding the diagnosis of di rections of motion that would initially relax the tissues, and their application in combined techniques. In Boscon, by 1944, some very promi nent physician teachers in the New England area had already been applying indirect methods extensively in their prac tices; however, the difficulty in communicating these skills was still a problem. In the 1940s, the Academy of Applied Osteopathy (now known as the American Academy of Osteopathy) initiated a na tional program ofeducation co i mprove the clinical skills of physi cians, for those proficiencies in practice that can be achieved with continual application of Still's principles. This was done through the implementation of postgraduate instruction. Harold Hoover was a part of this effort. His classification of direct and indirect manipulative methods included the following: 1. Direct technique: the method of moving one bone or segment of the articular lesion directly to a normal relationship with its neighbor. This is accomplished against the resistance of tissues and fluids maintaining the abnormal relationship.

2. Indirect technique: the method of moving one bone or segment slightly in the direction away from the direction of correction until the resistance of holding tissues and fluids is partially overcome and the tensions are bilaterally balanced, then allowing the released ligaments and muscles themselves to aid in pulling the part toward normal. Other body forces, including that of respiration, may be employed

(6).

Hoover's experiences with both of these methods of manipulation were beginning to channel his major interest roward the indirect (7) . Recognizing a functional model, he was reporting on his use of palpatory tests, palpable findings, and manipulative proce dures, especially those of the clinically effective indirect method. He often introduced his functional approaches in seminars. His presentation in New England in 1951 initiated an era of devel opment in the New England Academy of Osteopathy. Bian n ual study sessions, led by Charles Bowles, resulted in a series of three publications entitled "A Functional Orientation for Technic." In his initial report, Bowles wrote:

weakened elements of the ligamentous structure to be equal to or

This was not the birth of a new entity in osteopathy, but simply a

slightly in excess of the tension of those that were not strained. This is

new type of measuring srick for evaluating the Still lesion as a process

61.

of aberrared funcrion ... our funcrional invesrigarion had become formalized by using rhe parrern of a demand-response rransacrion,

FunctionaL Technique: An Indirect Method

Ceph/caudad

Translations

Z

insriruring morion demands (which could be named) wirh a morive han ' d, down

ro,

971

and rhrough a given segmenr, while assessing rhe

morion response of rhis given segmenr rhrough a palparory lisrening hand. To besr understand, follow, and conrrol this demand-response rransaction rherapeutically ar

a

segmenral level, cerrain specific in

sighrs seem necessary, namely:

Lateral

y

J. An undersranding of typical morion-demands and a system of annorarion rhar makes rhem easily communicable between operarors,

2.

An undersranding ofresponses which allows an accurare reporring and a useful evaluarion of rhe specific demand-response rransac rion raking place currenrly under rhe fingertips of rhe palparing or "Iisrening hand" during manipularion, and

3.

X Anterior/posterior

An undersranding of crireria for lesioned and non-Iesioned per formance, i.e., in terms of functional adequacy.

FIGURE 61.1. Coordinate system to ill ustrate straight-l i ne di rections

Thus the significanr funcrional informarion abour verrebral mo

WL. Segmental definition, part I: a focal point for diagnosis of somatic

tion or restricrion is not so much thar mere is motion or restriction,

of movement used to describe transl atory motion tests. (From Johnston dysfunction. JAOA. 1988;88:99-105, with permission.)

bur ramer how rhese morions and resrricrions change, and under what circumstances, and in response ro what demands. It is the response information that evenrually guides funcrional technic

(8).

It should be noted that these commenrs by Bowles are in conrrast ro guides based on anaromic concepts, and bony, muscular, or ligamenrous relations. By 1 96 1 , Lippincorr was expressing educational concerns sim ilar ro those of Ashmore. He reported srudenr confusion, as well as practice [[ends, that were leading h i m ro analyze and clarifY the various methods of correcting lesions. In "Basic Principles of Osteopathic Technique," he reporred:

being returned ro the position in which lesion formarion originally occurred, and only ro this position. When the joinr is returned

ro

position (indirect), the muscles promprly and gratefully relax

(10).

this

Since 1969, and possibly starring during the Bowles in itiative in New England i n 1955, interest has grown i n relation ro moror function, with a focus on the application of motion tests and palpable fi ndings for descriptive clinical research. A test pattern of passive gross motions evolved with standards relevanr ro the six elementary directions of the body's movement (Figs. 6 1 .1 and 6l.2) . These motions are:

It is evident that Dr. Stili treated his patients carefully, with due considerarion for the delicacy and the welfare of the tissues beneath

Rotation

his fingers. It is also evident that he imparred ro the students who

Z

came under his supervision mis wholesome respect for me tissues, the structures, and their functioning.Then, after the turn of the cen tury, it became popular with many of the vigorous and enthusiasric young doctors ro treat with vigor and emhusiasm. They developed techniques that would produce a "pop" regardless of the force re quired ro produce it. This gave them a sense of accomplishment bur it also gave osreopathy a reputation for being rough, painful, and

()

even dangerous, a stigma that still persists among the uninformed. Within a decade or two the trend turned back roward more careful

Axial Rotation

and inrelligent, bur perhaps less spectacular methods. The result is a wealth of technical procedures representing varied approaches ro the correction of osteopathic lesions. It is a decided advanrage for the physician ro have at his command a variety of methods whereby he can meet the needs of each individual patienr

f'

Flex.lExt.

y

(9).

During the 1960s and 1970s, the steadfastness of positional con cepts conrinued ro be reRected in the development of new tech niques. In 1 964 Lawrence H. Jones published his original article, "Sponraneous Release by Positioni ng," i n troducing the technique for manipulative treatment called srrain/counterstrain . Dr. Jones questioned:

o x

Is the muscular tension arranged so as ro splinr this joint, ro prevenr it from moving back inro its eccenrric position? No! The muscular tension resists any position away from the extreme position in which the lesioning occurred. Even the severest lesions will readily rolerate

Side-bending

FIGURE 61.2. Coordinate system to ill ustrate di rections of movement about axes used to descri be rotary motion tests. (From Johnston WL. Segmental definiti on, part I: a focal point for diagnosis of somatic dys function. JAOA. 1988;88:99-105, with permission.)

972 • • • • • •


Flexion/extension Side bending Rotation Translation from side to side Translation anteriorly/posteriorly Translation cephalad/caudad (traction/compression)

Verte bral C5

7

�T1

I. Passive gross motion tests provide a means to attain baseline palpatory information in medical problem solving for a mobile system :

2. Segmental somatic dysfunction is a complete asymmetry of its elementary motion functions: three rotary, three straight-line translatory, and respiratory (18). ( Respiratory was the seventh function, and takes under consideration the demands of inhala tion and exhalation on motor function.) Palpable recordable cues evident in response to these motion tests provide seven possible descriptors for the motion characteristics of each motor defect. 3. A fundamental unit of segmental somatic dysfunction (16,19) consists of a three-segment complex, as illustrated in Fig. 61.3. A central asymmetric segment is the primary defect. Mirror-image (opposing) motion asymmetries are present at the adjacent segments, above and below. (These are secondary and adaptive. implying a basis in somato-somatic reflex activity.) 4. A different organizational principle operates when pri mary defects are idemified a t a midline vertebra and a n adjacem rib at the same spinal level with identical motion asymmetries; this contrasts with the opposing asymmetries presented by mirror images (20). An example is illuStrated in Fig. 6l.4 at T2 and left rib 2. Accompanying this primary defect at the T2 level, note that there still are secondary m irror-image asymmetries at the adjacent segments above and below in both the midline ver tebral and left costal columns. Clinical research (21) has sup ported the premise that visceral afferents contribute to this char acteristic configuration of two segmental units, vertebra and rib, linked in similar pri mary motion asymmetries at the same spinal level. This preceding h istorical perspective puts one in mind of the classic tale of the blind men and the elephant, with each man describing the elephant according to the part being touched. From clinical palpatory experience, asymmetry (A) of joint po sition, restriction (R) of motion, and tissue texrure changes (T) are expressed in the mnemonic acronym A RT. Tenderness (T) has recently been added to the acronym, making it TART. with the first "T" representing tenderness. Each of the last three has emerged as a palpable sign of segmental somatic dysfunction, where motor function is asymmetric and its manifestations are

Right Costal 6

This test pattern allows implementation of an organized diag nostic process for describing the motor characteristics of neuro musculoskeletal dysfunctions. Investigations (11) using this test pattern have been advancing our knowledge about functional aspects of both regional and segmental somatic dysfunction, as follows:

Examining regional motor performance (12) Locating segmental motor defects (13,14) Characterizing the specifics ofa segment's motor dysfonction as a basis for designing manipulative interventions to address somatic dysfunction (15-17)

__

Left Costal

I"

__

4 5 6 FIGURE 61.3. Schema tic representa tion of three mobile columns in thora cic region, with a three-segment unit of dysfunction in vertebral column. X, location of primary functi onal defect a t T2, with resistance to shoulder/trunk rotation to right (short, solid arrow, with bar repre senting sense of resistance). In adjacent T1 and T3 segments, mirror image resistance to left rota tion is secondary (short, solid arrows with bars). Longer, open arrows without bars at each level represent sense of compl i ance with motion and a greater range of motion in direc tions opposite to directions of l i mited mobil ity. (From Johnston Wl. Soma tic manifestations in renal disease: a clinical research study. JAOA. 1987;87:22-35, with permission.)

Vertebral

C5

__

Left Costal

__

I�

Right Costal

6

__

7

__

I�

3

4-5-6

--

FIGURE 61.4. Schema tic representa tion of two primary motor asym metries at T2 spinal level, indi cated by X in vertebral and a dja cent l eft costal columns. Arrows with bars at T2 spinal level i ndicate resi stance in both columns to ri ght rotation of shoul ders/trunk. Secondary mirror image asymmetries of restricted motor function are indicated a t T1 and T3 spinal levels by bars on arrows for left rotation that is (again) present in both columns.

6/.

present in structure, motion, and tissue. The functional charac teristics of motor asymmetry emerge primarily ftom motion tests. These characteristics provide detailed descriptors to implement differential diagnosis and also establish basis for fhe classification of methods of mani pulation as direct and i ndirect.

Q) c

� Physiologic barrier

FUNCTIONAL TECHNIQUE

The term 'JunctionaL technique" refers to osteopathic manipula tive procedures that apply palpatory information gai ned from tests for motor Function, although the term is oFten applied in appropriately as a general synonym For "indirect." To be specific, in Functional manipulative procedures the palpable inFormation regarding all six degrees of freedom and respiration are used to address the dysfunctional aspects of segmental behavior. Passive gross motion testing identifies motion symmetry/asymmetry at an individual mobile segment. IF you can, temporarily set aside the interpretation of palpatory information about mobility in a Format For static concepts of j o i nt position-for example, a poste rior transverse process. I nstead, criteria For determining a mobile segment's behavior and its resistance to or compl iance with op posing directions of specifically induced passive regional motion tests are applied. The demonstration in Fig. 61.5 illustrates a

FIGURE 61.5. Single axial motion test of shoulders and trunk in rota tion to ri ght. (From Johnston WL. Segmental defini tion, part I: a focal point for diagnosis of somatic dysfunction. JAOA. 1988;88:99-105, with permission.)

973

FunctionaL Technique: An indirect Method

I ncrea sing resistance

---:.:::::==",==*===::....- R.

Range -X Segmental Behavior-Symmetric

FIGURE 61.6. Symmetric response to motion at a nonlesioned thoracic segment where only axial rotation is represented. Shown are equal i ni tial compl i ance to ri ght (R) and left (L), and then increasing resistance toward an equidi stant final anatomic end point. (From Johnston WL. Segmental defi nition, part I: a focal point for di agnosis of somatic dys function. JAOA. 1988;88:99-105, with permissi on.)

single axial motion test i ntroduced thtough the shoulders and trunk in rotation to the right. With the patient seated and arms Folded, right rotation of shoulders and trunk is introduced by the physician's right hand at the patient's right elbow. The fingers of the left hand monitor bilaterally the immediate response of par avertebral tissues overlying T6 transverse processes. To compare for response to rotation left, the operator stands to the left and the hand positions are reversed. Finding asymmetric behavior at T6, one can report resistance encountered at T6, For example, during shoulder trunk rotation right. (The test and the criterion are explicit, and the fi nding becomes clear in relation to the test used to elicit it, thereby attending to scientific method for first order reporting.) This is in contrast to applying locaL pressure prone at T6, encountering increased resistance to pressure on the left versus the right, and then reporting a posterior left transverse process, with limited rotation to the right of T6 on T7 within the concept of a j oint. As illustrated i n Fig. 61.6 for symmetric behavior, the initial resting level of m i n i mal muscle tone or tension at point X reAects the natural palpable resistance that the operator's fingertips sense as they lightly contact tissues overlying the bony segment at rest. Point X also illustrates there is palpable symmetry in a segment's i nitial compliance to move right and left with no rise on the tone scale at the initiation of movement. I ndicated also is the normally increasing resistance to range as motion approaches a physiologic and an anatomic barrier. Start with a compression test. The compression test is the ap plication of pressure through the fi ngers to sense any increased tissue tension at one segment compared with adjacent segments. Even at rest, a compression test of a dysfonctionaL segment will register the local increased resistance of that segment's deep mus culature; this can be illustrated as an elevation to Xl on a tone scale (Fig. 61.7). The fingertips mark the site of the increased reSistance to pressure. The segment's tissue tension in the marked area changes immediately on initiation of each passive motion test. Palpa tory cues reflect the immediately increasing resistance to pres sure in one direction (in this example, to the right) , while in the

974

VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment combination of translarory and rotary directions. The ob j ective is ro reach a sense of release of tissue tension at the fingertips, which are con ti n ually moniroring response at the dysfunctional segment.

Barrier

6. The release of restraint in the motor mechanism allows a return to m idline resting, unobstructed by any sense of the resistance previously encountered in the return direction.

Immediately decreasing resistance

L . ---------------- - - �r � X

------------- - - - - -R ange

R.

Primary Asymmetric Lesioned Behavior

FIGURE 61.7. Asymmetric behavior at a dysfunctional (Iesioned) seg ment. (From Johnston WL. Segmental definition, part I: a focal point for diagnosis of somatic dysfunction. JAOA. 1988;88:99-105, with permission.)

opposing direction they reAect an i mmediate sense of decreasing resistance ro pressure (i.e., a decreasing tension with increasing ease of motion). These palpable changes provide an indicaror of asymmetric motor function, ro monitor not only during di agnosis to guide accuracy, b ut also during treatment ro guide efficacy in the return to symmetric motor function. Treatment with Functional techn ique is a distinctive application of a n indi rect method of manipulation. Wel l-defined d i rections of passive motion are combined in their initial stages of increasing ease. A particular phase of active respiration also i ncreases this sense of ease in movement. As the responses ro each precise elementary di rection of increasing ease are summed up, the reduced tissue tension signals a rapidly im proving moror function palpable at the fingertips. Guidelines

A successful outcome is signaled by a sensed release of the segmental tissues' holding forces, which then allows a free return to a resting position, and a new tissue rone at rest. The segment's new functional symmetry is evident in the responses to further motion retesting. Increased resistance in response ro directions previously limited is no longer encountered. Examples of applying this functional method of palpa rory diagnosis and manipulative treatment are presented under " Examples of Functional Tech nique" later in this chapter. To memorize any technique for use as a manipulative procedure, without recreating each of the steps outlined above, this would be i nappropriate and probably clinically i neffective. Bowles (23) stated, "It is . . . the response information that eventually guides functional technic." Therefore, at a mobile segment, focus atten tion on the following: 1. The criteria for symmetric and asymmetric motor function 2. The orientation of motion testing ro the palpable findings of bony and tissue tension expressed at a dysfunctional mobile segment 3. The way that response at your fingertips, ro each direction of motion test, guides not only diagnosis but also the develop ment of each i ndividual manipulative procedure conceptual Basis

The following p hrases reveal the static positional concepts that emerged during osteopathy's early professional hisrory:

Certain procedural aspects offunctional technique help to ensure success in the application of an i ndirect method of manipulation For segmental dysfunction (22) . l.

Describing the lesion as a bone out of place, Exaggerating the lesion position, Rerracing the path of the lesion, Noting the position in which the lesion occurred, and Stacking positions ro balance the tension.

The in itial i ntroduction of motion in any one elementary direction is small (not range), with m i ni mal forces applied.

2. Motion directions are roward a sense of immediately increasing ease. This response manifests a decreasing sense of resistance ro pressure at fingers monitoring the tense dysfunctional seg ment (at the same time, motions are away from the opposing direction in which i ncreasing resistance is encountered) . 3. Single elements of rotary and translarory directions are com bined, effecting the control of a n eventual smooth rorsion arc for body movement. The order of i ntroduction of these elements is not important. 4. The final step of the functional procedure i nvolves request for a specific d i rection of active respiration, whichever direction ( i nhalation or exhalation) contributes further ro the increasing ease. For example, i f i nhalation, the request is for the subject to take a deep breath slowly and hold it brieAy. 5. This respirarory interval, adding to a continuous feedback of decreasing resistance, allows the operaror to fi ne-tune the

Bowles' comments about demandlresponse transactions and the motor coordination necessary for each bone ro be in the right place at the right time during demands for body movement strongly i ndicate that he was moving beyond static positional concepts. His conceptual bias for moror function called for the recognition of a mobile system and mobile segments, patterned ro act in concert with one another. Each mobile segment is a bone with articular surfaces for movement, and adnexal tissues under moror control; together, they respond ro precise functional demands ro: l.

Maintain postural position,

2. Carry out active movements, and 3. Allow passive movement. For Bowles, functional diagnosis and technique were "unique i n accuracy and u niversal in nontraumatic application" (24).

61.

Currently there is widespread recognItIon, but still limited understanding, of the neural control of these motor dynamics. In 1978, Stein (25) reviewed principles emerging from studies of the properties of interneurons and their application to the orga nization of the body's motor patterns. Fundamental concepts of command neurons and pattern generators furnished a baseline for continuing research in this field. This growing knowledge about neural networks and motor control systems has been re viewed by Getting (26) . Atsuta and colleagues' research presents an ongoing example (27). In areas where motion tests detect signs of segmental motor asymmetry, somatic proprioceptive and no ciceptive afferents (sensory impulses) acting through feedback loops effect adaptive changes in motor patterns. These changes are palpable as a three-segment unit of segmental dysfunction, which describes a basic unit of defective and adapted function. During functional technique, the release of holding forces (using minimal force) and the return to motor symmetry have been expressed as follows (28) : At the moment when the release of resistance forces is sensed, the response (conceprually) appears to be the result of a matching in

FunctionaL Technique: An Indirect Method

915

Findings

This patient has a dysfunctional T6 segment, locally resisting re gional rotation of shoulders and trunk to the right. Additional findings on shoulder/trunk rotation tests indicate that the in creasing ease in rotation left at T6 is accompanied by resistance to rotation left at T5 and T7. Other rotary motion tests reveal initial increasing ease at T6 to side bending left and to extension, and to initial inhalation on respiratory testing. These directions are resisted at T5 and T7. In the next test (Fig. 61.8A), the physician initiates right side bending of the trunk with moderate caudally directed force through the right hand, which is on the patient's right shoulder. The fingers of the physician's left hand monitor the response at T6. In the second test (Fig. 61.8B), trunk Aexion and extension are initiated, being careful not to introduce translatory aspects of movement (e.g., the patient is maintained in midline of the intersection of m idcoronal and sagittal planes). Slightly relaxed slumping supported by the physician's left arm initiates Aexion. Reversal of this rotary d irection (about the y axis of Fig. 6l.2) initiates extension. The physician's right fingers compare responses to these opposing d irections of motion.

movement function, in which the local segmental control becomes appropnate to the current, overall movement-a matching of ade quacy in physiologic response to specific motion demand. The re turn to local controlled compliance of the mobile segment within the whole complex movement restores the opportuniry for adequate part-to-whole functional relations of this segment within the mobile system. Basic knowledge abom proprioceptor and nociceptor stimuli as a source of reflex communication from somatic tissues to other so matic tissues is well established

(29).

The patient is in the seated position. As indicated in Fig. 61.9, the physician's left arm is over the left shoulder and under the right shoulder of the patient to allow easy introduction of side bending left and rotation left in the following functional application of an indirect method of manipulation.

Even at rest, in response to

only graviry and positional demands, the palpable findings of bony irregulariry and increased resistance of muscular tissue to pressure at dysfunctional segments reflect ongoing stimulation of proprioceptor sensors. During movement, these palpable cues to the traffic on affer ent pathways are highly erratic, since in some directions of ease they decrease whereas in opposing directions of resistance they increase. The sheer immediacy of the changes palpated during motion test ing and treatment suggests the moment-to-moment afferent moni roring by numerous muscle spindle stretch receptors and the resulting efferent control of muscle contractionlrelaxation as a physiologic ba sis for interpreting the response to osteopathic manipulation being reported here

Position

(28).

At vertebral levels where segmental motion asymmetry is present, the physical stress of daily demands for movement and position ing accounts for a major increase in somatic sensory afferent impulses reaching the spinal cord (30). A concept of afferent re duction has application where the palpable sense of decreasing resistance, monitored throughout a functional manipulative pro cedure, successfully restores symmetric motor function.

EXAMPLES OF FUNCTIONAL TECHNIQUE Thoracic, Lumbar, and Sacral Regions: Seated

The method described in the following example of functional technique (17) is applicable in the thoracic, lumbar, or sacral spi nal regions.

Treatment Procedure

1. Hold the patient to provide control in side bending left, rotation left, and extension in a smooth torsional arc. Each of these directions will begin to diminish the local tissue resistance being monitored at T6 during the manipulative p rocedure. 2. Using slight shifting of postural forces to control movement of the patient's body, three translatory tests can be completed. In Fig. 6l.10A, with patient's hips relatively fixed by sitting posi tion, a slight shift in the physician's body weight to the right and then to the left allows comparison of response of T6 to lateral translations of the patient's trunk. In Fig. 61. lOB, a slight shift in the physician's weight controls patient's shoulders and trunk, relative to the pelvis, to initiate anterior and then posterior trans lation motions for testing response at T6. In Fig. 61.1OC, for testing cephalad/caudad directions, the physician initiates slight l i fting cephalad through the parient's shoulders and trunk, and then caudad by applying mild body com pression; the segment's responses to opposing directions are monitored by the physician's right hand. In this example, movements are added with increasing ease in translations to the left, anterior, and cephalad. Testing had indicated increasing resistance in each opposing translatory di rection. Initial introduction of each appropriate di rection is more i m portant than extent of range in any one di rection alone. 3. The final component is to direct a slow inhalation by the patient. The additional element of increasing ease promotes an eventual release of the holding tensions at the dysfunctional

976

VII.


FIGURE 61.8. Additional rotary motion tests. A: Physician initiates right side bending of trunk. B: Trunk flexion and extension. (From Johnston WL. Segmental definition, part II: application of an indirect

method in osteopathic manipulative treatment. JAOA. 1988;88:211-217, with permission.)

segment. The release allows return to a central resting position without encountering the previous resistance in these opposing directions. 4. Following successful release, retesting confirms a return to compliance and symmetry in response throughout the T5-7 area.

2.

For the rotation test, introduce motion with the left hand. The right hand monitors for restricted motion response to the rotation left, with the third fingerpad of the right hand at the right, thumb at the left, and overlying the facet processes. (Hand placements are reversed to monitor the associated lim itations in rotation right at occiput and at C2.)

Cervical Region

In this example, the cervical region is examined initially in the seated position, followed by treatment in the supine position. Findings

The first cervical vertebra (atlas) is limited in head and neck rotation left. Diagnostic Procedure

Position No.2

The patient is supine; the physician sits at the head of the table as shown in Fig. 61.11. Positioning of the physician's arms with elbows supported on the knees provides comfortable support of the patient's occiput in the palms of the physician, who then monitors response to introduced motion. The third fingertips overlie cervical articular facets at C1 bilaterally to monitor response. As rotary motion tests continue, C1 responds with initial increasing ease in side bending right and flexion. During respiration, exhalation is easier.

Position No.1

The patient is seated; the practitioner stands behind the patient. l.

With the left hand, contact the frontal-parietal region, palm frontal, with fingerpads at the right, thumb at the left.

Treatment Procedure 1.

(the patient is supine) To small amounts of each of the three directions of rotary ease, add translatory components (of the

61.

Functional Technique: An Indirect Method

977

Costal Region

FIGURE 61.9. Positioning of patient and physician to facilitate initial

introduction of combined three rotary components toward a sense of increasing compliance (ease) in extension, left side bending, and left rotation. (From Johnston Wl. Segmental definition, part II: appl ication of an indirect method in osteopathic manipulative treatment. JAOA. 1 988;88:2 1 1-2 1 7, with permission.)

head in relation to the trunk) in straight-line directions of in creasing ease to the left, posterior, and caudal approximation . (Translatory testing in this example has indicated increasing resistance in each opposing di rection.) 2. The increasing ease accumulating at C1 during the initial in troduction ofthese six specific elements of motion is enhanced during a directed exhalation.

When diagnosing the motor functions of ribs, it is significant to recognize that their elementary function is respiratory. Ribs also function, however, within the context of routine gross body movements that i nvolve the thoracic spine and cage. Therefore, rib function is examined with the patient in the seated posi tion with fi ngertip contact over the rib angle to monitor a rib's response to the spinal test pattern of elementary passive gross movements (rotations and translations), as well as active respira tion. In principle, costal mobile units also function in association with movement of the upper extremities. Recogn izing their in termediary role in so much of the body's movement suggests that costal dysfunctions may show more complex characteristics of motor asymmetry because they have one major motor function (inspiratory/expiratory) and two subsidiary motor roles active in trunk and appendicular movement. This complexity becomes evident when the palpatory charac teristics of costal motor asymmetries are identified. There appears to be an element of simplicity, however, in the manner in which that asymmetry is organized. The primary movement of the ribs occurs in i nhalation and exhalatio n . It is this respiratory primacy that appears to dictate the remaining characteristics of the total motor asymmetry when a rib becomes dysfunctional. For example, if a primary costal defect is freer during exha lation and resists i nhalation, this respiratory feature distinctively patterns the motor dysfunction of that rib. This becomes ap parent when tested through the shoulders and trunk, with the patient seated, and through the ipsilateral arm with the patient in the lateral recumbent position. However, if the dysfunctional rib is freer during inhalation and resists exhalation, then the asym metric pattern of this rib's motor function is largely reversed from that of the preceding (exhalation) example. Ribs are also involved in asymmetric motor function asso ciated with afferen t input from visceral d isease. This distinctive category of a viscerosomatic component needs consideration sep arate from the two dysfunctions to be detailed here. They arise more strictly from the physical stresses incurred in this somatic regIOn. The following two examples illustrate the most common kinds of dysfunction in the rib cage (essentially somatic in origi n , rather than visceral) . One shows elementary limitation o n ex halation; one is l i mited in inhalation. The predominance of bucket-handle or pump-handle motion during the inspiratory and expiratory function varies throughout the rib cage and is not considered in these examples. Instead, each example is con cerned with monitoring a rib's response to specific demands for rotary and translatory aspects of passive motion tests. These are introduced through the shoulders and trunk of the seated pa tient and through the ipsilateral upper extremity when the pa tient is in the lateral recu mbent position. Each example of treat ment has two procedural components, one seated and one side lying.

3. The smooth torsion pathway for final release of tissue tension allows an easy return to a central resting position. 4. Reexamination in the seated position should reveal a return to symmetry in response to head/neck rotation tests including the occiput, C l , and C2.

Findings in Example 1

The right rib 3 resists exhalation. It predictably resists shoul derltrunk rotation left and side bending left in the seated position,

918

VI!. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment

FIGURE 61.10. Translatory motion tests. A: Patient in sitting position for comparison of response of T6 to lateral translations of trunk. B: Shift in physician's weight initiates anterior and then posterior motion testing at T6. C: Testing cephalad/caudad d i rections. (From Johnston WL. Segmental definition, part II: appli cation of an ind i rect method in osteopathic mani pulative treatment. JAOA. 1988;88:2 1 1-2 17, with permission.)

monitored with the right fingertips overlying the rib angle. Test ing adjacent ribs above and below demonstrates m irror-image asymmerries if right rib 3 is the primary functional defect. Procedure No. 1 : Concurrent Diagnosis and Treatment: Through the Trunk

1. Standing at the right of the seated patient, monitor directions of increasing ease of motion with the left fingers. 2. The right arm is over the patiem's right shoulder and un der the left to control initiation of motions through shoul ders and trunk during side bending and rotation ro the right ( Fig. 61.12A). 3. Tissue tension and limited mobil iry cominue to improve dur ing initial introduction of backward bending and translations

to the right and anterior. (They worsen during flexion and rranslations to the left and posterior.) 4. Direct the patient to inhale slowly and hold the inhalation phase momentarily as d irections of motion are carefully com bined in a smooth torsion arc of movement. This promotes a release and rerurn to a central resting position. 5. Retest shoulderltrunk movements, seated, to assess return to symmetry of these motion components. Procedure No.2 : Concurrent Diagnosis and Treatment: Through the Upper Extremity l.

The patient is in a left lateral recumbent position. Stand in front of the patient with the patient's right upper arm sup ported j ust cephalad to the elbow, as shown in Fig. 6 l .128, on the physician's left forearm. The patient's right hand hangs toward the floor.

2. The right fingers overlie the tissue tensionlrestricrion identi fied at the rib angle and monitor respiratory motion to confirm continuing resistance to exhalation. 3. Palpate for response to motiC'n tests introduced through the patiem's right arm. Typical findings include resistance to exter nal rotation (about the long axis of the humerus), abduction, and cephalad movements. 4. In the treatment procedure, monitor increasing ease to internal rotation, adduction, and caudad movements during a directed slow inhalation phase of the patient. 5. Following a successful release, retest the arm motion compo nents in the side-lying position. FIGURE 61.11. Supine position for cervical technique.

6. Following successful release in each of these two treatment components at right rib 3 resisting exhalation, retesting

61.


979

Procedure No. 1 : Concurrent Diagnosis and Treatment: Through the Trunk

1. Standing at the left of the seated patient, monitor di rections of increasing ease of motion with the right fingers. 2. The left arm is over the patient's left shoulder and under the right shoulder ro control initiation of motions through the shoulders and trunk during side bending left and rotation to the left, as shown in Fig. 6 1 .13A. 3. Tissue tension and limited mobility continue to i mprove as you allow initial slouched flexion over the left arm support and translate to the right and posterior. (They worsen during backward bending and translations to the left and anterior.) 4. Direct the patient ro exhale slowly and hold the exhalation phase momentarily as directions of motion are carefully com bined in a smooth torsion arc of movement to promote a release and return ro a central resting position. 5. Retest shoulder/trunk motions in the seated position.

FIGURE 61.12. E xample I: R ight rib 3 resists exhalation. A: In seated position, motions introduced through the shoulder/trunk. B: In left side lying position, motions introduced through the right arm.

throughout right ribs 2, 3, and 4 confirms return to func tional symmetry in this area of the rib cage. Findings in Example 2

Right rib 3 resists inhalation. During diagnostic testing, stand on the right to test rotation to the right, and on the left to test ro tation to the left. The right rib 3 resisting inhalation predictably resists shoulder/trunk rotation right and side bending right. This is monitored with the left fingertips overlying the rib angle. Test ing adjacent ribs above and below demonstrates m irror-image motion asymmetries, if the right rib 3 is the site of the primary dysfunction.

FIGURE 61.13. Example 2: Right rib position. B: In left side-lying position.

3 resists inhalation.

A: In seated

980

VI/. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment

Procedure No.2 : Concurrent Diagnosis and Treatment: Through the Upper Extremity I.

The patient is in a left lateral recumbent position. Stand in front of the patient. With the left forearm, support and intro duce motion th rough the patient's right arm, having it relaxed and folded at the elbow as seen in Fig. 6 l . 1 3 B.

2. The right fingers overlie the tissue tensionlrestriction identi fied at the rib angle and monitor response to respiratory tests to confirm continuing resistance to inhalation. 3. Palpate for response to motion tests introduced through the patient's right arm. Typical findings include resistance to inter nal rotation (about the long axis of the h umerus), adduction, and caudad movements. 4. In the treatment procedure, monitor increasing ease to exter nal rotation, abduction, and cephalad movements, during a di rected slow exhalation phase of the patient. 5.

Following release, retest arm motion components in the side lying position and retest inhalation and exhalation throughout right ribs 2, 3, and 4.

Although the description of these two examples of rib tech nique (exhalation restriction and inhalation restriction) begin with the seated phase followed by the side lying, the order is not necessarily important and can be optional. The physician's approach in functional technique is impor tant. Evaluate im mediately as each direction of motion is intro duced. Combine these m inor ranges in each direction, as de scribed, to produce a smooth torsion arc of motion during the appropriate final respiratory phase. This complements the con tinually monitored response of increasing ease. The palpable ten sion decreases to a sense of release, and the patient is returned to a resting state. Although these aspects of rib technique are pre sented as specific directions patterned to inhalation or exhalation restrictions, they should not be applied as if to copy a technique procedu re. Rather, test each direction to promote appropriate summation of increasing ease, and monitor decreasing tension throughout each manipulation.

Th oracic Cage: D i fferentiating S omati c and Visceral I nputs

The spinal cord provides communication pathways that conduct im pulses from sensory receptors in both musculoskeletal and vis ceral tissues. When noxious stimuli are persistent, the afferent bombardment contributes to palpable somatic manifestations of spinal dysfunction. Segmental motion asymmetries develop individuality in their dysfunctional behavior depending on the afferent source, somatic or visceral . From functional methods in descriptive research, Fig. 61.3 ill ustrates a th ree-segment configuration of vertebral motion asym metries that characterizes somato-somatic reAex activity. The primary dysfunction at the central segment demonstrates a complete asymmetric behavior in response to motion tests in troduced through the shoulders and trunk in the seated position; the secondary dysfunctions at adjacent segments display mirror image (opposing) motion asymmetries. The reAex basis for these secondary mi rror images becomes apparent when all th ree seg-

ments return to motion symmetry fol lowing successful response to a functional manipulative procedure that addresses only the central (primary) dysfunctional segment. In Fig. 6 l.4, the mi rror-image phenomenon is still evident. However, this time it accompanies central segments that present a different primary orientation. The primacy relates to a vertebra and one adjacent rib at the same spinal level presenting identical motor asymmetries, rather than opposing. The term linkage ap plies to this phenomenon, because both vertebra and rib respond to motion tests in identical fashion, as if they were now linked together as a single mobile unit. This dysfunctional unit's mo tion asymmetry is typically complete in rotary, translatory, and respiratory tests; secondary mi rror images exist at the adjacent coupled segments, as indicated. Clinical data from interexaminer (31) and longitudinal (32,33) studies with hypertensive subjects, as well as a controlled clinical trial with renal, hypertensive, and normotensive subjects (2 1 ) have supported the presence o f linkage as a somatic manifes tation of visceral disease. The characteristic motion asymmetries at several linkage sites are reproducible, and have been reported (20). Manipulative treatment at a l inkage site requires attention to two aspects of the motion behavior disturbed at such a dysfunc tional costovertebral level. The segmental locus demonstrates not only asymmetry to spinal motion tests in the seated position in duced through the shoulderslrrunk, but also in recumbent po sitions to motion tests introduced through the lower extremi ties. A manipulative approach to address the former behavior has been detailed for both diagnostic and treatment procedures, seated, in the preceding thoracic section of "Examples of Func tional Technique." However, maximum response at a linkage site also demands attention to motion behaviors related to the lower extremities (34). An example of diagnostic and treatment p roce dures follows. Findings

Examined in the seated position, the patient has segmental dys function at spinal level T5, with l inkage to left rib 5, and resis tance to inhalation locally (and to exhalation at adjacent segments above and below). There is also resistance to anterior translation, monitored at tissues overlying the transverse processes at T5 and the angle of left rib 5. Under these circumstances, positioning the patient prone (rather than supine) enhances posterior trans lation and begins to decrease the palpable tension locally, as a fi rst step in a functional procedure (35) . The physician now stands at the left of the prone patient, as illustrated in Fig. 61.14. With both legs initially resting on the table, begin with the right leg resting semiAexed. With plantar contacts of your right hand at the patient's right heel, control for the introduction of inversion and eversion motion tests of the whole right limb. Monitoring responses with the left hand in contact at the T5 left linkage site will reveal immediately increasing resistance to both di rections initiated. Sim ilar testing with the left leg will reveal asymmetric behavior; for example, with eversion there is once again resistance, while with inversion there is increasing compl iance. Note: For linked segments in the thoracic region, this char acteristic behavior during lower extremity tests is typical, in that

61.


981

sidebending right as compared with left, introduced through the shouldersltrunk. In such an instance, an expectation also exists for increased resistance to sidebending right compared with left when introduced through the head/neck. However, segments involved in linkage do not show accord in response to these two apparently similar sidebending tests. Instead, segmental resistance to sidebending

right

through the shoulderslrrunk will accompany resistance to sidebend

left introduced through the head/neck. This lack ofaccord serves as a convenient tool for use in diffirential diagnosis of fictive visceral influence in any spinal region dysfunction (34) [author's italics added ing

for emphasis) .

Comment: Regarding Somatic Manifestations of Visceral Input

FIGURE 61.14. Examination of l i n k age left s i te at T5 spinal level leads to treatment, prone, involving specific motion d i rections introduced through the ipsi lateral lower extremity. With appropriate control by ri ght hand support at the left knee, the operator mon itors response at the left hand con tacti ng the l i n ked costovertebral segments. (From Johnston WL. Segmental definition, part IV. Updating the di fferential for somatic and visceral i n puts. JAOA. 2001;5:278-283, with permission.)

responses are asymmetric to tests with the leg ipsilateral to the linked costal component, while resistance is present in both re sponses to tests with the contralateral leg. Procedure: Concurrent Diagnosis and Treatment of Costovertebral Linkage

Engage support at the knee for control of the patient's left leg semiflexed as illustrated in Fig. 6 1 . 1 4. Maintaining slight inver sion freedom, monitor responses at the T5 linkage site to com pare inversion with eversion, flexion with extension and cephalad with caudad directions of the l imb. Select and combine initial as pects of these other elementary directions of increasing ease. In Fig. 6 1 . 1 4, abduction of the limb laterally from the table, flex ion, and caudad directions are combined. With the finding of resistance to inhalation, the final decrease in palpable tension is maximized during a slow exhalation phase to release, followed by return of the leg to natural positioning on the table. When suc cessful, repeating the diagnostic tests involved with each leg will reveal a return to symmetry in these aspects of the dysfunctional behavior at T5. Note: Aparc from the linkage phenomenon, as recognized in the costovertebral region, an additional distinctive characteristic of visceral input is now applicable for those spinal levels lacking costal components, that is, in cervical, lumbar, and sacral regions. Our continuing interest in examination of viscerosomatic linkage sites has led to a descriptive study. The following excerpt details that characteristic: For example, consider any non-linked dysfunctional vertebral or costal segment that shows increased resistance to the seated test for

When spinal analysis identifies a site with palpable signs posi tive for visceral input, the search for the source of the visceral input narrows somewhat, based on the known distri bution of visceral afferent pathways via dorsal routes (36,37). Further, the palpable characteristics of the spi nal tissue changes presented at a site of visceral input bear directly on the time element involved. When historically connecting possibly relevant incidents of ill ness, recent/current paravercebral soft tissue changes trend to ward aspects of local prominence and congestion. On the con trary, when related illness is long-standinglrecurrent, there is a depressed area of the spinal musculature overlying the transverse processes at the vertebral site central to the visceral input. This sparse, deep, horizontal band of markedly increased tissue ten sion reflects the hypoxia associated with tissues that are subjected to prolonged, concentrated reflex action. In time, this action will be both pri mary visceral and secondary somatic, since the spinal dysfunction once initiated continues as a focus for motion stress, and becomes self-maintaining within continuing demands of the motor system. Innominate

The patient has an elementary kind of pelvic dysfunction, one with palpatory findings localized to one side of the pelvis, with asymmetric response to motion tests introduced th rough only the ipsilateral lower extremity (and no resistance encountered with tests introduced through the conrralateral limb). Findings

There is a tissue texture abnormal i ty (TTA) and limited mobility at the left ilium/gluteal region (at the level of 52). There is palpable resistance at the left innominate to external rotation (eversion) of the left lower limb. Diagnostic Procedure

1 . The patient is supine, with the left knee semi flcxed and the foot resting on the table; the physician stands at the patient's left. 2. Locate with the right hand the area ofTTA and limited mobil ity at the left i l ium/gluteal region, at the 52 level, and maintain contact throughout the procedure.

982

VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment procedures at a diagnosed focus of TTA, and restricted mobility, wherever these are evident on pelvic structural examination (35 ) . Specific directions of positioning a n d motion are then applied in a controlled manner to the pelvic location diagnosed, to ease i ncreasingly the holding forces of restricted motor function. Appendicular Regions

Note: There is a continuing application of principle here as the physician maintains use of the six elementary motions and res piration as functional tools for testing and reducing specific dys function in an appendage. FIGURE 61.15. Right lateral recumbent position for left innominate techniq ue.

3. With the left hand at the patient's left knee, in itiate internal and external rotation (moving knee roward right, then left) , revealing resistance palpated at the right hand to the initiation of external rotation (eversion). 4. Introduce similar comparison of internal and external rotation tests through the right semiAexed l imb, but monitor it at the right hand, reveal i ng left innominate compliance to both d i rections of the test.

Findings

In this example, the left knee fails to hyperextend. On exami nation in the supine position with the physician standing at the left side, the left knee lies slightly raised from the table surface when compared with the right. In this uncomfortable, sl ightly Aexed position, it is tenser to palpation than the right and resists further passively i ntroduced extension. A prominence is palpable at the anteromedial border of the joint i nterspace (tibiofemoral), indicating the edge of the medial semilunar cartilage. Position

Treatment Procedure

1. Position the patient right lateral recumbent. Stand in front, with left hand contact at the i n nominate, TTA at level S2 ( Fig. 61.15). Direct the patient to shift the pelvis slightly in anterior translation relative to the shoulders. Maintain this positional shift if this direction decreases tension at the S 2 level, compared with posterior translation. 2 . With your right hand supporting the patient's knees, intro duce Aexion through both legs together to localize action at the S2 sacral level monitored by the left hand.

The patient is supine and the left knee is Aexed; stand by the left side of the table. Procedures: Concurrent Diagnosis and Treatment I . The right palm spans the patellar area with the thumb fol lowing the lateral aspect of the joint i nterspace. The third finger follows the medial aspect, as indicated in Fig. 6 1 .16. This hand is keyed sharply to the distorted sense of rigid binding resistance

3. Now alter your support to the left leg only ( Fig. 61.15), with the right hand/forearm to monitor (in this example) the in creasing ease at your left hand in response to abduction of the limb (versus adduction), backward bending (versus Aexion ) , a n d caudal traction (versus cephalad). Each of these compo nents is combined during introduction of internal rotation (external rotation is resisted) . 4. Direct the patient in in halation (the direction of ease of the TTA). 5. During the fi nal component of directed inhalation ease, com bine these directional elements appropriately to achieve a pal pable sense of decreasing tension and then a release by the holding forces. Return the limb to its resting position with the patient in lateral recumbency. 6. Reexamining the motion tests supine indicates a return to symmetry of response at the left innominate, with reduced tissue tension of the left gluteal musculature. Variations in the findi ngs from those described for this ex ample simply require application of elementary motion testing

FIGURE 61.16. Appendicular example at the left knee. Right hand

monitors and supports. Left hand i ntroduces major motions in testing and treatment.

61.

where it is most apparem. Keep the comact light enough [0 ap preciate this palpable marker, yet fi rm enough in grasp [0 assist in the manipulative procedure. 2: The left hand firmly grasps above the left ankle [0 assist i n slowly bringing the knee up imo the freer direction of flexion. 3. Explore additional directions of motion test for the limb while it is supported in freedom from the table by both hands: these motions address the other rotary aspects, which are found [0 be freer in medial rotation and abduction. Begin the i ntroduction of these motions with the left hand and moni[Or response with the right. 4. Maimai n the initial introduction of rotary components. 5. Wh ile still moni[Oring response at the knee, the tests us ing rransla[Ory directions for the limb i ndicate increasing ease amerior, above the table (binding posterior), increasing ease [0 the left (compared with right), and cephalad (with binding i n caudal traction). The respira[Ory test indicates easier response [0 inhalation. 6. In the fi nal maneuver, the right hand comact at the knee guides the l ifting support anteriorly [0 the left, while the left hand comrols the amoum of each rotary motion in a cephalad direction via the distal tibiofibular contact. There is a proportionately larger amount of flexion i ntroduced, guided by the sense of continuing i ncreasi ng ease. (This aspect of the knee's template of motion has the greatest range.) 7 . Direct the patient [0 slowly exhale [0 promote the final release of holding forces. Mobiliry then allows an easier return imo improved extension range as the leg is guided back down on[O the table.

983


Applied Osteopathy; I n dianapolis, I N : American Academy o f Osteopa thy; 1 9 5 5 : 1 77- 1 9 1 . 9 . Lippincott HA. Basic principles o f osteopathic tech nique. I n : Barnes M W, ed . Yearbook of the Academy ofApplied Osteopathy. Carmel, CA: Academy of Applied Osteopathy; Indianapolis, I N : American Academy of Osteopathy; 1 96 1 :45-48. 1 0 . Jones L H . Spontaneous release by positioning. The DO. 1 964;4: 1 091 1 6. 1 1 . Johnsron WL I nterexaminer reliabiliry studies. Spanning a gap in med ical research. jAOA 1 982;8 1 : 8 1 9-829. .

1 2. Johnston WL Passive gross motion testing, parr I: its role in physical .

examination. jA OA. 1 982; 8 1 :298-303. 1 3 . Johnston WL, Hill J L. Spinal segmental dysfunction: incidence i n cer vicothoracic region. jAOA. 1 98 1 ;8 1 :67-76.

1 4. Johnston WL Kelso AF, Hollandsworth DL, Karrat J. Somatic mani ,

festations i n renal disease: a clinical research study. jA OA. 1 9 87;87:2235. 1 5 . Kelso AF, Grant RG, Johnston WL Use of thermograms .

to

suppOrt

assessment ofsomatic dysfunction or effects of osteopathic manipulative treatment. jAOA. 1 982;82: 1 82- 1 88 . 1 6. Johnston WL Segmental definition, parr I : a focal point for diagnosis .

of somatic dysfunction. jA OA. 1 988; 88:99- 1 0 5 .

1 7. Johnston WL Segmental definition, pan I l : application of an indirect .

method in osteopath ic manipulative treatment. jAOA. 1 988 ;8 8 :2 1 1 2 1 7. 1 8 . Johnston WL Segmental behavior during motions, 1 : a palpatory study .

of somatic relations. jA OA. 1 972;72:352-3 6 1 . 1 9 . Johnston WL H i l l JL. Spinal segmental dysfunction: incidence in cer ,

vicothoracic region. jA OA. 1 98 1 ; 8 1 :22-28. 20. Johnston WL Segmental definition, part I I I : defi nitive basis for distin .

guishing somatic fin d ings of visceral reflex origin. jA OA . 1 988;88:347353. 2 1 . Johnston WL Kelso AF, Hollandswonh DL, Karrat J . Somatic mani ,

festations in renal disease: a clinical research study. jA OA. 1. 987;87:2235. 2 2 . Johnston WL Friedman H D . Functional Methods: A Manualfo r Pafpa ,

tory Skiff Development in Osteopathic Examination and Manipulation of

CONCLUSION

Motor Function. I ndianapolis, TN: American Academy of Osteopathy; 1 99 5:44-45.

23. Bowles CH. A functional orientation fo r technic. I n: Page LE, ed. Year

The term functional technique applies [0 an indirect method of osteopathic manipulation in which the treatment procedure is organized around palpa[Ory i n formation gained from tests for mo[Or function. By payi ng attention [0 the feedback constantly moni[Ored by the fingertips, the physician will experience im proved psychomo[Or skill and proficiency in the use of this treat ment method, and in many other clinical procedures as well.

book of the Academy of Applied Osteopathy. Carmel, CA: Academy of Applied Osteopathy; 1 9 5 5 : 1 77-1 9 1 . 24. Bowles C H . Functional technique: a modern perspective. jA OA. 1 98 1 ;80:326-33 1 . 2 5 . Stein PSG. Motor systems, with specific reference

to

the control of

locomotion. Ann Rev Neurosci. 1 978; 1 :6 1 -8 1 . 26. Getting PA. Emerging principles governing the operation o f neural net works. Ann Rev Neurosci. 1 989; 1 2: 1 8 5-204.

27. Atsuta Y, Garcia-Rill E, Skinner RD . Characteristics o f electrically in duced locomotion i n rat i n vitro brain stem-spinal cord preparation. j Neurophysiol. 1 990;64:727-735.

REFERENCES

28. Johnston WL Segmental definition, parr II: application of an indirect .

method in osteopathic manipulative treatment. jA OA. 1 988;88:2 1 1 2 1 7.

1 . Ashmore EF. Osteopathic Mechanics. Kirksville, M O : Journal Printing Co; 1 9 1 5:72. 2 . McConnell CP. Osteopathic an, V jAOA. 1 935 ;34:369-374. 3 . McConnell CP. Osteopathic studies, IV jAOA. 1 93 1 ;3 1 :206-2 1 2. 4. Downing C H . Principles and Practice of Osteopathy. Kansas C iry, MO: Williams Publishing Co; 1 923: 1 62. 5 . Lippi ncorr HA. T he osteopathic technique ofWm. G . Sutherland, D.O. In: Northup TL, ed. Yearbook ofthe Academy ofApplied Osteopathy. Ann Arbor, MI: Edwards Brothers I nc; 1 949: 1 24. 6. Hoover HV Fundamentals of technique. In: Yearbook ofthe Academy of

Applied Osteopathy. Ann Arbor, M I : Edwards Brothers Inc; 1 949:25-4 1 . 7 . Hoover H V, Nelson CR. Basic physiologic movements o f the spine. In: Academy ofApplied Osteopathy Year Book. Ann Arbor, M I : Cushing Malloy I nc; 1 9 50:65. 8 . Bowles C H . A fu nctional orientation for tech nic. I n : Page LE, ed. Year

book of the Academy of Applied Osteopathy. Carmel, CA: Academy of

29. Henneman E. Organization of the spinal cord and its reflexes. I n: Mount castle VB, ed. Medical Physiology, 1 4th ed. Vol 1 . St. Louis, MO: CV Mosby; 1 980:762-786. 30. Johnston WL Osteopathic clinical aspects o f somatovisceral interaction. I n : Patterson MM, Howell J H , eds. The Central Connection: Somatovis

cerallViscerosomatic Interaction. In d ianapolis, I N : American Academy of Osteopathy; 1 992. 3 1 . Johnston WL, H i l l JL, Elkiss M L, Marino RV Identification of stable somatic findings i n hypertensive subjects by trained examiners using palpatory examination. jA OA. 1 9 8 2 ; 8 1 :830-836. 32. Johnston WL, Kelso AF, Babcock HB. Changes in presence of a segmen tal dysfunction parrern associated with hypertension, parr 1 : a shorr-term longitudinal study. jA OA. 1 99 5;4:243-2 5 5 . 3 3 . Johnston W L , Kelso AF. Changes in presence o f a segmental dysfunction parrern associated with hypertension, part [ I : a long-term longitudinal study. jA OA. 1 99 5; 5: 3 1 5-3 1 8 .

984 34.


Johnston WL, Golden

W).

Segmental definition, parr IV: updating the

differential for somatic and visceral inputs. jA OA.

35.

36.

Johnston WL, Friedman HD. Functional Methods: A Manualfor Palpa

Beal M C Viscerosomatic reAexes: a review. jAOA.

1 985; 1 2:786-

80 1 .

200 1 ;5:278-283. 37.

Johnston WL, Friedman H D . Functional Methods: A Ma/1l1alfor Palpa

tory Skill Development in Osteopathic Examination and Manipulation of

tory Skill Development in Osteopathic Examination and Manipulation of

Motor Function. I ndianapolis, I N : The American Academy of Osteopa

Motor Function. Indianapolis, I N : The American Academy of Osreopa

thy;

thy;

1 995:83-9 1 .

1 995 : 1 35-1 37.

OSTEOPATHY IN THE CRANIAL FIELD HOLLIS H. KING EDNA M. LAY

KEY CONCEPTS • • • • • • • •

H istory of osteopathy i n the cranial field, including the contribution of William G . Sutherland The primary respiratory mechanism Research indicative of primary respiratory mechanisms The mechanics of physiologic motion Strains D iagnosis via history, observation, and palpation Clinical problems requirin g treatment Principles of treatment

During my years in practice as an osteopathic physician, there never has been one regretfor having chosen this fieldfor my lift's work. Professional experience daily demonstrates the truth that the Science o/Osteopathy includes the key to the great physiological chemical laboratory, the human body, unlocking the living potent forces that heal. To the student lookingforward to a professional field 0/scientific research, and with the desire in his or her heart to render beneficial service to humanity, let me truly say: Osteopathy Provides The Golden Opportunity. -WG. SUTHERLAND, DO Osteopathy is a philosophy, a science, and an art. The study of osteopathy in the cranial field (OCF) offers a unique perspective on all three areas. Through persistent study of the i ntricate os seous armor that protects the brain and spinal cord, keen observa tion, and a compassionate dedication to relieve human suffering, William Garner Sutherland, DO, made a significant d iscovery about the central nervous system that is important i n osteopathy today.

HISTORY

William G. Sutherland, DO, DSc (Hon) (1873- 1 9 54) was an early student of Dr. A. T. Still. Sutherland graduated from the American School of Osteopathy i n Kirksville, Missouri in 1 899. While a student, he observed a mounted disarticulated skull. The sphenoid and the squamous portions of the temporal bones caught his attention, and he remembers:

W i l l i a m G. Sutherland, DO, DSc (Hon)

As T stood looking and thinking in the channel of Dr. Still's philoso phy, my attention was called to the beveled alTicular surfaces of the sphenoid bone. Suddenly there came a thought; I call it a guiding thought-beveled like the gills of a fish, indicating articular mobility for a respiratory mechanism (I).

He dismissed the thought but it kept returning, as if goading him ro study the details of the various articulations of the skull. Sutherland was an original thinker, and his application ofStill's philosophy is recognized as "one of the most i nnovative ideas to be advanced by a member of the osteopathic profession" (2). Anatomy books at that time stated that the sutures of the cran i um were immovable. This, however, did not deter Sutherland. He was determined to understand why the articular surfaces have such

986

VII.


a unique design, and he persevered until he understood that the design was accommodative to the function of the cenrral nervous system (CNS), cerebrospinal fl uid (CSF) , and dural membranes, all of which function as a unit. He named this functional unit the primary respiratory mechanism (PRM). Sutherland established his practice in M i nnesota and devoted 30 years to study, original research on himself, and observation of his patients before he began to share his discovery with his col leagues. The remarkable results he obtained with patienrs aroused the i nterest of other physicians. They prevailed on h i m at his home to teach them his method of treatment. The classes and the i nterest grew, slowly but steadily, because those who were able to learn the concept and apply this method of osteopathic diagnosis and treatment had similar results of relieving patients of pain and distressful conditions when other forms of treatmenr failed to help. As more physicians studied and practiced this method of osteopathic treatment, they formed an organization, the Osteo pathic Cranial Association, for the purpose of j oining together to promote further study, support research, and publish l iterature to help educate physicians and laypersons. This membershi p organization later changed i ts name t o the Cranial Academy and became a component society of the American Academy of Osteopathy. In 1953 Dr. Sutherland, with Drs. C. Handy and H. Magoun, Sr, established the Sutherland Cranial Teaching Foundation, Inc., for the purpose of continuing the teaching of the cranial concept. Dr. Sutherland had established that an accurate diagnosis and successful treatment required sensitive and proficienr palpation that could not be learned from a book; expert i nstructors using hands-on teaching and repeated verification were needed. Dr. Still's teachings also provided these basic principles:

CLassification ofDisease, Ninth Revision (ICD-9) delineates cod ing for somatic dysfunction of the cranium. Competency test ing of osteopathic manipulative treatment (OMT) to treat this dysfunction is available to nonspecial ists and specialists alike. In recent years, the American Osteopathic Association (AOA) has received numerous research grant proposals from both cl ini cians and basic scientists to study the mechanisms and/or efficacy of this approach; the AOA has fu nded several of these projects (6-10) . I nstruction in OCF, also commonly referred ro as cranial osteopathy (CO), has been a part of standard training in de partments of osteopathic pri nciples, practice, and manipulative medicine in all osteopathic medical schools. Concepts and termi nology pertaining to OCF/CO have been developed and defined by the Educational Council on Osteopathic Principles (ECOP) of the American Association of Colleges of Osteopathic Medicine (AACOM ) . They have been published in the Glossary of Os teo pathic Medical Terminology which appears annually in AOl\s Yearbook and Directory of Osteopathic Physicians ( 1 1) . As the federally recognized accrediting body for residency training programs within the osteopathic medical profession, the AOA has approved the Basic Standards for Residency Training in NeuromuscuLoskeLetaL Medicine and Osteopathic ManipuLative Treatment. OCF/CO is one of the OMT models within these basic standards. The AOA also is the federally recognized body charged with approval of certifying boards within the osteopathic medical profession. The AOA has chartered the American Osteo pathic Board of Neurom usculoskeletal Medicine. This certifying board administers written, oral, and practical examinations that include items relating to OCF/CO.

PRIMARY RESPIRATORY MECHANISM

The body functions as a unit • The body possesses self-regulatory and self-healing mecha nisms • Structure and function are reciprocally i nterrelated • Rational treatment is based on application of these three principles •

Dr. Sutherland's discovery and teachings have supplied knowl edge and methods that clarify and expand on the science of os teopathy. Prior to Dr. Sutherland's work, the body was treated as if the head was incapable of having somatic dysfunction. OCF is osteopathy of the entire person because the inher ent force that manifests from within the head region functions throughout the body; therefore, this form of diagnosis and treat ment affects the whole person rather than being limited to the cran ium. Furthermore, the position of the head atop the verte bral column affects the postural balance of the entire neuromus culoskeletal system. For example, if the cranial bone structures have been brought i n to a state of imbalance through trauma, the cran ium will cause compensatory changes throughout the neuromusculoskeletal system in order to keep the equilibrium apparatus efficient i n its function. The insights and techniques derived by Dr. Sutherland's ex pansion of basic osteopathic principles are increasingly inte grated into osteopathic teach ing and care (3-5). T he InternationaL

Primary refers to first in i mportance; Dr. Sutherland considered thoracic respiration secondary to the PRM. By thi� he meant that the physiologic centers that control and regulate pulmonary respiration, circulation, digestion, and elimination are located in the floor of the fourth venrricle and depend on the function of the CNS ( 1 2) . Respiratory refers to the exchange of gases and other metabolites at the cellular level. Mechanism implies an in tegrated machine, each part in working relationship to every other part. The PRM is described as having five anatomic-physiologic components, described in the following sections. Inherent Motility of Brain and Spinal Cord

The inherent motion of the CNS is a subtle, slow, pulse-wavelike movement. It is described as having a biphasic cycle, which may have a rhythmic nature. The entire CNS shortens and thick ens during one phase and lengthens and thins during the other ( 1 2) . As the cerebral hemispheres develop in fetal life, they grow, lengthen, and curl or coil within the developing cranium in the shape of a pair of ram's horns. This embryologic development may account for the anatomic and physiologic p rocesses pro ducing the specific motion characteristics described as the'PRM is palpated. In words still relevant today Lassek described the brain as being "vibrantly alive . . . incessantly active . . . dynamic

62.

. . highly mobile, able to move forward, backward, sideward, circumduct and to rotate." He further stated: ·

The normal, human brain is a wondrous, enormously complex, mas ter organ which can be only made by nature. There are probably approximately rwenty billion neurons in the central nervous system of man and it runs on a mere 25 wattS of electrical power (12).

Fluctuation of Cerebrospinal Fluid

The CSF is formed by the choroid plexuses and circulates through the ventricles, over and around the surface of the brain and spinal cord through the subarachnoid spaces and cisternae. Thus, the CSF is i nside and outside of the CNS, bathing, protecting, and nourishing it. Fluctuation is defined as a wavelike motion of fluid in a natural or artificial cavity of the body observed by palpation or percussion ( 1 3). From the perspective of Sutherland's concept of the PRM, as the CNS shortens and lengthens in a biphasic rhythmic motion, the ventricles of the brain change shape slightly and the Auid moves concurrently. Furthermore, the combined motility of the CNS and the fluctuation of CSF mani fests as a hydrodynamic activity as well as a bioelectric i nterchange throughout the body. Stated simply, this combined activity of the CNS and CSF functions both as a pump and as an electric generator.

Mobility of Intracranial and Intraspinal Membranes

The meninges surround, support, and protect the CNS. The dura mater, the outermost of the three coverings, is composed of two layers of tough fibrous tissue. The outer layer of dura mater lines the cranial cavity, forming a periosteal covering for the inner aspect of the bones, and extends through the sutures of the skull to become the periosteum on the outer surface of the skull. The inner layer of dura mater covers the brain and spinal cord and has redupl ications named the falx cerebri and the tentorium cerebelli. These sickle-shaped structures arise fro m a common origin along the straight sinus and i nvest the various bones of the cranium. The two layers of dura mater are blended or fused in certain areas and are separated in other areas, forming the intradural venous sinuses. The dura mater extends down the spinal canal with firm at tachment around the foramen magnum, to C2 and C3, and to the lower lumbar and sacrum at the level of the second segment. The falx cerebri arises from the straight sinus, attaching to the occiput, parietals, frontals, and the crista galli of the ethmoid. The two halves of the tentorium cerebelli arise or originate at the straight sinus and attach to the occiput, temporals, and sphenoid bone. The spinal and cranial dura and its reduplications respond to the i nherent motion of the CNS and fluctuation ofCSF and move through the biphasic cycle, inAuencing the bones of the crani um and the sacrum. Sutherland named this functional anatomic unit, consisting of the dura mater withi n the cranium and spinal canal, the reciprocal tension membrane (RTM) ( 1 2) . It has also been referred to as the core l ink ( 1 2) because i t transmits forces by linking the cranium to the sacrum. Influences such as trauma

Osteopathy in the Cranial Field

987

and postural strains that affect one part of the mechanism have been clinically observed to affect the entire unit of function. Articular Mobility of Cranial Bones

The most dramatic and debated phenomenon of the PRM has been the articular mob i l i ty of the cranial bones. Careful study of the design of the various articulations of the cranium and face and the RTM and its i n A uence on the motion of the bones led Sutherland to an u nderstanding of the mechanical design and relationship of the inherent motility of the CNS and CSF. At birth, the cranial bones are smooth-edged osseous plates with membrane and/or cartilage between them. With growth and mo tion the edges of the plates develop sutures between them that develop in a way that allows for a m i nimal amount of motion and yet provides protection for the brain. The debate and research are reported subsequently. Involuntary Mobility of Sacrum Between Ilia

The cranial dura is continuous with the spinal dura; the spinal dura extends through the vertebral canal into the sacral canal , attachi ng at the level of some lumbar segments and the second sacral segment. Careful study of the design of the articular sur faces reveals that the sacrum may move on one or several postural axes i n relation to the ilia (pelvic bones) . In addition to these vol untary or postural movements, the sacrum also responds to the i nherent motility of the CNS, to the A uctuation of the CSF, and to the pull of the intracranial and i ntraspinal membranes with an involuntary movement that can be observed by palpation in the living body. This slight rocking motion occurs around a trans verse axis (called the respiratory axis) . Normally, the involuntary motion of the sacrum is synchronous with the involuntary mo tion of the occiput, each bone being inAuenced by the rhythmic pull of the spinal and cranial dura mater. Appreciation of the five phenomena of the PRM in theoret ical and practical terms requires an i ntegration of the anatomic and physiologic factors substantiated by empirical research, and experience-derived applications d iscussed subsequently. Try to vi sualize this physiologic unit o f function with all five components moving slightly but steadily in the living body from before birrh until death. Becker ( 1 4) summarizes its influence on the rotal body economy as follows: Health requires that the PRM have the capacity ro be an involuntary, rhythmic, auromatic, shifting suspension mechanism for the intri cate, integrated, dynamic interrelationships of its five elements. I t is intimately related r o the rest o f the body through its fascial con nections from the base of the skull through the cervical, thoracic, abdominal, pelvic, and appendicular areas of the body physiology. Since all of the involuntary and voluntary systems of the body, in cluding the musculoskeletal system, are found in fasciaJ envelopes, they, too, are subjected ro the 10 ro 14 cycle-per-minute rhythm of the craniosacral mechanism in addition to their own rhythms of involuntary and voluntary activity. The involuntary mobility of the craniosacral mechanism moves all the tissues of the body minutely into rhythmic flexion of the midline structures with external rotation of the bilateral structures and, in the opposite cycle, extension of the midline structures with internal rotation of the bilateral structures 10 ro 14 times per minute throughout life.

988

va.


RESEARCH INDICATIVE OF THE PRIMARY RESPIRATORY MECHANISM Inherent Motility of Brain and Spinal Cord: Research

Since Lassek's time, m uch research has confirmed the inherent motility of the brain and spinal cord. Greitz and colleagues (15) offer diagrams of the brain movement and describe motion in certain areas in the range of 1 .0 mm to 1.5 mm. While their con cern, in part, was how this motion affects the clarity of magnetic resonance i maging, the evidence of substantial motion is well documented. Feinberg and Mark (16) report the velocity in the anterior cortex and corpus callosum as 0.4 ± 0.25 m m/sec and i n the basal ganglia and foramen o f Monro a s 0.63 ± 0.5 mm/sec. Poncelet and co-workers state, " I n summary, brain motion ap pears to consist of a single displacement in systole followed by a slow return to the initial configuration in diastole. This displace ment incl udes a descent of the m idbrain and brain stem toward the foramen magnum, with velocities increasing with proximity to the foramen magnum (:::;2 mm/sec) and medial compression of the thalami on the third ventricle (:::; 1. 5 m m/sec)" (17). Enz mann and Pelc report, "Peak brain displacement was in the range of 0.1 mm to 0.5 mm for all structures except the cerebellar tonsils, which had greater displacement 0.4 mm ± 0.16" (18). Basic science research by Wolley and Shaw (19), Clark (20), and Hyden (21) was cited by Magoun (12). Wolley and Shaw report rhythmic contractions of the of oligodendroglial cells of the CNS. Clark reports research on cats which showed "waves or cycles of 8-12 per m i nute occur . . . not related to the respi ratory rare or heart rate." Hyden shows that glial cells, grown i n tissue culture, pulsate contin uously. Magoun cites this research as supportive of the concept of the motili ty of the brain and spinal cord. This line of research, central to the PRM concept, has cont i n ued to be ofgreat interest to physiologists, radiologists, and neurologists. The majority of the mass of the brain is com posed of non neural cells called glia. Glia cells contain actin and myosin, which are capable of contractile motility. Examination of Fetal human astroglia by i mmunofluorescence staining was car ried out by Abd-EI-Basset and Federoff who found, "contractile units, suggesting that the stress fibers in astroglia may be con tractile. Contractile stress fibers would enable astroglia to exert rension on the matrix surrounding them, thus facilitating rapid changes in cell shape" (22) . Related research by Dani and asso ciates (23) shows active waves of astrocytic Ca2+ in the rat hip pocampus in response to neural activity. Propagation of the cal cium wave was usually within 5 to 6 seconds from the beginning of neural sti mulation, and under constant stimulation produced waves at the rate of 2 per m i nute. These findings are indicative of a regular periodicity propagated by biochemical activity of astroglia. Fluctuation of Cerebral Spinal Fluid: Research

That the CSF fluctuates is no longer controversial. It is the nature of production of rhe fl uctuarions that has not been completely determined by scien tific research. A comprehensive review of the extrinsic Factors aFfecting CSF was made by DuBolay and

colleagues (24). They cited research correlating heart rate with pulsatile CSF in dogs going back to 1896 (25) and discussion on the relationship between CSF and blood flow going back to 1877 (24) . In 1971 DuBolay summarized the vascular-CSF rela tionship issue thusly, "The majority of workers throughout these seven decades have become convinced that the 'cardiac' CS F pres sure rise measured in the ventricles, at the cisterna magna and in rhe lumbar theca, is caused by the rhythmic arterial input of blood to the cranial cavity. Their conclusions are based upon: [1] Timing in relation to the carotid pulses and ECG and various venous pulses and heart sounds . . . [2] Upon the character of the pulse wave . . . [3] Upon its alteration by obstruction elsewhere in the vascular system . . . . A very few have suggested as a result of their experiments that the 'cardiac' CSF pulse has a venous rather than arterial characteristics" (24). DuBolay further states, "Most authors, e.g. Becher, (27) had envisaged the arterial in flow to the head as causing an expansion of the brain and of the vessels within the basal cisterns. O'Connell (28) suggested that the brains' [sic] expansion, by compressing the third ventricle, might constitute a CSF pump [authors' italics added for emphasis]. The observations of Falkenheim and Naunyn (29) , of Knoll (30), and of Becher (27)-in dogs for the most part-drew attention to the effects of respirarion upon CSF pressure" (24). DuBolay's summary has nor been modified or challenged and appears to be current today, though much more research with more refined instrumentation has been done. DuBolay's discus sion of relationships between respiration and CSF pressure, and that the third ventricle might in some way be a CSF pump ap peared to support Sutherland's formulation of the PRM. Mobility of Intracranial and Intraspinal Membranes

That this anatomy i ndeed exists as described has never been dis puted, but few, other than practitioners of OCF/CO, have ex amined the physiologic i m plicarions or even carried out research pertaining to this phenomenon of the PRM. In a study of spinal cord motion, Levy and associares (3 1 ) compared normal subjects with patients who had tethering of spinal cord structures due to spinal dysraphism (e.g., spina bifida), cord compression, or tumor. Their data were in velocity dimen sions but based on empirical displacement of spinal dura tissue. Their data showed healthy subjects to have a spinal CSF flow rate of 12.4 ± 2.92 mm/second, subjects with spinal dysraphism 2.12 ± 1.69 mm/second, and subjects with cord compression 1. 87 ± l.4 mm/second. They furrher elaborate their findings wirh the nature of CSF flow, "The origin of cord pulsations is comparible wirh a direct transfer of morion From brain pulsa tions. In our cases, rhe riming of cord impulse coincided wirh the onser of the caudal phase of flow in the spinal canal. This is in agreement with the observation thar rhe caudal morion of rhe brain leads to reversal of CSF flow by expulsion of cranial CSF, thereby generating a wave of CS F rhat propagares and de scends into the spinal canal" (31). That these phases offlow, based on analysis of brain and spinal dural tissue displacement, were empirically demonstrated, is suggestive of continuity of morion in these structures and the reciprocal nature of the connection between intracranial and i ntraspinal membranes.

62.

An unusual approach was taken by Kosropoulos and Kerami das (32) on a male cadaver that had been embalmed for 6 monrhs. The brain tissue was removed through [wo cur windows, leaving · imact the three divisions of the dural membranes. The measure menr used was a piezoelectric e1emem arrached ro the falx cere bri with the motion recorded by oscilloscope. Application of the frontal lifr cranial rreatmem maneuver then produced a 1.44-mm elongation of the falx cerebri and a parietal lift produced a l.08-mm elongation. Even on embalmed tissue, application of the sphenobasilar compression maneuver produced a -0.33-mm movemenr, and the sphenobasilar decompression maneuver a +0.28-mm movemem of falx cerebri. The observable motion of dural membrane tissue by cranial bone pressure is a unique demonsrration of the cominuity of cranial bone and dural-fascial structures, and supports Sutherland's formulation of the PRM with regard ro the core l ink.

Articular Mobility of Cranial Bones: Research

Despite modern statemenrs that the cranial bones do not move (33), there is ample evidence demonstrating that cranial sutures are consrructed in such a way ro allow for motion, and other studies tha� have measured some degree of cranial bone motion (Fig. 62.1). Those who hold that there is no cranial bone motion cite ev idence that cranial sutures ossifY by a certain age, and are not capable of motion (33,34). However, Pritchard and colleagues (35) studied the hisrology of cranial sutures in humans and five other species, and were anlong the earl iest researchers ro seriously question the complete ossification of cranial sutures. "Oblitera tion of sutures and synosrosis of the adjoining bones, ifit happens at aLI (author's italics added for emphasis), occurs usually after all growth has ceased. In the great apes synosrosis of all sutures occurs im mediately after growth has ceased, but in man and most laborarory animals sutures may never completely close. These dif ferences have been attributed ro the differences in the degree of developmem of the masticatory apparatus" (35). Retzlaff, with collaborarors in a number of studies confirmed, and refined the Pritchard study. Retzlaff and associates state, "Gross and microscopic examination of the pariero-parietal and pariero-temporal cranial sutures obtained by auropsy from 17

Cambial

Uniting

Middle

Capsular

FIGURE 62.1. H istology of cra n i a l sutures. (From Magoun H I . Osteopa thy in the Cranial Field, 2nd ed. K i rksville, MO: J o u rn a l Pri nting Com pany; 1966, with permission.)

Osteopathy in the CraniaL FieLd

989

human cadavers wi th age range of 7 ro 78 years shows that these sutures remain as clearly idemifiable structures even in the oldest samples" (36). Other studies by Retzlaffand colleagues (37) delin eated sutural elemenrs comraindicating ossification and demon strated the presence of vascular and neural structures in the su tures. These studies also showed the presence ofnerve and vascular tissue substantial enough ro supply the needs of connective tissue activated beyond mere bony sutural adhesions and ossification. Additionally, Retzlaff and colleagues (38) traced nerve endings from the sagirral sinus through the falx cerebri and third ventri cle ro the superior cervical ganglion in primates and mammals. Empirically demonstrated cranial bone motion in animals is well documemed. Michael and Retzlaff(39) demonstrated cranial bone (parietal) mobility in the squi rrel monkey. In significam work, Heisey and Adams (40,41) and Adams, Heisey, and others (42) demonstrated parietal bone mobil i ty in cats as a function of laborarory-induced fluctuation in CSF volume. Demonstration of human cranial bone motion is suggestive of support for the P RM phenomena, but has involved studies with few subjects. In 1971, Frymann (43) reported cranial bone excursions ranging 0.0005 ro O.OQ1 inches. She used an elec tronic, spring-loaded, strain-gauge apparatus and was able ro show dyssynchrony be[Ween cranial bone motion and thoracic respirarory motion. Heifitz and Weiss, using technology similar to Frymann's found, ''A definite increase in the bitemporal di mension of the imact skull was associated with the rise in rcp [imracranial pressure] over 15 mm Hg in our [wo comarose pa tiems. This increase was detectable with ordinary strain-gauge technology" (44). Using force transducers, Tettambel and asso ciates (45) showed differences be[Ween heart rate, respirarory rate, and a third rhythm which appeared ro be associated with the PRM of 30 subjects be[Ween the ages of 16 ro 71. In a substamial body of work, yet ro be replicated, Zanakis and co-workers (46) demonstrated human parietal bone motion. The objective measure used was infrared reAecrors on acupunc ture needles "anchored" in the parietal bones, and movement was measured by a camera in a "kinematic system." Regular repeti tive motion frequencies ranged from 7 ro 12 cycles per minute, and the rotal excursion ranged 20 ro 200 microns, with the ab solute diameter of the skull changing by 2.2 milli meters over a lO-second period (46). The rate and amplitude characteristics were replicated and a further conclusion that "motion of cranial bones is not a simple 'hi nge' operation, but a complex motion involving more than one axis of movemem" was reached (47). Lewandowski and associates (48) concluded, " Movement of the parietal bones therefore appears ro be movemem abour the cranial sutures alone." Among the more promising ongoing research on cranial bone motion is that of Moskalenko and colleagues (49-51). A recem publication speaks not only ro cranial bone motion but also ro intracranial Auid volume characteristics suggestive of changes in consistem with a rigid calvarium. Moskalenko and co-workers state: It has been shown that the cranial dimensions in healthy people un dergo continuous changes in the frontal and sagittal sections with a mean amplitude0.380.21 mm (N 18) and a maximum deviation of up to 1 mm. Two-channel bioimpedence [sic] imaging (60 kHz) =

990

VII.


of the human head, with electrodes placed in fronto-occipital and bitemporal positions and with further analysis of the resulting curves in the rwo-dimensional X (one channel)-Y (another channel) coor dinate system, revealed the ellipsoid shape of the recorded data with a 0.23 0.16 axis ratio (N 26) characteristic of the presence of an antiphase, or reciprocal, component. Owing to this the cranial cav ity volume increases by 12-15 mL under natural elevation of the intracranial pressure. The prevalence of periodic movements with a frequency of 6-14 cycles per minute was observed by means of spec tral analysis of 3-minute sections of continuous recording in one of the channels (50) . =

Moskalenko and colleagues (51) further describe an i n teraction berween i nt racranial hemodynamics and CSF circulation which com bined to give a frequency of 6 to 12 cycles per m inute. "It was found that slow oscillations of the bio-impedance [sic] (BIM) in the frequency range 0.OS-0.2 Hz were of intracranial origin and were related to the mechanisms of regulation of the blood supply to and oxygen consumption by cerebral tissue, as well as with the dynamics of the CSF circulation" ( 5 1 ). Utilizing laser-Doppler flowmetry, Nelson and co-workers (52) demonstrated that the Traube-Hering-Meyer (THM) os cillations were highly correlated with PRM rhythmicity. They report PRM and THM rates of 5 to 1 0 cycles per m i nute, and state, "The results of this study indicate that the PRM oscillation occur simultaneously, though they may not represent the exact same phenomenon" (52). Involuntary Mobility of Sacrum Between Ilia: Research

Empi rical research by Weisl has substantiated this phenomenon of the PRM (53). Further research by M i tchell (54), Pruzzo ( 5 5), and M i tchell and Pruzzo (56) demonstrates a horizontal axis of sacral motion located anterior to the second sacral segment. Their research also reports sacral movement characteristics consistent with Weisl's findings. The S2 axis has become known as the respiratory axis of the sacrum. This "southern pole" of the PRM awaits the type o r research effort applied in the demonstration of cranial bone motion.

MECHANICS OF PHYSIOLOGIC MOTION

The overall shape of the skull is that of a relative sphere with its inferior surface i ndented. The terminology used to describe the directions of motion of the various bones is similar to that for the motions of the spine and extremi ties. M idline bones move through a flexion phase and an extension phase during their biphasic cycle. Paired bones move through external rotation and internal rotation during the cycle. The flexion phase of m idline bones is simultaneous with external rotation of paired structures. The extension/internal rotation phase occurs reciprocally. The sphenoid and occiput (midline bones) form the key ar ticulation at the sphenobasilar symphysis (or synchondrosis) i n the base of the skull . This is a cartilaginous u n i o n up to the age of 2 5 years and thereafter has the resi liency of cancellous bone (57). This articulation is slightly convex on its superior surface. With flexion of this joint there is slight increase in this convex-

ity. The motion of each midline bone occurs around a transverse axis. The other midline bones of the mechanism are the ethmoid, vomer, and sacrum. They are moved through the biphasic cycle in response to the pull or influence of the dural membranes that are influenced by the coiling and uncoiling of the CNS and the fluctuation of the CSF. The motion is i n itiated from within the living body and is referred to as inherent motion or involuntary motion. The overall motion of the cranium is sim ilar to the motion of the chest during respiration, but the rwo do not occur si multaneously. Thoracic respiration occurs 12 to 16 cycles per m inute in adults and up to 44 cycles per minute in newborns (5S); the most frequently encountered motion of the P RM nor mally occurs 1 0 to 1 4 cycles per minute (12). During flexion of the m idline bones, palpation senses that the head widens slightly i n its transverse diameter and shortens slightly in its anteropos terior diameter. The area where the coronal and sagittal sutures join, called bregma, descends. This widening occurs as the paired bones move toward external rotation. With extension of the midline bones, the head narrows and lengthens slightly as the bregma ascends, and all paired bones move toward i nternal rotation. During the biphasic cycle, the osseous cranium changes shape slightly but its volume remains essentially constant; the research of Heisey and Adams (40) and Moskalenko (50) suggests there is enough cranial bone compli ance and "sutural stretch" to allow as much as a 15-mL i ntracranial fluid volume change. During flexion, the sacrum is influenced by the spinal dura and core link and moves posterosuperiorly at its base while the apex moves anteriorly toward the pubes. During extension, the base moves anteriorly and the apex moves posteriorly. This motion occurs around a transverse axis i n the area of the second sacral segment posterior to the sacral canal and is called the respiratory axis of the sacrum. The other axes of sacral motion are postural axes (Fig. 62. 2). The inherent motion of the cranium is not visible but it is palpable. This motion is perceived as a subtle, soft, slight move ment of fluid (CSF) and semifluid (CNS) inside an osseous case. The first attempts at this palpatory exercise may not reveal any thing, or you may feel the subject's thoracic respiration transmit ted through the neck to the head. If the breathing is a distraction, ask the patient to hold their breath for a moment. If you can still sense the rhythm i c motion i n the head, the inherent motion is coming from within the cranium. With palpatory experience, one learns to distinguish berween these different motions. Follow these steps to palpate this rhythmic motion: 1 . Position the patient supine, with the head 8 to 10 inches from the head of the table. 2. Sit comfortably at the head of the table with your forearms resting on the table and your hands placed on the sides of the patient's head. Have the patient move up or down on the table to comfortably accommodate to your relaxed posture (see Fig. 62.S). 3. Contact the patient's head lightly, allowing the fi ngers and part of the palms to gently conform to the curvature 'of the head. (It is essential that the palmar surface of all the fingers, not the thumbs, contact the head because the nerve endings

62.

�

Sphenoid

Squama of the occiput

��'-h'rlf.H'---- Atlas

1I��"'""""Tt--+-- Third cervical

Dural sheath of spinal cord

v.�-'I cCl)

u

40

:I

a

e

60

70

80

90

30

LL

22

1

20 Mortality With OMT •

Without OMT

Shock

10

8

0

T8 T7 T6 T5 T4 T3 T2 T1 T1 T2 T3 T4 T5 Location Dysrhythmia

FIGURE 72.1. Response of 50 patients with myocardial infarction. (Adapted from work by Ed Stiles, DO.)

Left Thoracic Spine

Right Thoracic Spine

FIGURE 72.2. Location and incidence ofthoracic somatic dysfunction in 94 cardiac patients. (From Kuchera ML, Kuchera WA. Osteopathic Considerations in Systemic Function, rev. 2nd ed. Columbus, OH: Greyden Press; 1994, with permission.)

72. Efficacy and Complications certain acute visceral diseases. It is hypothesized that these findings correlate with the anatomy of the proximal vagus nerve in relation to the second cervical vertebra. B~al and Kleiber evaluated 70 patients prior to angiography. Specificity for both positive and negative cervicothoracic palpatory findings in patients with and without coronary artery diseases was 79o/o (33). Many other authors have reported on the efficacy of manipulation in managing coronary heart disease, but no controlled studies have been performed (34,38). Nevertheless, these authors have identified similar clinical findings and results associated with the addition of manipulative treatment to an overall management plan. Similar studies have been done for spinal levels ofsomatic findings associated with pulmonary diseases (39,40). Authors report a strong dominance of problems located in the upper thoracic and C2 region of the spine. Many of these authors report beneficial outcomes associated with osteopathic manipulative treatment (OMT) . Howell and associates (41) reported on the efficacy ofOMT in 17 patients who showed improvement in the severity score over a 1-year time frame. Miller (42) reported on a study of 23 patienrs with chronic obstructive lung disease randomly assigned to a treatment or control group. With the exception of OMT, the treatment received by all patients was the same. Although there was a small change in the mean viral capacity of the treated versus the untreated group, this parameter was not considered statistically significant. What did prove to be clinically significant was a clear improvement in functional capacity of the treated group with reduction of cough, increased walking capacity, less dyspnea, and fewer respiratory tract infections. Numerous other observational studies and pilot projects suggest the value of continuing use of manipulative treatment to enhance self-healing mechanisms in patients with systemic illnesses. For example, two pilot studies suggest that preoperative and postoperative OMT reduce the incidence of atelectasis (43) and ileus, respectively (44). In subsequent randomized, researcher-blinded trials, Sleszynski and Kelso (45) demonstrated similar outcomes using thoracic lymphatic pump OMT compared to using incentive spirometry in prevention of postcholecystectomy atelectasis. Study patients developing atelectasis had earlier recoveries and were quicker return to preoperative forced viral capacity and forced expiratory volume in 1 second values than the incentive spirometry groups. Radjieski and Lumley (46) demonstrated significant length of stay reduction when OMT was added to in a randomized, controlled study to the care of hospitalized patients with pancreatitis (mean reduction, 3.5 days). In another randomized, controlled study, Noll (47) demonstrated that the addition ofOMT resulted in shorter length of stay and shorter duration of intravenous antibiotic use in geriatric hospitalized patients with pneumonia. Some reports suggest that OMT can be effective in decreasing blood pressure and aldosterone levels in hypertensive patients (48-50) . Other OMT research reports suggest that fibromyalgiarelared tender points can be decreased, with improved quality of life measures (5 1- 53). T he value ofOMT as part of health promotion in preventive practices is noted by osteopathic pediatricians and may extend to

1147

opportunities to enhance the efficacy of certain immunizations. In respect to the latter, Jackson and co-workers (54) documented data to support enhanced immunologic response in subjects who received lymphatic and splenic pump OMT. Measel had also documented this in earlier studies (55). The value of promoting health through prevention of degenerative change and maximizing function through reduction of biomechanical risk factors is more fully discussed in Chapter XX. Simons and Travell document (56) improved visceral fu nctions when related somatic components are corrected with manipulative treatment and other manual neuromuscular release techniques. Problems that improved include: Supraventricular tachyarrhyrhmia Gastrointestinal functioning Reduced recurrences of peptic ulcer disease Korr, drawing from his and others' published research, has hypothesized about neurophysiologic factors, such as segmental facilitation and sympathetic nervous system factors that contribute to these phenomena (57).

COMPLICATIONS AND CONTRAINDICATIONS Although manual treatment methods have been used for centuries, little has been recorded regarding morbidi ty and mortality arising from their use. The earliest documentations were recorded as case histories in various journals. Complications associated with various procedures have been reported only recently. Most center on impulsed thrust manipulations and focus on isolated case reports of manipulation of the upper cervical spine. Greater interest in the gathering of data regarding these problems began in the 1980s. Attempts were made to identify the actual incidence, nature, and causes of the injuries. Any discussion of complications must make a clear distinction between symptom exacerbation and true complication. Even though uncomfortable, symptom exacerbations following manipulative treatments are often normal , temporary outcomes of the treatment process. This is particularly true following changes associated with long-term, chronic tissue texture abnormalities and a resulting short-term acute inflammatory response. True complications are those that worsen the patient's pathologic condition or result in developmem of new injury or disorder as a direct result of the manipulative treatment. When describing manipulative treatment conrraindicarions, one must also differentiate between absolute and relative facto rs. There are few absolute contraindications, but many are relative. If the condition being treated risks worsening when activating forces of a particular technique are apt to create harm, it constitutes a relative contraindication. Other manipulative techniques that use different activating forces may however be appropriate and useful.

Incidence A true incidence of complications is difficult to identi fy. Most studies arrive at similar conclusions: major, serious, or significant complications range from 1 in 400,000 to 1 in 1 million (Table 72.1) (58-69).

1148

VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment TABLE 72.1. POSSIBLE SERIOUS CONSEQUENCES OF MANIPULATION REPORTED IN THE WORLD LITERATUREa Preexisting Condition

Incidence

Unilateral atresia of vertebral artery

1:400,000 to 1:1,000,000

Sequelae

Vertebrobasilar artery sequelae Locked-in syndrome Wallenberg syndrome Vertigo/dizziness/posterior headache Aneurysm/dissection subintimal tears Intraluminal clot Transischemic attack/stroke Death

Prior neck trauma including prior traumatic cervical manipulation

Cervical cord compression

Agenesis of odontoid process Odontoideum Down syndrome with: agenesis of transverse axial ligament odontoid developmental variation Ligamentous laxity in : severe rheumatoid arthritis other rheumatologic disorders Posterior osteophytes

1:1,000,000

Exacerbation of disc disease 4 1.4 2 sequestration and acute radiculopathy Thrombosis anterior spinal artery Dissecting hematoma of internal carotid 43 Paralysis of diaphragm 44 Hearing loss Horner syndrome 45 Herniation of thoracic disc 46 Rib fracture Spinal meningeal hematoma 47 Thoracic spine fracture/discitis Cauda equina syndrome• 8- 52

Disc disease

Rare

Osteoporosis/metastasis Concurrent anticoagu lation A lcoholic patient Disc herniation

Very rare Very rare Very rare Very rare Very rare Very rare 1:1,000,000 Very rare Very rare 1:1,000,000

•in a survey of the literature, only approximately 5% of these rare seque lae have occurred as a result of osteopathic physicians using osteopathic manipulative techniques.

Dvorak and Orelli (70) surveyed members of rhe Swiss Manual Medicine Society in 1981. The survey reports a serious incidence of l in 400,000 procedures, most of which were mobilization with impulse (HVLA) with considerable accompanying rotation . Of 1,408 reponed complications, 1,255 were associated with cervical procedures. Most were minor co mplications, such as verrigo. More serious complications included 10 patients with altered consciousness, 12 with loss of consciousness for as long as 5 minutes, and 11 with an undefined neurologic disturbance. Four underwent surgery. The Swiss survey reports less frequent complications relating ro the lumbar spine, with most complaints related to an increase in subjective pain. Although rhe Swiss survey did nor involve U.S. osteopathic techniques, irwas among one of the first careful reporrs on manipulative rrearmenr-relared morbidity. It also highlights the low risk involved with these procedures. In addition, in a 199llecrure to students at rhe MSU College of Osteopathic Medicine, Dvorak reported a ze ro incidence of manipulative treatment complications throughout the 1980s when cervical manipulations were modified ro principally use muscle energy/posrisomerric relaxarion (MET) procedures. Parijn (7 1) identified 93 papers yielding 129 cases of significant manipulation-related complications. He notes that of the reports:

67% (85 cases) involved chiropractors 5% involved physical therapists 5% involved European osteopathic practitioners 2% were unknown 2% were self-i nduced 2% were performed by unqualified persons 18% (23 cases) were unspecified The most frequent significant complication (65%) involved vertebral artery injury. Other complications included: Cauda equina syndrome (12%) Ruptured lumbar disc (6%) Cervical fracture and/or dislocation (5%) Thoracic disc rupture (2%) Other occurrences (less than 1o/o each) All appeared to involve HVLA activations. Vertebral artery complications occurred in a younger gro up than might be anticipated, with a mean age of 35 to 40 years. Male and female distributions were equal. Despite these occurrences, spontaneous vertebral artery dissection is more likely to occur during normal daily activities, such as looking backward over one's shoulder. Koss (72) reporrs on rhe higher incidence of side effects from medications when compared with manipulative procedures. He

72. Efficacy and Complications notes that 5% of hosp ital adm issio ns result from adverse drug reactions and that 36% of patients o n an internal medicine service had a_n adverse reaction to a drug or diagnostic or therapeutic procedure.

Choice of Osteopathic Technique Because a wide variety of mild to assertive impulsed (thrust) manipulative techniques are availab le to U.S.-educated osteopathic physicians, it is difficult to list or generalize absolute contraindications for the procedures. Rather than rely on one method, one shou ld tailor treatment to the individual patient's circumstances. An essenrial key is the practitioner's familiarity with the approaches discussed in this text. Kleynhans (73) divides causes of manipulative complications into two categories: physician-related and patienr-related. Physician-related prob lems include: D iagnostic errors Lack of manual ski lls Lack of interdisciplinary commun ication and consultation with those who are specially skilled in manipulative techniques Kleynhans reports that patient-related problems arise from physical intolerance to the procedures as well as pathologic and structural factors. Other factors are often pertinent: Personal expectations of both physician and patienr Previous experiences with other practitioners Subjective pain responses Other psychological and behavioral factors Congenital abnormalities Osteophytes Atheromatous plaques Active arthritis Joint instabilities Physician examination and diagnostic errors can lead to improper o r inappropriate use of manipulation, with complications potentially occurring. For example, using manipulation in the absence of an appropriate physician encounter runs the risk of delayed diagnosis of potentially life-threatening diseases, such as cancer and heart disease. Anecdotal reports of such problems are common. Properly performed history, physical, and testing procedures avoid this pitfall. Lack of diagnostic and manipulative treatment skills can result in: Poor choice of manipulative procedures Use of manipulation in a contraindicated situation Improper soft tissue preparation Incorrect patient positioning Poorly app lied techniques that use excessive force Final ly, history of trauma severe enough to raise the suspicion offracture, dislocation, or neurovascular insult requires that imaging procedures be performed before manipulation is undertaken.

1149

High Velocity, Low Amplitude Thrusting HVLA thrusting (mobi lization with impulse) techniques reportedly cause the most serious complications, occurri ng in l of 400,000 procedures to 1 in 1 million procedures. They are designed to apply low-amp litude planar and rotational forces along planes of both single and multiple joint systems. The most frequent of the severe complications are neurovascular accidents following manipulations of the upper cervical spine. These include: Occipitobasilar strokes (Wallenberg syndrome) Vertebral artery compression with thrombosis Arterial dissections Cerebellar infarctions Vascular complications occur primarily with the use of cervical rotatio nal forces with the head extended on the neck. The risk increases when the neck is moved away from the midline. Injuries at Cl and C2 are more prone to create vascular complications than are other cervical regions. Several living and cadaveri c studies have shown that during rotation, the extracranial portion of the vertebral arteries can be occluded on the side opposite to the rotation (i.e., rotation right can occlude the left verteb ral artery) (74). Fortunately, decreased blood Aow to the brain as a result of cervical rotation is a rare complication, arising only in the presence of a significant preexisting compromise of the other vertebral artery, often congenital. Basmajian states, furthermore, "The cervical spine is, without doubt, quite resistant, and the atheromatous vertebral arteries are quite tole rant." (75). Patients with rheumatoid arthri tis and Down syndrome are also at particular risk to cervical direct method manipulation because the odontoid ligament is likely to be weakened and susceptible to rupture. Severe complications are less frequent in the lumbar and thoracic spi ne. Increased pain reports are most common in this group. Complications also may include fractures in patients with the fo llowing underlying conditions: Osteoporosis Metastatic bone disease Bone infections Vertebral tuberculosis Cauda equina syndromes have occasionally been reported in conjunction with the use ofHVLA procedures.

Muscle Energy When indicated, MET procedures are effective direct method alternatives for HVLA. MET is most effective when a specific joint or muscle is involved and when patienr cooperation and operator forces can be well controlled. Posttreatment discomfort and complications are uncommon. The most frequent complications are temporary increases of pain . MET is not effective for someone if muscle contracting increases pain or if proper patient positioning cannot be achieved. Abso lute MET contraindications are fractures and severe neuromuscular injuries involving potential treatment sites.

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Counterstrain Counterstrain technique is a gentle, nontraumatic, indirect manipulative treatment. Posttreatment pain can occur several hours after the procedure, particularly in antagonist muscles, but this is usually well accepted by patients who have been informed of this possibility. Take care to avoid combined upper cervical hyperrotation and hyperextension. Stop treatment immediately if the patient reports any unusual neurologic sensations. Anecdotally, one documented case of counterstrain-related stroke has been reported in Europe during formal course teaching. A 38-year-old physical therapist, with unknown vascular disease but with many risk factors including smoking, sustained an internal carotid artery stroke after multiple classroom procedures. The complication was documented by angiography. It had not been previously reported (R. Ward, personal communication, 1993). Avoid positioning that fails to relieve pain and discomfort, as well as positions that produce dizziness or radicular pain. Osteoporotic patients should avoid positions that require extreme forward bending of the thoracolumbar spine.

Craniosacral Osteopathically based cranial manipulations, with their potential for providing valuable help in a wide variety of cases, also can create problems when used by the unskilled. For example, unanticipated lassitude and temporary emotional reactions ranging from tears to laughter occur at times. Uncomfortable side effects include: Nausea Vertigo Lightheadedness Headache Loss of appetite Sleep problems Most are temporary and respond to rest. If problems occur in the clinic, the gentle use of CV4 techniques usually calms the reaction. In the hands of nonprofessionals, serious complications have occurred. One author (E.L.D.) reports the case of a young man who developed hypopituitarism following an unskilled and forceful cranial treatment. After several months of hormone treatment and osteopathic treatment for the cranial dysfunctions, he had a favorable recovery.

Prevention of Complications Proper diagnosis and treatment of any kind, including manipulative procedures, occur when one links the patient's background and presenting history with present circumstances. This includes: Mechanism of injury Medication use and abuse Exercise levels Lifestyle factors Memal and emotional well being

A well-performed history and physical examination, including a careful, osteopathically oriented history and physical examination, complete this essential process. The application of osteopathic principles associated with functional anatomy, biomechanics, and manipulative skills reduces the potential for complications. Histories of trauma, joint and soft tissue diseases, infectious diseases, and cancer are major considerations. When appropriate, include blood work and imaging studies. Another line of defense is the appropriate choice of manipulative procedure. Indirect and neuromuscular-activating methods are typically safe and effective. If HVLA procedures are considered, explore the risk-to-benefit ratio. Most complications have occurred with HVLA maneuvers in the upper cervical spine during combined extension and rotation. Statistically, there is less chance of injury if cervical flexion and side-bending maneuvers are used. Take care to keep the neck in the midline, remembering the basic rule of spinal motion: modification of motion in one plane limits motion in all other planes. Following manipulative treatment, pain or soreness may be prevented if the patient remains well hydrated and refrains from overexertion. Finally, the broader the manipulative armamentarium possessed by the clinician, the better the chances for safe and effective outcomes.

OSTEOPATHIC PRACTICE GUIDELIN ES Disease and dysfunction-based allopathically designed medical practice guidelines have been created and are under continued development for a wide variety of diagnoses. For example, the American Association of Family Physicians established a guideline for depression after more than a year in development and at a cost of more than $1 million. Such MO-oriented guidelines are often difficult to implement for osteopathically oriented physicians because they do not allow for the wide range of patient responses (i.e., the host). As a parallel but distinctive health care system (76), osteopathic medicine is ill served by directly adopting another group's standard of practice as anything more than partial guidelines in the strictest sense of that word. In general, osteopathically oriented guidelines consider both the host and the etiologic factors. They should include an appropriate osteopathic diagnosis that incorporates palpatory diagnosis and potential manipulative treatment relatively early in the evaluation and treatment process, respectively. Goals of manipulation within an osteopathic practice guideline may include: . Resolution of primary somatic dysfunction Resolution of secondary somatic dysfunction Improvement of homeostatic mechanisms (e.g., respiratory, circulatory, immune, etc.) Reduction of inappropriate afferent neural stimuli (especially from segmentally related somatic and visceral structures) Significant somatic dysfunction is that which reduces the body's ability to recover, compensate, and repair itself. Psychologically, it is typically the somatic component that causes the patient discomfort and concern. It is also the somatic component of a

72. Efficacy and Complications problem that prevents the patient from functioning with a high level of efficiency. This is of particular importance for patients such .as high-level athletes and ballet dancers. Functional disorders of other systems affected by a primary disorder need to be a part of osteopathically oriented practice guidelines. The strategy is to reduce or remove identifiable lingering elements of somatic dysfunction to improve the body's ability to: Compensate Repair Recover Improve health Final ly, osteopathicall y oriented practice guidelines include all related elements relating to the diagnosis, treatment, and longterm health-enhancing strategies embodied in the application of osteopathic principles.

CONCLUSION OMT has the potential for complications and side effects, but the risk is low. Properly selected and app lied osteopathic procedures are beneficial for a wide variety of human ailments and health-enhancing activities. Palpatory diagnosis and manipulative treatment enlists the patient's cooperation in the process of maintaining health and overcoming the detrimental effects of somatic dysfunction. In general , the benefits far outweigh the rare and usually minor risks. Serious complicatio ns have occurred wirh the work of some practitioners but are only anecdotally documented in the practice of American-trained osteopathic physicians. Osteopathically based manipulative treatment is tailored to the individual patient's needs in a context of total health care that is in the patient's best interests. When osteopathic treatment is appropriate, it should be performed with gentleness, care, and skill.

REFERENCES I. Goldstein M, ed. The Research Status of Spinal Manipulative Therapy. Bethesda, MD: Department of Health, Education and Welfare; 1975. NIH publication 76-998. 2. Korr IM. The Neurobiologic Mechanisms in Manipulative Therapy. New York, NY/London , England: Plenum Press; 1978. 3. Greenman PE, ed. Concepts and Mechanisms ofNeuromuscular Functions. Berlin , Germany: Springer-Verlag; 1984. 4. Beurger AA, Greenman PE, eds. Empirical Approaches to the Validation ofSpinal Manipulation. Springfield, I L: Cha rles C Thomas; 1985. 5. Parrerson MM , Howell JN. The Central Connection: Somatovisceral/Viscerosomatic interaction. Proceedings of the 1989 American Academy ofOsteopathy International Symposium. Athens, 0 H: Un iversiry Classics, Ltd; 1989. 6. Willard FH , Parrerson MM. Nociception and the Neuroendocrine-Immune Connection. Proceedings of the 1992 American Academy of Osteopathy International Symposium. Athens , OH: University C lassics, Ltd; 1994. 7. Kwoh K. Development of research protocols to study the efficacy of osteopathi c manipulative treatment. In Sirica, ed . Current Challenges to M.D.s and D. O.s. Proceedings of a Conference. New York, NY: Josiah Macy, Jr. Foundation; 1996:263-270. 8. Kuchera ML. G lobal alliances: advancing research and the evidence base. jAOA . 2002;102(1):4-7.

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9. Parker GB, Tupling H, Pryor DS. A conrroll ed trial of cervical manipulation for migraine. Aust N Zj Med. 1978;8:589-593. I 0. Sloop PR, Sm ith DS, Goldenberg E, er al. Manipulation for chronic neck pain: a double-blinded controll ed study. Spine. 1982;7:532-535. II . Gross AR, Aker PO, Quartly C. Evid ence-based review of the literature: manual therapy in the treatment of neck pain. Rheum Dis Clin North Am. 1996;22(3):579-599. 12. Hurwitz EL, Aker PO, Adams AH, et al. Manipulation and mobilization of the cervical spine. A systematic review of the literature. Spine. 1996;21 (15): 1746-1760. 13. Shekel le PA, Adams AH, Chassin MR, et al. Sp in al manipulation for low back pain. Ann Intern Med 1992: I 17:590- 598. 14. Koes BW, Assendelft WJJ, von der Heijden GJMG, et al. Spinal manipulation and mobilisation for back and neck pain: a blinded review. Br Med j 1991;303: 1298-1303. 15. Blomberg S. A pragmatic approach to low-back pain including manual therapy and steroid injections: a multicentre study in primary health care. 1993. Acta Universitatis Upsaliensis: Comprehensive Summaries of Uppsala Dissertations from the Faculty ofMedicine 394. 16. Waagen GN, Haldeman S, Cook G, et al. Shorr-term trial of chiropractic adjustments for the relief of ch ronic low back pain. Man Med. 1986;2:63-67. 17. Gibson T, Grahame R, Harkness J, et al. Contro ll ed-wave diathermy treatment compariso n of short wave with osteopathic treatment in nonspecific low back pain. Lancet. 1985:1258-1261. 18 . Dyer C. Osteopathic vs med ical manipulation in clinical trials. Br Osteopath j 1983;15:65-67 . 19. Fitzgerald M, Stiles E. Osteopathic hosp itals' so lution to DRG's may be OMT. The DO. November 1984:97-10 I. 20. Andersson GBJ, Lucente T, Davis AM, eta l. A comparison of osteopathic sp inal manipulation with sta ndard care for patients with low back pain. N Englj Med1999;341(19):1426-143l. 2 1. Blomberg S, Hallin G, Grann K, et al. Manual therapy with steroid injections-a new approach to treatment of low back pain. A controlled multicenter trial with an eva luation by orthopedic surgeo ns . Spine. 1994; 19(5):569-577. 22. Koes BW, Bourer LM, van Mameren H, et al. Randomised clinical rrial of manipulative therapy and phys iotherapy for persistent back and neck comp laints: results of one year follow up. Br Med J 1992;304(6827):60 1-605. 23. Pope MH, MacDonald L, Haugh L, et al. A prospective randomized three week trial of spinal manipulation, transcutaneous muscle stimulation, massage and co rset in the treatmenr of subacute low back pain. j Manip & Physiol Therap. 1994; 17(4):287-288. 24. C herkin DC, Deyo RA, Battle M, et al. A compa rison of physical therapy, ch iropractic manipulation, and provision of an educationa l booklet for the treatment of patients with low back pain. N Eng! J Med. 1998;339(15): I 021-1029. 25. Brodin H. Inhibition-facilitation technique of lumbar pain treatment. Man Med. 1987;3:24. 26. Data comp iled by Labor and Industry co mputers in Florida (FCER, 1988, Arlington, VA: FCER; 1988) and Co lorado (Denver, CO: Tillinghast; 1993). 27. Cantieri MS. Inpati ent osteopathic manipulative treatment: impact on length of stay. Available at: http: //www.o hhpf. org/research96.html. Accessed May 3 1, 2002. 28 . Kelso AF. A double-blind clinical study of osteopathic findings in hospitalized patients: progress report. ]AOA. 1970;70:570-592. 29. Nicholas N. Correlat ion of somatic dysfunction with visceral disease. JAOA. 1975;75:426-428. 30. Smith LA, et al. An Atlas of Pain Patterns: Sites and Behavior of Pain in Certain Common Disease ofthe Upper Abdomen. Sprin gfield , IL: C harles C Thomas; 1961 . 3 1. Nicholas AS, DeBias DA, Ehrenfeuchter W, et al. A somatic compo nent to myocardial infarction. Br Med j. 1985;29 1: 13- 17. 32. Beal MC. Palparory testing for so matic dysfunction in patients with cardiovascu lar disease. JAOA. 1983;82:73-82. 33. Cox JM, Gorbis S, Dick LM, et al. Palpable musculoskeletal findings in coronary artery disease: results of a double-blind study. ]AOA. 1983;82:832-836.

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34. Rogers JT, Rogers RC. The role of osteopathic manipulative rherapy in the treatmenr of coronary heart disease. JAOA. 1976;76:23-31. 35 . Robuck SV. Osteoparh ic manipulative therapy in organic heart disease. In: AOA Yearbook. Indianapolis, IN : American Academy of Osteopathy; 1956:11 -25. 36. Parriquin OH. Osteopathic management of coronary disease. In: AOA Yearbook. Indianapolis, IN: American Academy of Osteo pathy; 1956:75-79. 37. Koch RS. A somatic componem in hearr disease. }AOA. 1961 ;60:92-97. 38 . Srookey JR. OMT for angina. Osteopathic Symposium. May 1975:16-18 . 39. Beal MC, MorlockJW. Somatic dysfunction associ a red wirh pulmon ary disease. jAOA. 1984;84: 179-183. 40. Koch RS. Structural patterns and principles of treatmem in rhe asthmatic patienr. In: AOA Yearbook. Indianapolis, IN : American Academy of Osreopathy; 1957:7 1-72 . 4 1. Howell RK, Al len TW, Kappler RE. The inAuence of osteopathic manipulative therapy in the managemenr of patienrs with chronic lung disease. JAOA. 1975;74:757-760. 42. Miller WD. Treatment of visceral disorders by manipulative treatmem. In: The Research Status ofSpinal Manipulative Therapy. Bethesda, MD: U.S. Deparrmenr of Health, Education , and Welfare; 1975:295-30 I . 43. Henshaw RE. Manipulative and posroperative pulmonary comp li cations. The DO. 1963;4(1 ): 132-133. 44 . H erman n E. Posroperative adynamic ileus: its prevention and treatment by osteopathic manipulation. The DO. 1965;6(2): 163-164 . 45. Sleszynski SL, Kelso AF. Comparison of thoracic manipulation with in centive spirometry in prevenring postoperative atelectasis. JAOA. 1993;93(8):834-838, 843-845. 46. Radj ies ki JM, Lumley MA, Cantieri MS . Effect of osteopathic manipulative treatment on length of stay for pancreatitis: a randomized pilot study. JAOA . 1998;98(5):264-272. 47. Noll DR, Shores JH , Gamber RG, et al. Benelirs of osteopathic manipularive trearmem for hospiralized elderly patienrs wirh pneumonia. }AOA. 2000; I 00(12):776-782 . 48. Northup TL. Manipulative management of hypertension. JAOA . 1961 ;60:973- 978. 49. Mannino JR. The application of neurologic reAexes ro rhe treatmenr of hyperrension. JAOA. 1979; 10:607-608. 50. Mannino JR. The application of neurological reAexes ro the treatment of hypertension. JAOA . 1979; 12:225-23 1. 5 1. Lo KS, Kuchera ML, Presron SC,Jackson RW. Osteopathic manipulative treatmem in libromyalgia syndrome. JAOA. 1992;9: 11 77. 52. Rubin BR, Gamber RG, Correz CA, et al. Treatment options in libromyalgia sy ndrome. JAOA. 1990;90:844. 53 . Rubin BR, Gamber RG , Shores J, et al. The effect of trearmem options on perceived pain in libromyalgia syndrome. JAOA. 1991 ;91: I 032. 54. Jackson KM , Steele TF, Dugan EP, et al. Effect of lymphatic and splenic pump techniques on the ami body response to hepatitis B vaccine: a pilot study. }AOA. 1998;98(3): 155- 160. 55. Measel JW. The effect of lymphatic pump in the immune response: I. Preliminary studies in anribody response to pn eu mococcal polysaccharide assayed by bacterial agglutination and passive hemagglutin ation. }AOA. 1982;82(1):28-3 1. Also: Measel JW, Kafity A. The effect

of lymph atic pump on the B and T cells in peripheral blood. JAOA. 1986;86:608. 56. Simons DG , Travell JG, Simo ns LS. Trave/L & Simons' Myofascial Pain and Dysjimction: The Trigger Point Manual. Vol 1. Upper Half of Body. Baltimore, MD: Williams & Wilkins; 1999. 57. Korr IM. The spinal cord as organizer of disease processes: Ill. Hyperactivity of sympathetic inn ervation as a commo n factor in disease. JAOA. 1979;79(4):232-237 58. Wolff HD. Akute Wurzelkeompression durch zervika len Bandscheibenseq uester nach gezielrer Handgrifftherapie. Man Med 1989;27: 14- 15. 59. Hooper J. Low back pain and manipulation. Med j Aust. 1973; I :549557. 60. Beatty RA. Dissecting hematoma of the internal ca rotid artery following chiropractic cervical manipulation . J Trauma. 1977; 17:248-249 . 61. H effner J E. Diaphragmatic paralysis following chiropractic manipulation of the cerv ical spi ne. Intern Med. 1985; 145:562-564. 62. Grayson MF. Horner's syndro me after manipulation of th e neck. Br Med }. 1987;295: 1381- 1382. 63. Lanska OJ, Lanska MJ, Fenstermaker R, er al. Thoracic disk herniation associated with chirop ractic sp in al manipulation. Arch Neurol. 1987;44 :996-997. 64. Darberr 0, Freeinna DG, Weis AJ. Spina l meningeal hematoma, warfarin therapy and chiropractic adj ustment. }AMA. 1970;2 14:2058. 65. Dan NG, Saccasan PA. Serious complications of lumbar spinal manipulation. Medj Aust. 1983;2:672-673 . 66. Richard J. Disk rupture with cauda equ in a syndrome after chiropractic adjustment. NY J Med. September 1967:2496-2498. 67. Malmivaara A, Pohjola R. Ca uda eq uin a syndrome ca used by ch iropraxis on a patient previously free of lumbar spine symptoms. Lancet. 1982;2:986-987. 68. Schvarrzman P, Abelson A. Complications of chiropractic treatment for back pain. Post Grad Med. 1988;83:57-6 1. 69. Quon JA, Cassidy JD , O'Conner SM, et al. Lumbar intervertebral disc herniation: treatment by rotation al manipulation. J Manipulative Physical Ther. 1989; 12:220-227. 70. Dvorak J, Orelli FV. How dangerous is manipulation to the cervical spine? Case reporr and results of a survey. Man Med 1985;2: 1-4. 7 1. Parijn J. Comp lications of manual medicine: a review of the literature. Man Med. 1991 ;6:89-92. 72 . Koss RW. Quality assura nce monitoring of osteopathi c manipulative treatment. JAOA. 1990;90(5):427-434. 73. Kleynhans AM. Comp lications of and contraindications to spinal manipulat ive therapy. In: Haldeman S, ed. Modern Developmellls in the Principles and Practice of Chiropmctic. New York , NY: Appleto n-Ce nturyC rofts; 1980;359-384. 74. Heinking K, Kappler R, eta!. Vertebral artery blood Aow during cervical extension and rotation as assessed by co lor Aow duplex ultrasound. }AOA. 1995;95(9) :548. 75. Basmajian JV Grant's Method of Anatomy, 8th ed. Baltimore, MD: Williams & Wilkins; 1983. 76. Gevitz N. Parallel and distinctive. The philosophic pathway for reform in osteopathi c medical educatio n. JAOA. 1994;94:328-332.

SOMATIC DYSFUNCTION H. JAMES JONES

KEY CONCEPTS • • • • • • • • • •

Definition of somatic dysfunction Anatomy and physiology of somatic dysfunction Facilitation and sensitization Mechanoreceptors Spinal cord response to nociception Somatovisceral and viscerosomatic relationships Dorsal horn response to peripheral nociception Central descending inhibition of nociception Myofascial responses to states of immobilization Some proposed effects of osteopathic manipulative treatment (OMT) in relation to somatic dysfunction

INTRODUCTION The Glossary of Osteopathic Terminology defines somatic dysfunction as "impaired or altered function of related components of the somatic (body framework) system: skeletal, anhrodial, and myofascial structures, and related vascular, lymphatic, and neural elements" (1). The diagnosis of somatic dysfunction is supported by visual and palpable findings of Tissue texture changes, Asymmetry of structure, Restriction of motion, and Tenderness to palpation (TART) (1). Palpable temperature changes have also been stated to correlate to areas of somatic dysfunction (2). This chapter will explore the underlying neurophysiologic concepts and theories that support this diagnosis and irs treatment by a variety of manipulative procedures. The diagnostic term "somatic dysfunction" was accepted by rhe International Classification of Diseases-Abridged, Ninth Revision (ICDA-9) in 1973. Ir supplanted the older terms such as "osteopathic lesion'' and "osteopathic lesion complex" (2). In the 19th century, m usculoskeleral motion restrictions and visceral disorders were thought to occur due to "anatomical abnormalities followed by physiologic discord." lr was reasoned that trauma was a large parr of the cause of various disorders. The musculoskeletal dysfunctions that A.T. Still and others found to be amenable to manipulation were thought to be due to an alteration in the position of joints and their mechanics. Manipulating the joints into proper alignment enabled restoration of normal

function. Progress in neurologic and biochemical sciences in the 20th century elucidated the nature of musculoskeletal (somatic) dysfunction. Current concepts include the understanding of the role of modulation of central nervous system (CNS) processes as well as changes in the nature of the connective tissues. T he effectiveness of osteopathic manipulative medicine can be appreciated in light of this understanding.

ANATOMY AND PHYSIOLOGY OF SOMATIC DYSFUNCTION Somatic dysfunction consists of neural, vascular, and con nective tissue adaptations . The activity and condition of body tissues (the soma) are partly influenced via excitation and inhibition of nerves that emerge from the CNS . Joint stiffness, myofascial fi brotic changes, and eventual joint contracture can occur from excessive activity of CNS mediated alpha-motor neurons that may provoke a state of increased contraction (hypertonicity) of muscles innervated by those nerves. Associated with these articular and periarticular changes wi ll be distortions of the body's fascial connective tissue architectural matrix. T his can res ult in alterations of blood and lymphatic Aow to rhe contracrured tissues, conceivably eliciti ng states of relative ischemia and hypoxia and alterations of the local tissue chemical milieu. Osteopathic manipulative treatment (OMT) is designed to alleviate deleterious neurologic processes and connective tissue ab normalities that comprise somatic dysfunction .

Faci I itation In areas of somatic dysfunction, the physiologist Irvin Korr theorized that a large portion of these neurons are kept near their points of depolarization, making them more sensitive to the production of an actio n potential. The action potential would be conveyed via nerve axons to the final end organ (e.g., in the case of alpha-motor neurons, the end organ would be the myoneural junction of the muscle). This concept has been termed facilitation in rhe osteopathic medical literature (3) and sensitization by others (4-6). The facilitated state may then lead to alterations in muscle tone, resulting in myofascial connective tissue stiffness, contracture, and pain. Repeated or strong stimuli tend to elicit a decremental response in most types of nervous receptors (7) .

1154


INJURY/ DEGENERATIVE CYCLE

l l,. l ll

TISSUE INJURY~ BIOCHEMICAL IMBALANCE

t

FLUID

"-......INFLAMMATION

~3~~~STION ~

t

RELEASE OF PROSTAGLANDI NS/ BRADYKININS

PH, ~

DECREASED INCREASED LACTIC ACID, INCREASED HYPOXIA

t/

~

Mechanoreceptors

---DECREASED PAIN ~ GAG

t

MUSCLE GUARDING

MUSCLE SPASM"-....

DECREASED BLOOD/ LYMPH FLOW

ritative chemicals, such as bradykinins, prostaglandins, calcitonin gene-related peptide (CGRP), and so forth , into the surrounding tissue environment, which play an integral role in facilitation and promulgation of somatic dysfunction (9). Associated with these adaptive changes may be local tissue biochemical alterations denoted by the loss of connective tissue lubricants (glycosaminoglycans [GAGS]) that would manifest themselves as further impaired myofascial and joint fl exibility (10) (Fig. 73. 1).

t

EARLY ONSET FATIGUE

NEURAL HYPERSENSITIVITY FIGURE 73.1. Injury/degenerative cyc le.

H owever, in the case of nociceptors (nervous recepmrs that convey a noxious se nsa tion), repeated noxious stimuli appear w lower the activation energy necessary w provoke an action potential that is co nveyed along the nerve axon (8). Therefore it is believed that nociceptors play an integral ro le in the facilitation process. T he vo lleys of afferent input can be derived from a whole host of somatic and/or visceral insults, including physical or chemical trauma or even the effects of a sedentary lifestyle. With tissue damage there is the elaboration of proinflammatory and neuroir-

In order to understand how manipulation resolves somatic dysfunction, it is necessary to be awa re of the anato my and physiology of the mechanoreceptors and co nnective tissue involved. Various kinds of mechanoreceptors th at respond to noxious stimuli are known as nociceptors. Cutaneous nociceptors are described on the basis of their relative size, degree of myelination, and their responsiveness to different kinds of noxious stimuli (11 ). In primates the most prominent ty pes of nocicepto rs include A-delta (Ao) mechanical nociceprors (12), Ao mechanical heat nocicepmrs (13), and C polymodal nociceptors (which respond w heat, chemical, and mechanical stimuli) (6). In 1967, the British neurologist, Barry Wyke, building on the work of Polacek, described an articular nervous receptor system (Table 73. 1) that is responsive to mechanical stimuli (14-16) . Subsequently, others have corroborated the existence of mechanoreceprors that exist in the ce rvical (17), thoracic ( 18), and lumbar spinal joints (19), as well as the intervertebral discs themselves (20). Mechanoreceptors are also found in ligam ents, knee joint menisci, the articular discs of the temporomandibular joint (21 ), and in the gut (22,23), pulm o nary bronchi (24), and cardiac tissue (25). The nomenclature for mechan oreceptors relates to the A-afferent and B-a./ferent systems ori gin ally proposed by Prechtl and Powley (1990) (26). T he A-afferent system is characterized by encapsulated nerve endings, large myeli nated fibers, low thresholds of depolari zation, discriminative to uch and proprioception, and a lin e-labeled system . T he B-afferent system is

TABLE 73.1. MECHANORECEPTORS AS DESCRIBED BY BARRY WYKE, MD Type

Location

Recept or Appearance

Physi ologic Fu nction

Stratum fi brosum of ligaments and joint capsu le

Laminated Ruffini-like corpuscles

Active during movement and at rest Low threshold for activation Slowly adapting

II

lntraarticu lar and extraarticu lar fat pads Junction of the synovial an d f ibros um of th e joint ca psule

Laminated, pacinian -like shaped corpuscles

Active at the onset and ending of movement Low threshold for activation

Ill

Col lateral ligaments A bsent in interspinous ligament s of the cerv ical spi ne region

Golgi-Tendon Organ (GTO)-Iike corpuscles

Active at end of joint range of motion High threshold for activation Slowly adapting

IV

Joint capsule, ligaments and articu lar fat pads Absent in synovia l tissue

Free nerve endings Lattice-like endings

Active only in response to extreme mechanical or chemical irritation High threshold for activation Slowly adapting

73. Somatic Dysfunction TABLE 73.2. COMPARISON OF THE PRECHTL AND POWLEY SYSTEM OF NOMENCLATURE WITH THE WYKIAN NOMENCLATURE Prechtl and Powley System

Wykian System

A-Afferent Division Encapsulated nerve endings, larger diameter myelinated fibers, low thresholds of depolarization, discriminative touch, proprioception, line-labeled system

Type I, Aa fibers Type II, A{J fibers

B-Afferent Division Naked nerve endings, typically smaller diameter. unmyelinated nerve endings (except A8 fibers which are myelinated), high thresholds of depolarization, nociception, pain and a frequency-labeled system

Type Ill, A8 fibers Type IV, (-fibers

characterized by naked nerve endings, small unmyelinated nerve fibers, high thresholds of depolarization, nociception, pain, and a frequency-labeled system. The types I and II mechanoreceptors of the wykian system of nomenclature correspond to the A-afferent system, A-alpha (Aa) and A-beta (Af3) fibers, respectively. The types III and IV mechanoreceptors correspond to the B-afferent system, A8 and C fibers, respectively (Table 73.2). Afferent nerve fibers from muscle that correspond to the types III and IV mechanoreceptors appear to function as nociceptors (26,27). During states of ischemia, some type IV muscle afferents appear to be activated more strongly (28).

The Spinal Cord Response to Nociception Manipulation has been known to alleviate pain in various musculoskeletal conditions. In order to understand how manipulation intervenes in the nociceptive process, it is necessary to first understand the spinal cord response to acute nociceptive input (which can be symptomatic or asymptomatic). Primary afferent nociceptive fibers (types III, A8) reach the spinal cord via the dorsal roots and synapse in the dorsal horn of the spinal cord in Rexed laminae I, II, V, and X (29). C-fiber (type IV) nociceptors synapse primarily in the substantia gelatinosa (lamina II) of the dorsal horn (30) . Primary nociceptive afferent fiber terminals contain neuropeptide-laden vesicles . Some of the putative peptides are substance P (SP) and CGRP (31 ,32). The neuropeptides interact with receptors in the dorsal horn, resulting in the activation of second messenger systems leading to long, slow depolarization (33) . These depolarizations then invoke the opening of N-methyl-d-aspartate (NMDA) voltage-gated ion channels (34) and transcription factors producing proteins of the endogenous opioid class such as dynorphins (35). These cascade of events lowers the thresholds for activation of certain dorsal horn cells known as wide dynamic range (WDR) neurons (36). Additionally, the same nerve endings contain excitatory amino acids (EAA) (glutamate and aspartate) that are believed to cause a rapid excitatory synaptic ion-gated transmission (37).

Wide Dynamic Range Neurons Three different classes of neurons involved in nociception that reside within the dorsal horn of the spinal cord are low threshold mechanoreceptors, nociceptive specific neurons, and WDR neurons

1155

(36). Convergence of Af3, A8, and C fibers on the WDR neurons may contribute to the perception of allodynia (an ordinarily nonnoxious stimulus is perceived, because of a change in central processing of the stimulus, such as a painful sensation).

Responses to Painful Stimuli Information conveyed to the CNS by nociceptors includes the activation of both excitatory and inhibitory circuits. The excitatory signals result in transmission of nociceptive input to higher centers via ascending nervous tracts such as the lateral spinothalamic tract (LSTT) neurons (38). Inhibitory circuitry is found in both the dorsal horn of the spinal cord and in more rostral supraspinal control systems activated by discharges in ascending tracts. Local inhibitory circuits are believed to involve interneurons containing inhibitory amino acid neurotransmitters, and y-aminobutyric acid (GABA) (39). Pep tides of the opioid class, such as enkephalin and, as mentioned earlier, dynorphin, are also thought to contribute to the inhibitory circuitry of the dorsal horn (40,41). Serotonin and norepinephrine function as inhibitory neurotransmitters in the terminals of descending pain control systems (42).

Ascending Tracts Nociceptive information conveyed from the dorsal horn (after synapsing with first order A8 [III] and C fibers [IV]) to more rostral CNS centers for processing and interpretation include the LSTT (pain and temperature). From the substantia gelatinosa (lamina II), second order axons cross via the ventral (anterior) white commissure and then ascend rosrrally via the LSTT. At least a portion of the LSTT tract below the face projects to the ventroposrerolateral (VPL) nucleus of the thalamus in primates and humans (11). Pain sensation from the face, cornea of the eye, the sinuses, cranial dura, temporomandibular joint labial mucosa, and cheeks is conveyed via the trigeminal nerve (V) through irs sensory ganglion (43). The ganglion is known as the semilunar or gasserian gangl ion (44). The central processes of the gasserian ganglion form a descending traer known as the spinal traer ofV after entering the pontine brainstem region. Terminals from this tract form synapses with the spinal nucleus of V Axons from the spinal nucleus of V cross to the contralateral side of the spinal cord and ascend as the ventral (anterior) trigeminothalamic tract to the ventroposteromedial (VPM) nucleus of the thalamus. From the VPM and the VPL, third order axons project to the somatosensory cortex of the parietal lobe of the brain where the full nuance of the nociceptive sensation is experienced as pain (44). Emotional-affective features of pain perception involve other parts of the CNS as well.

Response of Ventral Horn Neurons to Peripheral Nociception Peripheral nociception induces increased firing rates and sensitivity of a-motor neurons within the ventral horn of the spinal cord (45). Conceivably, this would result in increased hypertonicity of muscle and associated myofascial structures subserved by those neurons leading to states of increased muscle contraction and spasm that will manifest themselves as the palpable changes that osteopathic physicians denote by the TART acronym. Concomitantly, the convergence of somatic primary afferent and visceral

1156


afferent fibers onto dorsal horn neurons will result in alterations in sympathetic nervous activity. Aihara and colleagues and Kimura and colleagues demonstrated that nociceptive input conveyed to midthoracic (T6-9) somatic tissues increases sympathetic outflow to the stomach, inhibiting peristalsis (46,47).

Somatovisceral and Viscerosomatic Relationships Louisa Burns, DO, was one of the first osteopathic researchers to suggest that a connection existed between affectations of the somatic and visceral tissues. In a series of experiments performed primarily on rabbits bred specifically for the purpose, experimentally produced spinal "strains" were induced in her animal population. The strains were described as manually tractioning the anesthetized prone animal by grasping the animal's legs, and while the traction was maintained, hyperextending and rotating the spine until a "slight slipping" or maladjustment of the spinal articular surfaces was readily palpable. Burns reported that the paraspinal muscles in the experimentally lesioned areas of her rabbits were different than those of her controls. She noted an increase in the lactic acid content, edema of the striated muscle fibers, and congestion of small blood vessels and capillaries associated with muscle fibrosis in her lesioned animals (48). In anesthetized animals devoid of emotional factors, Sato demonstrated that somatic afferent nerve stimulation (skin pinching or brush stroking) is capable of regulating visceral functions in a variety of domains. Gastrointestinal motility is inhibited by stimulation of the abdominal skin; cerebral blood flow is increased by stimulation of the hind or forelimb in animal models (49). Jorgensen and Fossgreen (50) studied 39 patients with complaints of upper abdominal pain without demonstrable organic abnormalities contrasted with 28 healthy control subjects, and compared them blindly with regard to back pain (P value less than 0.00 1). Back pain was reported in 72% of the patients who complained of upper abdominal pain versus 17% of the control subjects. Seventy five percent of the patients with complaints of back pain manifested abnormalities on physical examination localized to the lower thoracic and thoracolumbar regions of their backs; the very same neurologic levels that innervate the gastrointestinal tract. These findings suggest a connection between the abdominal and back pains, based upon the concept of viscerosomatic or somatovisceral reflex loops with reference patterns directed either from or to the viscus or to or from the skin, muscles, tendons, ligaments, and associated myofascial structures. Interestingly, Jorgensen and Fossgreen were able to demonstrate in their study that 51 o/o of the patients experienced symptoms of irritable bowel syndrome and 41 o/o reported heartburn, both of which were strongly correlated to their complaint of back pain. In a blinded controlled clinical trial, palpatory evidence of somatic dysfunction in left upper thoracic vertebral segments were found in 70 of 99 patients with coronary artery disease (CAD) (51) . Frobert and co-workers (52) demonstrated significantly more degenerative bony changes on cervical spine radiographs in symptomatic patients (30 women and 18 men) with chest pain but with normal electrocardiograms, normal echocardiograms, and normal coronary angiograms compared with asymptomatic control subjects (10 women and 8 men) . Further, physical examina-

tion demonstrated abnormal palpatory musculoskeletal findings in the anterior and posterior chest wall at thoracic vertebral levels T1-6 and in the muscles ofthe neck and shoulder girdle of the symptomatic patients.

Response of Dorsal Horn Neurons to Peripheral Nociception Primary afferent nociceptive input to the dorsal horn results in generator potentials of adjacent terminals of other afferent fibers. Under conditions of peripheral inflammation, action potentials are conducted backwardly (antidromically) along the afferent axons to its parent tissue. This phenomenon is known as a dorsal root reflex (DRR) (53). Antidromic conduction of DRRs may result in the elaboration of neuropeptides (i.e., SP of adjacent nerve terminals contributing to the inflammatory [and hence TART changes] process) (54).

Central Descending Inhibition of Nociception (55) The descending inhibition of nociception begins at the level of the hypothalamus and prefrontal cortex, which permits hormonal and emotional influences to interact and affect the nociceptive experience. In the rostral pons, in an area known as the periaqueductal gray (PAG), cells in response to nociceptive afferent input elaborate opioid neuropeptides (enkephalin) and the inhibitory amino acid, GABA. Additional inhibitory contributions from the locus coeruleus (LC) consist of norepinephrine (noradrenaline). Descending fibers from the PAG synapse on the nucleus raphe magnus (NRM) and nucleus reticularis paragigantocellularis (NRP) with the resultant elaboration of serotonin (5-hydroxytryptophan). Subsequently these cells activate inhibitory neurons that proceed via the dorsolateral funiculus and terminate in the dorsal horn of the spinal cord. Within the dorsal horn, multiple synapses occur with local inhibitory circuitry with the elaboration of multiple enkephalinergic neuropeptides, GABA, a-adrenoceptor release of norepinephrine (noradrenaline), and glycine. The presence of the inhibitory agents effectively hyperpolarize (makes it more difficult to mount an action potemial) any second order neuron transmission of nociceptive information along spinothalamic pathways, blocking the conduction of noxious stimuli to the somatosensory cortex of the brain.

Myofascial Responses to States of Immobilization The nonfibrous portion of collagen connective tissue is known as the "ground substance." It is composed of linear polymers of repeating disaccharide units collectively known as gfycosaminogfycans (GAGs) and water. Within connective tissues there exist several types of GAGs: hyaluronic acid, chondroitin-4-and-6-sulfate, keratan sulfate, derma tan sulfate, and heparin sulfate. Typically GAGs are bound to a protein and are referred to collectively as proteogfycans (56). The function of GAGs is to maintain a certain critical collagen imerfiber distance owing to their large hydrophilic capacity, thus permitting the expression of normal myofascial flexibility by allowing these collagen fibers to move freely against one

73. Somatic Dysfunction

another (57). Woo and colleagues (58) and Akeson, Arnie!, and ochers (9,59) provide evidence that physiologic joint motion appears ro function as a cell signal (ligand) that stimulates fibrocyres embedded within a connective tissue matrix ro elaborate GAG into the surrounding tissue milieu. Saari and associates (60) monirored responses ro joint mobilization in patients with rheumaroid arthritis. Utilizing a radiolabeled, hyaluronatebinding assay, they were able ro determine that joint mobilization increased the serum concentration of the GAG. As alluded to previously, owing ro their large capacity ro uptake and bind water, the GAGs function as connective tissue "lubricants" inhibiting the formation of excessive adhesive cross-links by maintaining a certain critical distance between collagen fibers. However, some cross-linking is necessary ro impart physical strength and integrity ro the tissue. Cross-links consist chemically of aldol condensations between aldehydes (61). In human collagen, major types of cross-links are: dihydroxylisinonorleucine, hydroxylysinonorleucine, and histidino-hydroxymerodesmosine (56,61). Hisrologic evidence suggests that joint fibrosis may occur within as little as 4 days after the onset of joint immobilization (62). This has been seen in states of immobilization, such as would occur with casting an extremity after a fracture, or in bedbound patients who have incurred either orthopedic or neurologic insult and essentially mold ro the shape of the bed or wheelchair within which they reside. In the case of individuals who work in sedentary occupations, a dearth of physiologic deformation (and hence loss of cell signal) ro the joint and adjacent periarticular connective tissue fibrocytes may have similar effects. With decreased physiologic connective tissue deformation, this will presumably result in a decreased production of GAG, with a decrease in tissue uptake of water, and therefore permits collage n fibers ro physically approximate one another. When a certain cri tical collage n interfiber distance is achieved, excessive crosslinkage adhesio ns will develop that impair myofascial mobility. If the excessive cross-linking is not subjected to physiologic deformational stresses, it will result in eventual joint and periarticular con rractu re. Conceivably, vascular structures, such as blood and lymph vessels traversing an area of TART-associated somatic dysfunction, because of the disrorrions ro the connective tissue architecture, may lead ro localized regions of ischemia and hypoxia altering the chemical environment of the tissue, followed by sti mulation of nociceprors. Type IV (C) and possibly type III (A8) nociceprors embedded within the joint and adjacent soft tissues will be further provoked as the individual attempts ro impart normal movement upon a now dysfunctional and adaptively shortened connective tissue matrix. This will result in the cascade of events leading ro nociception, pain, and palpable TART changes as described previously.

SOME PROPOSED EFFECTS OF OSTEOPATHIC MANIPULATIVE TREATMENT IN RELATION TO SOMATIC DYSFUNCTION "Manipulation" is thought ro be derived from the Latin term manus (hand) or manipulare (rouse the hands). Manipulation in a generic sense cannot be viewed as the exclusive domain of any

1157

particular manual medicine-oriented practitioner in so much as it is practiced on a worldwide basis by osteopathic physicians, chiropracrors, physical (physio) therapists and others (63). Some practitioners make a distinction between "mobilization" versus "manipulation" ro indicate that mobilization procedures generally refer roan oscillarory, rhythmic type of physical maneuver and manipulation refers ro a "thrusting" type of physical maneuver directed against an area of dysfunction of the body (64). OMT is described as the therapeutic application of manually guided forces by an osteopathic physician to improve physiologic fun ction and/or support homeostasis, which is acco mplished via a variety of techniques (1). (Fig. 73 .2). A compelling rationale can be mounted that the many myriad forms of manipulative expression practiced by a variety of practitioners simply represent different points on a treatment armamentarium spectrum and that the putative co nnective tissue, vascular, biomechanical, and neurophysiologic effects are mediated through final common pathways. Thus practitioners of the manipulative arts tend ro describe the various approaches as separate and discrete techniques, possibly because that permits an easier understanding of the complex relationships governing this body of technique. It is probably more likely that manipulative techniques employ multiple interlinking mechanisms, often deployed simultaneously.

SOMATIC DYSFUNCTION

[l

[l OPTIMUM HOMEOSTASIS AND FUNCTION FIGURE 73.2. Somatic dysfunction mediated via osteopathic manipu lative technique.

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Soft Tissue and Myofascial Release Thus soft tissue and myofosciaf release techniques may function primarily via the interdiction of excessive cross-linkage adhesi~ns ~y imparting physiologic motion to a given area ofTAR:r. Th1~ will provoke the fibrocyte imbedded within the dysfunctional tissue to produce more GAG with the resultant u_rtak~ of ~ater and restoration of appropriate collagen connective tissue mterfiber distance and the full free expression of myofascial flexibility and pliability (9, 10,57-62). . . During the loading and unloading of a connective tissue, the restoration of the final length of the tissue occurs at a rate and to an extent less than during deformation (loading). These differences represent energy loss in the connective tissue system. This difference in viscoelastic behavior (and energy foss) is known as hysteresis (or "stress-strain") (64). It can be illustrated by a stressstrain or hysteresis curve (Fig. 73.3). Loading the connective tissue to the point ''X' on the hyster~sis curve will result in an "elastic" deformation, with the connective tissue upon release of the load returning to near baseline length . Stressing the connective tissue to point "B" and beyond (the "pl~s tic" range) will result in disruption of so many of the connect~ve tissue cross-links that a sustained lengthening of the connective tissue will result. In the case of a contractured myofascial tissue, such as a tendon or ligament, the soft tissue or myofascial manipulative technique may interdict the TART changes associated with somatic dysfunction, at least in part, via this model. Myofascial techniques are divided into direct (the operator engaging a TART-associated area of somatic dysfunction with a palpatory sense of greatest tissue resistance) and indirect techniques (wherein the operator engages the tissues in the direction of _less p~lpatory resistance). Even in areas of less palpatory myofasC!al resistance, this would not imply that there is an absence of cross-link formation. Rather it simply indicates that the end feel imparted to the operator's palpating hands is perceived as qualita_tively l~ss resistant than when engaging a soft tissue or myofasc1al barner directly. When the deformational load proceeds to the point "C" on the hysteres is curve, then the design characteristics of a given tissue are exceeded and so m any of the cross-links supporting the tissue are disrupted that the tissue loses coherence and structural integrity, resulting in failure of that tissue. If we are talk-

ing about a muscle tendon or a ligam ent, then those tissues are torn. If we are discussing bone, then the bone sustains a fracture (60,61).

Articulatory Techniques Articulatory techniques are described as low velocity/low, moderate, or high amplitude manipulative techniques that carry a jo_int and its adjacent soft connective tissue though a range of monon designed to restore mobility (1) . These techni~ues are o~t~n referred to as joint mobilization by physical therapists. In addmon to proposed connective tissue effects, articulatory techniques may function predominantly by the activation of joint mechanor~ ceptors (types I and II [Aa and A.B]) within an area of somatic dysfunction. Joint mechanoreceptors of types I and II (Aa and A.B) are faster conducting fibers compared to type III (A8) and IV (C) nociceptors. Conceivably, a preponderance of non noxious activity within the faster conducting axo ns, as they are conducted to the level of the dorsal horn, synapse with local inhibitory circuitry of the enkephalinergic and GABA types. This inhibits the transmission of nociceprion via second order neurons to the thalamus and subsequently to the somatosensory cortex. This may explain the phenomenon that occurs when an individu~ in~d~er tently strikes their thumb with a hammer. The concussive 111Jury activates type III (A8) and IV (C) mechanoreceptors within the tissues and joints of the rhumb which are conveyed rostrally to the spinal cord and supraspinal centers (thalamus) via the LSTT. Activation of a-motor neurons in the ventral horn produce an action potential conducted to the muscle of the involved digit. In response to the painful stimulus, the individual immediately reflexively withdraws his or her digit and typically shakes It back and forth in a rhythmic and oscillatory manner. Presumably this activates the larger and faster conducting mechanoreceptor endings located in the metacarpophalangeal joint of the digit. This generates an action potential that is conducted along large diameter afferent axons to the dorsal horn of the spinal cord w:th the inhibition of nociceprion via interactions with tl1e inhibitory dorsal horn circuitry and with contributions from descending cenrral inhibitory systems as discussed previously. The central pain inhibitory pathway also plays a role in this process, but with a larger latency.

Strain-Counterstrain

Lossof~r----T~r

Energy Necking and Failure of the Tissue

Toe Region

Strain (Degree of Deformation) FIGURE 73.3. Hysteresis curve.

~

Lawrence Jones, DO, developed strain-counterstrain techniques (65). Strain-counrerstrain is an OMT that is described as a system of diagnosis that considers the somatic dysfunction tO be a continuing, inappropriate strain reflex. The dysfunction is inhibited by applying a position of mild strain (typically the joint position of relative comfort), followed after a brief period of sustained positioning, by slowly repositioning the j~inr in the oppo~ite direction of the initial mild strain (2). Penpheral somatic msults elicit nociceptive input to the spinal cord as previously discussed via type III (A8) and IV (C) afferents. Pain provokes the individual to attempt to reflexively withdraw from the noxious stimulus. Synapses with y-motor efferent fibers ca us~ the muscle spin~le apparatus (intrafusal fibers) to shorten, wh1ch causes a relative length mismatch between the intra- and extrafusal muscle fibers

13. Somatic Dysfunction in areas of somatic dysfunction. Type Ia and II afferents, sensing the length mismatch between the intra- and extrafusal muscle fibers, generate action potentials mediated via the a motor neurons and axo ns, whi ch result in hypertonicity of the motor units and hence muscle shortening innervated by particular a-motor neurons. All of these events then perpetuate the cycle of somatic dysfunction. When presented with this scenario, if the individual attempts to lengthen th e maximally shortened muscle rapidly, it is suggested that the shortened muscle begins to report itself in a position of strain well in advance of achieving a neutral length. Strai n-countersrrain techniques then may interdict the pain of somatic dysfunction by initially placing the dysfunctional joint in a position of relative shortening of the muscles that surround and attach to the osseous structures. By placing the muscle in a relative shortened position, it is believed that this inhibits inappro pri ate proprioceptive input regarding the length mismatch between agon ist and antagonist muscles (66). The muscle jointcomplex is held in this relative position of comfort for several seconds, then slowly repositioned to neutral in order not to provoke a nociceptive proprioceptor response. Van Buskirk (67) and Bailey and Dick (68) have proposed that a purely proprioceptive reflex model to explain the effects of counterstrain techniques appears inadequate. They suggest that nociceptive reflexes contribute to the paradigm of so matic dysfunction, probably mediated via type III and IV nociceptors.

Muscle Energy Muscle energy techniques are osteopathic manipulative interventions first developed by Fred Mitchell, Sr., DO (69). They are described as OMTs in which the patient's joint(s) are positioned against a restrictive motion barrier and held immobile. The patient uses muscular effort agai nst an unyielding operator counterforce to elicit direct reflex inhibition of agonist muscles or indirect reflex inhibition of antagonist muscles (70). Muscle energy techn iques are often used to mobilize joints, to strengthen weak muscles, to stretch tight muscles and fascia, and to improve circulatio n. G uissard and colleagues (71) studied the effects of different types of stretching maneuvers on motor neuron excitability of the human triceps surae muscles (gastrocnemius and soleus) as a function of the Hoffman (H) refl ex. The H reflex is an electromyographic representation of the degree of activity of the anterior horn (a- motor neuron) excitability. The H reflex is normally present at birth. After 6 months of age it is present in the gastroc-soleus, fl exor carpi radialis, and has been recorded in the hamstri ng and quadriceps muscles (72). In their study, Guissard and colleagues examined three different types of stretching maneuvers ro the triceps surae musculature of their subjects. They were able to determine that a "contract-relax" maneuver (similar in execution to muscle energy technique) , in which the subjects contracted their agonist triceps surae against an unyielding counterforce, followed by relaxation of the muscle with the ankle joint repositioned (stretched) to a new range of motion during the relaxa tion period, and an antagonist-contraction of the tibialis musculature with similar repositioning of the ankle joint during the post- isometric relaxation period, was a superior stretching maneuver than simply static passive stretching of the agonist

1159

triceps surae muscles. During the period of stretching, the H reflex was depressed. This indicated that a-motor neuron excitability, which could conceivably contribute to increased states of muscle hypertonicity and hence the TART changes associated with somatic dysfunction that would inhibit any stretching maneuver, were also depressed. In the physical therapy literature, Schenck and co-workers were able to demonstrate significantly improved lumbar extension spine range of motion in a group of 26 volunteers subjected to muscle energy techniques with limited initi al lumbar range of motion (73).

High Velocity/Low Amplitude Thrusting H igh velocity/low amplitude (HVLA) thrusting techniques (sometimes referred to as mobilization with impulse or thrust) are described in the osteopathic literature as direct techniques that engage a restrictive joint/connective tissue barrier. A short (low amplitude), quick (high velocity) operator force is then applied to the joint to elicit release of the restriction (1). The exact mechanisms of HVLA techniques remain enigmatic (74). Postulated mechanisms may include alterations in cross-link adhesions that impair joint and myofascial mobility (59,75). In other words, from a connective tissue/biomechanical perspective, perhaps a part of what HVLA techniques do is disrupt the connective tissue adhesions that impair joint arthrokinematics by functioning closer to the "C" region of the hysteresis curve. Other postulated mechanisms include the production of afferent discharges from skin receptors, muscle spindles, mechanoreceptors, and free nerve endings in the zygapophysial joints and adjacent connective tissue of the spine, as well as in peripheral joints (76). T he afferent discharges then would synapse on dorsal horn inhibitory circuitry as discussed previously, leading to inhibition of a-motor neuron pools in the ventral horns of the spinal cord. Dishman and Bulbulian conducted a study of 17 subjects (1 0 men and 7 women) in which spinal mobilization without thrust and spinal manipulation with thrust were employed. The amplitude of the tibial nerve/gastrocnemius H reflex was suppressed transiently during the mobilization and/or manipulation procedures. This was consistent with attenuation of a-motor neuronal excitability (74). Conceivably, this results in a state of decreased firing of the motor units innervated by those a-motor neuronal pools, ultimately leading to improved myofascial fl exibility. As the flexibility of the soft connective tissue architecture is restored, blood and lymph flow may improve within these regions (77).

SUMMARY AND CONCLUSIONS Somatic dysfunction is a complex paradigm that likely involves interlinking mechanisms from the biomechanical, connective tissue, neurophysiologic, vascular, and affective (emotional/behavioral) domains. Currently the lifestyle foundations that promote somatic dysfunction are beginning to be better elucidated. The role of OMT in ameliorating somatic dysfunction , while not completely understood, appears to function at simultaneous multimodallevels employing a variety of mechanisms .

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REFERENCES 1. Ed uca tio nal Counci l on Osteopathic Pri nciples. Glossary of Osteopathic Terminology. Washingron, DC: American Association of Osteopathic Colleges; 200 1. 2. Denslow J S. Pathologic evidence for the osteopath ic les ion: the known , unknown and co ntroversial. In: Beal M C, ed. Selected Papers ofjohn Stedman Denslow, DO. Indianapolis, IN: American Academy of Osteopathy; 1993:1 54- 160. 3. Korr I. T he neural basis of the osteopathic lesion. In: Peterson B, ed. The Collected Papers ofIrvin M. Korr. Colorado Springs, CO: American Academy of Osteopathy, 1979: 120-127. 4. Beck PW, Handwerker HO. Bradykinin and seroroni n effects on various types of cutaneous nerve fibres. Pflugers Arch. 1974;347:209-222. 5. Co hen RH , Perl ER. Contributi ons of arachidonic acid derivatives and substance Pro the sens itization of cutaneous nociceprors. j Neurophysiol. 1990;64:457-464. 6. LangE, Novak A, Reeh PW, Handwerker HO. Chemosensitivity of line afferents from rat skin in vitro. J Neurophysiol. 1990;63:887-901. 7. Burgess PR, Perl ER. Cuta neous mechanoreceptors and nociceprors. In: lggo A, ed. Handbook ofSensory Physiology. Be rlin , Germany: SpringerVerlag; 1973:29-78. 8. Bessou P, Perl ER. Response of cutaneous sensory units with unmyelinated fibers to noxious stimuli . J Neurophysiol. 1969;32: I 025-1043 . 9. Akeson WH, Arnie! D. Immobility effects of synovial joints: the parhomechanics of joi nt contracture. Biorheology. 1980;1 7:95-110. 10. Akeso n WH, Arnie! D. The con nective tissue response ro immobility: a study of the cho ndroitin 4 and 6 sulfate and derma ran su lfate changes in periarticular connective tissue of contro l and immobilized knees of dogs. Clin Orthop. 1967;5 1:190-197. I I . Willis WD. The Pain System. The Neural Basis ofNociceptive Transmission in the Mammalian Nervous System. Basel, Switzerland: Karger; 1985. 12. Perl ER. Myelinated afferent fibres innervating the primate skin and their response to noxious stimuli . J Physiol. 1968; 197:593-615. 13. LaMotte RH , T hai hammer JG, To rebja uork H E, Robinson CJ . Peripheral neural mechanisms of cutaneous hyperalgesia following mild injury to heat. J Neurosci. 1982;2:765-78 1. 14. Wyke B. T he neurology of joints. Ann Royal Colt Surg England. 1967;4 1( 1):25-50. 15. Polacek P. Receptors of the joints. Their structure, variability and classifi catio n. Acta Fac Med Univ Brnnesis. 1966;23: 1- 107. 16. Dvorak J, Dvorak V. Neuropathophysiology of the apophyseal joints. In: Manual Medicine Diagnostics. , New York, NY: Georg Thieme Verlag; 1984:chapte r 2. 17. McLa in RF. Mechanoreceptor endings in human cervical facet joints. Spine. 1994; 19(5) :495-50 1. 18. McLain RF, Pickar JG. Mechanoreceptor endings in human thoracic and lumbar facet joints. Spine. 1998;23 (2): 168-173. 19. Yamashita T, CavanaughJM, EI-Bohy AA, et al. Mechanosensitive afferent units in the lumbar facet joint. J Bone joint Surg. 1990;72-A(6):865870. 20. Roberts S, Eisenstein SM, Menage J, et al . Mechanoreceprors in intervertebral discs, mo rpho logy, distribution , and neuropeptides. Spine. 1995;20(24) :2645-265 1. 2 1. Zim ny ML. Mechanoreceptors in articular tissues. Am] A nat. 1988;182 ( 1): 16-32. 22. Yokoyama S, Ozaki T. Effects of gut distension on Auerbach's plexus and intestinal muscle.jpnj Physiol. 1980;30(2):143- 160. 23. Acca rino AM, Azpiroz F, Malagelada JR. Selective dysfunction of mechanosensitive intestinal afferents in irritable bowel synd rome. Gastroenterology. 1995; 108 (3):927-931. 24. Sa nt'Ambrogio G, WiddecombeJ. Reflexes from airway rapidly adapting receprors. Respir Physiol. 200 1;125(1-2):33-45. 25. Kamkin A, Kiselva I, Wagner KD, er al. Mechanically induced potentials in fibroblasts from human right atrium. Exp Physiol. 1999;84(2):347356. 26. Prechtl JC, Powley TL. B-afferents: a fundamental division of the nervous system mediating homeostas is? Behav Brain Sci. 1990;1 3:289331.

27. Kumazawa T, Mizumura K. T hin-fibre receptors responding ro mechanical, chemical and thermal st imulation in the skeleta l muscle of the dog. j Physiol. 1977;273: 179- 194. 28. Mense S, Stahnke M. Responses in muscle afferent fibres of slow conduction velocity ro co ntractions and ischemia in the car. J Physiol. 1983;342:383-397. 29. Light AR, Perl ER. Sp inal termination offunctional ly identified primary afferent neurons with slowly cond ucting myelinated fibers. j Comp Neurol. 1979; 186:133- 150. 30. Sugiura Y, Lee CL, Perl ER. Central projections of identified, unmyelinated C afferent fibers inn ervating mammalian skin. Science.l986; 234:358-361. 31. Carlton SM, McNeill DL, Chung K, Coggehall RF. Organization of calcitonin gene-related peptide immunoreactive terminals in the primate dorsal horn. J Comp Neurol. 1988;276:527-536. 32. De Lanerolle NC, LaMotte CC. Ultrastructure of chemical ly defined neuron systems in the dorsal horn of the monkey. Substance P immunoreactivity. Brain Res. 1983;274:3 1-49. 33. Liu H, Brown JL, Jasmi n J E, et al. Synaptic relationship between substance P and the substance P recepror: li ght and electron microscope characterization of the mismatch between neuropep tides and their receptors. Proc Natl Acad Sci USA. 1994;91: 1009-1013. 34. Traub R]. The spinal co ntributi on of substance P ro the generation and maintenance of inflammarory hyperalgesia in the rat. Pain. 1996;67: 151 - 161. 35. Coderre TJ, Katz J, Vaccarina AL, er al. Contribution of central neuroplasricity ro pathological pa in : review of clinical and experimental evidence. Pain. 1993;52:259-285. 36. Maixner WR, Dubner DR, Kenshalo MC, er al. Responses of monkey medullary dorsal horn neurons during rhe detection of noxious hear stimuli. J Neurophysiol. 1989;62:437-449. 37. DeBiasi SN, Rustioni A. G lutamate and substance P coexist in primary affere nt terminals in the superficial laminae of the spi nal cord. Proc Natl Acad Sci USA. 1988;85:7820-7824. 38. Carlton SM, Westlund KN, Z han g D, era!. Calciron in gene-related peptide contain ing primary afferent fibers synapse on primate spinorha lmic traer cells. Neurosci Lett. 1990;109:76-8 1. 39. Ca rlron SM, Hayes ES. Light microscopic and ultrastructural analysis of GABA-immunoreactive profi les in the monkey sp inal cord. J Comp Neurol. 1990;300: 162-182. 40. LaMotte CC, de Lanerolle NC. Ultrastructure of chemically defined neuron systems in the dorsal horn of the monkey. 11. Methionineenkephalin immunoreactivity. Brain Res. 1983;274:51-63. 41. Takahash i 0, Shiosaka S, Traub RJ, er al. Ultrastructural demonstration of synaptic connections between calcitonin gene-re lated peptide immunoreactive axo ns and dynorphin immunoreactive dorsal horn neurons in a rat model of peripheral inflammation and hyperal gesia. Peptides. 1990; II: 1233-1237. 42 . LaMorte CC, de Lanerolle NC. Ultrastructure of chemically defined neuron systems in the dorsal horn of the monkey. Serotonin immunoreactivity. Ill. Brain Res. 1983;274:65-77. 43. Fix J. Neuroanatomy, 2 nd ed. Baltimore, MD: Williams & Wilkins, 1995. 44. Gi lman S, Newman SW. Manter and Gatz's Essentials of Clinical Neuroanatomy and Neurophysiology, 8th ed. Philadelphia, PA: FA Davis Co; 1992. 45. Schaible HG , Grubb BD. Afferent and spi nal mechanisms of joint pain. Pain. 1993;55:5-54. 46. Aihara Y, Nakamura H, Sa to A, et al. Neural contro l of gastric motility with specific reference to cuta neo-gastri c reflexes . In: Brooks C, ed. Integrative Functions of the Autonomic Nervous System. New York, NY: Elsev ier, 1979. 47. Kimura A, Sato A, Saro Y, et al. Sin gle electrical shock of a somatic afferent nerve elicits A and C reAex discharges in gastric vagal efferent nerves in anesthetized rats. Nettrosci Lett.. 1996;210:53-56. 48. Burns L. Viscero-sensory and somaro-visceral sp inal reAexes. JAOA . 1907;7:51-60. . 49. Saro A. Reflex modulat ion of visce ral functions by somat ic afferent activity. In: Patterson MM, Howel l JN , eds. The Central Connection: Somatovisceral!Viscerosomatic Interaction, Proceedings ofthe 1989 American

73. Somatic Dysfunction Academy ofOsteopathy InternationaL Symposium. Ath ens, 0 H , University C lass , Ltd; 1992:53- 72. 50. Jorge nsen LS, Fossgreen J. Back pain and spin al pathology in pati enrs wi th fun ctio nal upper abdomin al pain. Scand J Gastroenterol. 1990;25( 12) : 1235- 124 1. 5 1. Beal MC, Kleiber GE. Somatic dys fun cti o n as a predi cto r of co ron ary artery disease. JAOA. 1985;85(5) :302-307. 52 . Froberr 0, Fossgreen J, So nd ergaa rd- Pertersen J, et al. Musculoskeletal pa th ology in patients with angin a pecto ris and no rmal coronary angiograms. J Intern Med. 1999;245(3) :237-246. 53. Sluka KA, W illis W D , Westlund KN . T he ro le of do rsal root reAexes in neurogenic inA ammario n. Pain Forum. 1995;4: 14 1- 149 . 54. Raja SN , Meyer RA, Ringkamp M , et al. Peripheral neural mechanisms of nocice.pri on. In : Wa ll P, Melzack R, eds. Textbook ofPain. Edinburgh, Scotland: C hurchiii -Li vingstone; 1999 :36. 55. Co usins M, Power I. Acute and posto perative pain. In: Wall P, Melzack R, eds. Textbook of Pain. Edinburgh, Sco tland: C hurchiii- Livin gsto ne; 1999:458- 460. 56. Srryer L. Biochemistry, 3rd ed. New York, NY: WH Free man and C o, 1988:chapter II . 57. Ca ntu Rl , G rodin AJ. Myofoscial Manipulation Theory and Clinical Application. Ga ith ersburg, MD: Aspen Pub licatio ns; 1992 . 58. WooS, Ma tth ews JV, et al. Co nnective tissue res po nse to immobili ty. Arthritis Rheum. 1975; 18:257-264. 59. Akeso n WH, Amiel D, et al. Co llage n cross- lin king alterati ons in the joinr conrractures: changes in th e redu cible cross links in periarticular co nn ect ive tissue after nine weeks o f immobiliza tio n. Connective Tissue Res. 1977,5: 15- 19. 60. Saa ri H , Konttin en YT, No rdstrom D . Effect of joint mobilization on serum hya lu ronate. Ann Med. 199 1;23 ( I ):29-32. 6 1. Ski nner H CW. Bone: cel lul ar and molecular o rga nization. In : Albright JA, Brand RA, eds. The Scientific Bmis of Orthopaedics. New York, NY: Appl eto n-Ce ntury-Cro fts, 1979:chapte r 4. 62. Sa lter BB. Royal College Lecture: Preventi on of arthriti s through preservatio n of ca rtil age. J Can Assoc Radio/. 198 1;32 : 5- 7.

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63. Haldeman S, H ooper PD . Mobiliza ti on, manipulatio n, massage a nd exercise fo r the reli ef of muscul oskeletal pain . ln : Wall PO , Melzack R, eds. Textbook of Pain, 4 rh ed. Edinburgh, Sco tland: C hurchiii- Li vin gston e; 1999:1 399-14 18 . 64. No rdin M , Frankel YH . Basic Biomechanics ofthe MuscuLoskeletal System, 2nd ed. Philadelphia, PA: Lea & Febi ger; 1989. 65 . Jo nes LH , Kusunose RS , G oerin g E K. Strain-Counterstrain. Bo ise, 10: Jo nes Srrain-Counrerstrain , lnc; 1995 . 66. Matthews PBC. Proprioceptors and the regulati o n of move ment. ln: To we AL, Luscher ES, eds. Handbook ofPhysiology, Section 1, The Nervous System, Vol ll, Part I. Bethesda, M 0 : America n Phys io logical Society; 198 1. 67. Van Buskirk RL. Nocicepti ve reAexes and the so mati c dys fun cti o n: a model. JAOA. 1990;90 (9), 792-8 09. 68. Bailey M , Dick L. Nocicepti ve co nsideratio ns in treating with co unterstrain . JAOA. I 992;92 (3):334-34 1. 69. Mitchell F. The Muscle Energy Manual, Vo l I. Lansin g, Ml; 1995 . 70. Goodridge JP. Muscle energy techniqu e: definiti on, ex pl anatio n, methods of procedure. JAOA. 1981;81 (4) :249- 253. 7 1. G uissa rd N, Duchateau J, H ain aut K. Muscl e stretching and moton euro n excitability. Eur j Appl Physiol. 19 88;58:47- 52. 72 . De Li sa JA, Mackenzie K, Baran EM . Marmal ofNerve Conduction Velocity and Somatosensory Evoked Potentials, 2 nd ed . New York, NY: Rave n Press, 1987. 73. Schenck RJ , M ac Diarmid A, Rousselle J. T he effects of muscle energy technique on lumbar range o f motion. J Man Manipulative Ther 1997;5(4): 179- 183. 74. Di shman JD , Bulbulian R. Spin al reAex attenuatio n associated with spin al manipul ation . Spine. 2000;25( 19) :25 19-2525 . 75 . Enneking W, H orowitz M . The intraarticular effect of mobilizati on o n th e hum an kn ee. J Bone joint Surg. 1972;54(A): 973- 985. 76. Vandeenenabeele F, C reemersJ , Lambrichts l, et al. Enca psulated ruffini like endings in human lumbar facer joints. J A nat. 1997; 191 :57 1- 573. 77. Sucher BM. Thoracic o utlet sy ndrome-a myofasc ial vari ant: Parr I . Pathol ogy and diagnosis. JA OA. 199 0;90 (8) :6 86-696.


SECTION

VIII BASIC AND CLINICAL RESEARCH FOR OSTEOPATHIC THEORY AND PRACTICE

INTRODUCTION ALBERT F. KELSO BERNARD R. RUBIN

Osteopathic philosophy suggests a broader basis in rhe 21st century for continued advancement of irs theory and practice. A. T. Still's experience with deaths in his family initiated his search for a new treatment to replace medicine. His search identified manipulative techniques used to restore the body's capacity to heal itself. The philosophy that the body behaves as an integrated unit is derived from the application of his findings. His practice, based on treating the osteopathic lesion as the intervention to restore the body's inherent capacity to heal itself, assumed that the treatment affected the entire person. The principle of the body behaving as an integrated unit is evident in the research throughout osteopathic history. The same question faces osteopathic philosophy, theory, and practice that faces the chicken and the egg, "which came first? " The introduction of rhe osteopathic lesion (somatic dysfunction) and treatment of the whole person initiated Smith's use of the skiagraph (a forerunner to the radiograph) to study circulation (1). Still's research focused on reflex mechanisms contributing to the integration of the somatic system functions with other body structures and functions. Osteopathic philosophy and principles assume that somatic dysfunction or its components (segmenral, cranial, appendicular, and visceral) have a response to treatment rhar involves the whole person. This assumption is difficult to support with some scientific methods, although they can provide detailed explanations. Structural and functional mechanisms are altered at multiple sites during progression from an acute to a chronic condition, and only longitudinal studies provide clara on changes occurring during the course. The acceptance in both clinical and basic sciences that the body behaves as an integrated unit to the presence of somatic dysfunction or the body's response to its treatment needs longitudinal, evidence-based support.

BACKGROUND FOR A RESEARCH MODEL Models of a system to be studied increase the efficiency of research. Advancement of osteopathic health care is supported by documenting patients' health outcomes obtained in epidemiologic studies; mechanisms of integration are supported by basic or clinical research contributions to knowledge. The earliest clinical explanations for manipulative treatment of somatic dysfunction (initially identified as an osteopathic lesion) attributed favorable responses to the whole-body response. Satisfied osteopathic patients in the 19th and 20th century supported the founding and early development of rhe osteopathic profession. Their experience with osteopathic treatment influ-

enced state legislatures to approve establishment of osteopathic schools, colleges, and universities, and acceptance of osteopathic physicians into government positions. It is a continuing challenge to explain the patients' change in health status as an outcome of osteopathic health care. Patients, students admitted to osteopathic schools of medicine, and state or federal government positions manned by osteopath ic medical graduates expect advances in osteopathic theory and practice to keep the profession abreast of scientific knowledge. In 1892, The American School of Osteopathy (now the Kirksville College of Osteopathic Medicine or KCOM) included William Smith, a physiologist, in irs faculty. Smith added his discipline to the basic science curriculum . His repmation in using xerography to investigate circulation is widely recognized . The A. T. Srill Research Institute and early osteopathic faculty researchers supported the osteopathic somato-somatic and viscerosomatic reflex concepts by application of neurophysiologic information. Beginning in 1919, Sutherland published his search for information and an anatomic and physiologic explanation for the effects of cranial manipulative treatment. In the middle of the 20th century, Denslow and the KCOM faculty made major basic science contributions to osteopathic theory and concepts in reflexive and behavior research. Subsequent osteopathic research has strengthened the knowledge base created by these early conrributors. However, evidence on the course of somatic dysfunction remains a continuing challenge. Development of a model for research efforts is proposed to focus and faci litate research that advances osteopathic theory and practice.

DEVELOPMENT OF A MODEL Some clinical and most basic science research on somatic dysfunction provides cross-sectional data on single and multiple interactions of a stimulus (environmental change), the body's reactions to the dysfunction, and its response to imervenrions (experimental variables). Outcome variables are observed or measured in molecular, cellu lar, or organ systems, or as behavior. In vivo research in man or animals that uses longitudinal rather than cross-sectional studies identifies a sequence of responses to a stimulus. The stimulus site remains constant but may develop, as indicated by local changes accompanying a stimulus. Effects of the stimulus on other body sires involve observed or measured responses to multiple molecular, cellular," organ , and systemic reactions. Reactions to stress are observed or measured as changed function, behavior, or structure. Cannon's triple

Introduction response in the skin is an example of a stressor (change in environment) that elicits local changes in skin. The stressor and associated local re.sponses create neural and humoral signals that initiate reactions at remote sites. Selye's syndrome (2), produced by diverse noxious reactions, is the beginning of extensive research, including many theories and applications to health care. This reference provides information to develop an osteopathic model for research on the osteopathic principle that humans behave as an integra red un ir.

A PROPOSED MODEL FOR RESEARCH TO ADVANCE OSTEOPATHIC THEORY AND PRACTICE An osteopathic model similar to the Selye model can be used to investigate osteopathic philosophy, theory, and practice. Immediate success is likely to require years of effort, but less than the seventy-five years thus far devoted to early physiologic stress models. The suggested model to advance osteopathic theory assumes that observations of a total body response include: • Internal cr external environmental stress that initiates reactions at remote sites and that can be reliably observed or measured. • A reliable course description for the stimulus and integrated responses, which also requires standard, clinically observed descriptions and guidelines to enable data from collaborating scientists or other research reports to be pooled. • The philosophy that the body behaves as an integrated unit requires knowledge of the role of somatic dysfunction as a stimulus and research on the sequence of responses beginning with the acute changes and continuing in subsequent reactions.

CON SIDERATIONS RELATING TO THE PROPOSED MODEL The nature of a stimulus is an important factor. Is the site and reaction stable and unchanging? Some stressors, Cannon triple response in the skin to a nociceptive stimulus, for example, release neural and humoral signals that target multiple structures and functions distributed throughout the body. However, local changes in skin characterize a "triple response" that follows the response to the noxious insult. A cutaneous red reaction, axon reflex, and local vascular changes appear almost instantaneously and occur as local responses. Neural and humoral signals generated during these local changes initiate the neural reflexive and endocrine or humoral controlled behavioral and metabolic responses. Whether the whole-body response will undergo the same or similar course to Selye's stress response depends on the validity of assuming similarity between the two models. Published information on disturbances in any system, organ, cell, or molecular reaction to a known stressor provides information for formulating a model and research design. Progress from Cannon's and Selye's stressor and stress reactions to our current knowledge of stress provides a large body of evidence to support integrated adaptation to stress. It will be a challenge to initiate and develop a similar body of evidence-

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based knowledge. Acceptance of evidence-based support for the clinical aspects may require answers to questions about somatic dysfunction. When is somatic dysfunction a sign that the stressor is directly related to the somatic dysfunction? When is somatic dysfunction a response stressor initiated by some other internal or external environmental change? Are the whole-body responses to interventions used for treating the somatic dysfunction different for the dysfunction's direct and indirect relationship to the stressor?

AUTHORS AND THEMES In the following chapters, the authors discuss the history of osteopathic medical research and introduce reviews of methods of basic and clinical research, discussing how they specifically relate to current and future osteopathic physicians. Historic and methodological information is important to create a sound research plan, protocol, and subsequent publication. Each of the authors in this section reviews research methods that are practical and applicable to understanding the types of osteopathic research that has been done in the past and what challenges lie ahead. The details of what hypotheses, methods, and types of analyses are needed for a given project may change frequently, so knowledgeable consultants assist researchers in keeping current and timely. Five chapters in this section are devoted to clinical investigation. These five chapters review and discuss fundamental principals of research and offer ways that each type of research has relevance to osteopathic medicine. Heath and Gevitz review somatic dysfunction and relevant osteopathic research efforts over the last 20 years. Patterson explains the basic science approach to designing and implementing research projects that have been used to try to explain the theoretical basis for osteopathic medicine. Snow, Licciardone, and Gamber have written a timely chapter dealing with outcomes research, which is designed to study clinical end results of a given therapy. The authors review the existing data to assess the efficacy of osteopathic manipulative therapy in one specific entity-low back pain. Rubin introduces the concepts of clinical research in the context of pharmaceutical research. Good clinical practice guidelines are explained as a method to show osteopathic physicians the methods used to produce rigorous research studies. Foresman, D'Alonzo, and Jerome have written a chapter dealing with biobehavioral research in osteopathic medicine-research involving mechanisms of disease modification thorough mind-body interaction. Lastly, Patterson has predictions for future developments and challenges facing osteopathic medical research. His long career in osteopathic medical research uniquely positions him to note that the future of the profession is linked to research advances.

CONCLUSION The osteopathic profession has embraced research from the beginning of its existence. Basic, clinical, biobehavioral, and outcomes research provide evidence regarding the nature and importance of osteopathic medicine to health. Research must involve all parts of

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the osteopathic health care system. Therefore, practicing osteopathic physicians, clinical faculty members at osteopathic medical schools, and basic and clinical researchers all share the responsibility to investigate the unique aspects of osteopathic medicine. Clinical research must adhere to accepted practice, including the ethical standards regarding the protection of research subjects as governed by an institutional review board. Therefore, osteopathic physicians must be knowledgeable of these requirements and adhere to them. The future of osteopathic medical research has never been brighter. Researchers who read this section will note great detail paid to the role of research design, methods, and ideas, as well as the use of statistics to analyze data. These areas are important whether one is discussing basic research, outcome research,

clinical pharmaceutical research, or biobehavioral research. In investigating osteopathic theory and practice, it is critical ro develop sound research protocols. Research collaboration among all interested parties serves to promote advances in osteopathic medicine based on a solid research framework.

REFERENCES 1. Co le WV. Hisrorical basis for osreopathic rheory and practice. In: Northrup GW, ed. Osteopathic Research: Growth and Development. Chicago, IL: American Osteopathic Association; 1987. 2. Selye H. The general adaptive syndrome and the diseases of adaptation . J Clin Endocrinol Metab. 1946;6:117-173.

FOUNDATIONS FOR OSTEOPATHIC MEDICAL RESEARCH MICHAEL M. PATTERSON

KEY CONCEPTS • The forces that have shaped the research programs of the osteopathic profession • What constitutes osteopathic research? • Who does research in the osteopathic profession? • Ethical considerations in doing osteopathic research in animals and humans • Mechanisms underlying osteopathic concepts and their research basis • Types of research design and their uses • Considerations in osteopathic clinical research • The question being asked is the most important part of osteopathic research • Characteristics of good osteopathic clinical research • Potential pitfalls in osteopathic research

DEVELOPMENT OF RESEARCH IN THE OSTEOPATHIC MEDICAL PROFESSION

Early Research (1874 to 1939) Research began in the osteopathic profession before the formal in ception of rhe profession itself. A. T. Srill was a true researcher, practicing ob ervation, questioning his observations, trying new ways of thinking, and refining his hypotheses about his practice. He did nor do what would now be regarded as organized research, bur in facr, he did research ar the basic level in a way rhar is still ar rhe basis of almost all medical research. He observed, srudied, questioned, and constructed testable hypotheses. The ideas and philosophy that have become rhe osreoparhic profession and rhar undergird much of rhe research in rhe profession today came our of his questioning. Soon after Srill founded the first school in Kirksville in 1892, his students began ro do formal research inro the concepts he espoused. Ar first, these research endeavors were mainly devoted ro inquiries into rhe anomalies that became known as the "osteopathic lesion," which is now called somatic dysfunction. Skiagraphy, a crude form of x-ray, was used before 1900 ro try ro find

evidence of rhe structural abnormalities attributed ro the osteopathic lesion. Soon after, animal models were used ro determine rhe acwal physiologic effects of rhe palparory findings rhar made up the "lesion" (1). In 1906, the American Osteopathic Association (AOA) formed a research center, rheA. T. Still Postgraduate College of Osteopathy, and called for donations ro fund ir. The name was changed ro the A. T. Still Research Institute in 1909, and about $16,000 was raised ro support its efforts. Ir was nor until about 1913, when the Institute opened in a dedicated building in Chicago, that research under Wilborn]. Deason began. Funding continued robe a problem, even after Louisa Burns was appointed Director, and the Institute struggled ro meet its modest needs, despite calls from the AOA for more research and support. Over the ensuing years, Burns produced a body of work investigating the effects of spinal "lesions" in a rabbit model. The results ofher studies indicated that artificially produced strains of specific vertebral segments produced a somewhat reproducible constellation of changes in function of organs and tissues innervated from rhe area of strain. These changes were later substanriared by Wilbur Cole using various neural stains (2) . Burns published four books (3-6), a collected work (7), and several reports from the lnsrirute that, unfortunately, are nor widely available today but that contain much of value ro rhe modern researcher. he continued her work until the early 1950s. During the first third of the 1900s, research in rhe profession was encouraged at several osteopathic schools (8). This research included studies on basic neural and physiologic mechanisms underlying somatic dysfunction and the effects of osteopathic treatment on symptoms and immune function. Much of this research would on ly be considered suggestive by roday's standards, but formed the basis for lines of study produced later within rhe profession.

The Second Period of Research (1940 to 1969) In 1938, J. S. Denslow began a path of inquiry rhat would lead ro a program of research that literally defined rhe modern research era in the profession. He became convinced rhat ro bring increased credibility ro the profession, research based on the latest research standards and published in highly recognized journals would have ro be done. This research would have to show the basic mechanisms underlying rhe osteopathic lesion (9). He

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received training from internationally known biomedical scientists, including Ralph Gerard, and began a program of studies aimed at understanding the characteristics of muscle activity in relation ro palparory diagnosis. Joined by I. M. Korr in 1945, and by several others at Kirksville, they expounded the concept of the facilitated segmenr (10- 12). This conceptual framework was to dominate much of the osteopathic thinking about the basis for palpation and treatment to the present day. During the 1950s and 1960s, the research base of the profession did not expand gready. The Bureau of Research, founded by the AOA in 1939 to fund research projects, supported fledgling efforts at several schools, bur except for the Denslow/Korr project, no research efforts of a full project nature were begun. Several studies, such as those on joint mechanics (e.g., Beckwith), were published (13), bur in general, research in the profession progressed slowly during this rime. After World War II, the profession was busy training a flood of returning soldiers and adjusting ro the new post-war world. However, in the late 1950s, a threat ro the life ro the profession emerged. Culminating in the merger of the California Osteopathic and Medical Associations in 1962, the danger that the profession would be eradicated by takeover was very real. The years from 1960 ro 1969 were years of uncertainty about the profession's future. In 1969, a new osteopathic school was founded in Pontiac, Michigan, as the first of 10 new schools founded between 1969 and 1980. The threat of death by merger was over, and the profession began a period of expansion and organizational prosperity unparalleled in irs history. Unfortunately, it was during this period of uncertainty and threat that the profession missed our on the tremendous expansion of biomedical research facilities and effort that resulted from World War II. The expansion of the National Institutes of Health (NIH), with its emphasis on biomedical research and irs funding of new laborarories and programs, fueled an explosive growth of the biomedical research community in the United States. The osteopathic profession was unable to rake advantage of this early expansion. By the rime new schools with university bases were established in the 1970s, this first wave of biomedical research expansion was over.

The Third Period of Research (1970 to 2000) With the founding of new schools and expans ion of the five original schools remaining after the California merger (Kirksville, Chicago, Kansas City, Philadelphia, and Des Moines), the profession finally achieved a base for producing increased amounts of research. The schools began ro hire more research-trained faculty, and the political arms of the profession began to more actively encourage research endeavors. The AOA began actively promoting research through the Bureau of Research and the annual Research Conference. Awards were established to honor research productivity, such as the Louisa Burns Award (1969), the Gurensohn/Denslow Award (1984), and the I. M. Korr Award (1999). Swdent research efforts were recognized as viral and began to be encouraged more actively, for example, with the establ ishment of the Burnett Osteopathic Student Research Award. More importandy, the basis of research programs was established at many of the new schools and rejuvenated at some of the original schools,

especially at Kirksville, where, beginning in 1970, Denslow and Korr oversaw the hiring of facu lty specifically for research efforrs. The Michigan State University College of Osteopathic Medicine formed a Department of Biomechanics specifically devoted to osteopathic research. Many of the other schools began to provide funds from their operating budgets to seed research programs and encouraged faculty and students to engage in research projects. In the early 1970s, NIH funding was awarded for the first time in many years for research in an osteopathic school. In the years of the 1970s and 1980s, funding for research at osteopathic instiwrions from sources outside the profession itself grew tremendously, with many NIH and other grants being awarded. With encouragemenr from the Bureau of Research and individual schools, several osteopathic students undertook joint D.O.-Ph.D. studies designed to further careers as clinician researchers. Many of these students have entered successful research appointments at osteopathic or other institutions. Also in the decade of the 1990s, research requirements were instituted in many osteopathic residency programs. These requirements were aimed at familiarizing the residents with research methods and thinking, and have been expanding into some of the Osteopathic Postgraduate Training Institutes (OPTis) within the profession. Thus, at the end of the 20th century, the amount of research being accomplished in the osteopathic profession was at an alltime high. However, a step was missing.

The Fourth Period of Research (2001 onward) The research efforts in the profession by 2000 were both at an all-time high and increasing rapidly as research efforrs at schools and at hospitals reached maturity and gained recognition. However, the profession lacked another element that had characterized many research efforts sponsored by the NIH. In the 1980s and 1990s, the NIH had sponsored a series of centers of excellence as foci for directed research efforts around the nation. The research efforts of the osteopathic profession had not yet matured sufficiendy to support such an endeavor. By about 1997, several organizations in the profession, including the Louisa Burns Research Committee of the American Academy of Osteopathy (AAO), the AOA Bureau of Research, the American Association of Colleges of Osteopathic Medicine, and others were beginning to discuss the formation of such a center. By 1999, it had become evident that NIH funding for such a center would probably not be available and that the profession would have ro commit funds from its own resources. By 2000, funds had been secured for this enterprise, and requests for a center were sent ro the .Osteoparhic Medical Schools. Five schools responded with plans for developing a center for osteopathic research. The award, announced at the AOA Research Conference in October 2001 , went ro the College of Osteopathic Medicine at the University of North Texas Health Science Center. The Texas school had been building its research infrastructure for several years and had a solid research record. The development of a center sponsored by the profession itself and devoted to research in manipulative medicine is the logical next step in the development of a mature ~esearch enterprise in the osteopathic profession. This center is expected ro become a coordinating and centralizing force in developing

74. Foundations for Osteopathic MedicaL Research mature research efforrs into rhe fundamental questions faci ng rhe profession. Ir should help arrracr natio nal fund ing and foster collaqorarion within the osteopathic research community. Thus, the next phase of research development in the osteopathic profession has begun. This chapter wi ll provide information on the basics for conceptualizing resea rch on topics germane to osteopathic medicine and some of the challenges faced by investigato rs designing research in these topics.

WHAT IS OSTEOPATHIC RESEARCH AND WHO DOES IT? A definition for osteopathic research has eluded politicians and osteopathic researchers since irs inception. Why would this question be asked? It is often asked in rega rd to whether a research project should be funded by an osteopathic fund ing agency, such as the AOA Bureau of Research. It may be asked to determi ne whether research should be included in osteopathic publications. It can be a condition for whether students are to be included in a research project. Whether research is "osteopathic" or nor has both political and practical implications. In this regard, several definitions of osteopathic research have been pur forward at vanous nmes.

Research Under Osteopathic Auspices Perhaps the broadest definition is that osteopathic research is any research done under osteopathic ausp ices. T his defi nition implies that any research, basic or clinical, no marrer what the subject matter, is osteopathic when performed at an osteopathic institution or under the control of an osteopathic institution. Under this rubric, research on any topic could be considered osteopathic. This is obviously too broad.

Research on Topics of Special Interest to the Profession Some topics in biomed icine have historically been of greater interest to the osteopathic profession than others. For example, the actions of the nervous system in controlling various auto nomic functions and the effects of man ipulative treatment on im mune function have been topics of investigation for many years. At rimes, efforts have been made to define lists of such topics as the ones that define osteopathic research. The problem here is that new avenues of inquiry are constantly being fo und that apply to the clinical and theoretical topics of the profession, and no one list can be devised that will cover or predict them all.

Research on Osteopathic Manipulative Treatment Definitions of osteopath ic research have at times been restricted to those studies attempting to determine efficacy or value of osteopathic treatment. This approach leaves out the entire area of mechanism inquiry that seeks to explain the basis of treatment efficacy. Obviously, this is too narrow a view.

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Any research into biologic mechanisms, because osteopathy is holistic, therefore encompasses everything Although ecumenical, this is not a definition because it says nothing. It would assume that there are no basic theoretical underpinnings to the osteopathic philosophy or practice that have or should be identified, thus that there is no definition of osteopath ic medicine. If this were so, there would be little basis for the profession to exist.

A New Definition of Osteopathic Research Attempts to define a priori the scope or type of research that is considered osteopathic seem doomed to failure . However, perhaps there is one way to determine whether research is osteopathic: To require the investigator to explain how the hypothesis and expected find ings of their research would be relevant to the theory, mechanisms, or practice of osteopathic medicine. That is, investigators must have sufficient understanding of the basic principles of osteopathic medicine to explain how rhe interpretation of their data would impact osteopathic medicine. They must know enough about the perspectives of the profession, its theoretical basis, and/or its clinical practice to coherently build bridges from their studies to the profession. If they cannot do that, then, although their data may be interesting, important, and even cutting edge, it is not osteopathic. Perhaps someone else can bui ld those bridges, but until that happens, it is not osteopathic research. It is of great value to have physician researchers and PhD researchers who expend the time and intell ectual energy to understan d the profession's theoretical and clinical perspectives, because the res ults of any study must be interpreted within some context. If the context is that of osteopathic medicine, the data are much more likely to be correctly used in understanding the profession's basic questions. Th us, anyone can do osteopathic research, provided that they make the intellectual effort to become fami liar with the profession's clinical, theoretical, and/or historical experience. Otherwise, they are doing interesting research that must be interpreted by others to be useful to the osteopathic profession. The burden of proof that research is osteopathic lies with the investigator.

HOW DO RESEARCHERS BECOME AWARE OF THE THEORY OR CLINICAL ASPECTS OF THE PROFESSION? Although trained osteopathic physicians can be expected to be familiar with the background necessary to relate research findings to their profession, such is not the case with many bas ic scientists (including many currently at osteopathic institutions) or researchers outside the profess ion. Cultivating basic scientists who understand the clinical tenets of the profession and training basic scientists to gain such understanding pays off in increased theory bui lding and data interpretation. One excellent way to begi n the process of understanding osteopathic principles and practice is to ask PhD and other non-DO faculty to attend osteopathic manipulative treatment (OMT) courses.

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VI!!. Basic and Clinical Research for Osteopathic Theory and Practice

Experience in learning and receiving manipulative treatment is also an enlightening experience. However, researchers are trained to investi ga te new areas of knowledge and to ask questions of those areas. Basic scientists and others within the profession can easily access books and journals relevant to their osteopathic understanding. This book is a good start in that journey. A second source is th e journal ofthe American Osteopathic Association, where revi ews, original research articles, and case stud ies are available. Other sources, such as A. T. Still's Autobiography (14) or his Osteopathy Research and Practice (15) , are useful. Other books, such as Northup's books on the profess ion ( 16) and research (2), are useful in helping the basic scientist understand the profession . As much as the resea rcher must be expected to find and read materials pertinent to his or her understanding, so must those knowl edgeabl e in the profession be willing to help promote the necessary understanding. Osteopathic physicians and students must be willing to discuss their beliefs and clinical observations with often skeptical scienti sts. The experience of the 1989 AAO symposium (17) is illustrative of this point. Several internationally known basic scientists were assembled for 2 days of discussion prior to the symposium itself. They question ed the attending osteopathic phys icians about th e experiences of the profession , and co nsented to having osteopathic manipulative treatment. Rarl1er than being antagonistic to the largely anecdotal clinical observati ons, th ey were uniformly supportive and excited by them. Several altered their prepared talks to reAect their new understanding and have maintained active contact with the profession since. In fact, one is actively training DO students in his laboratories. Active and open communication about ideas most often leads to excitin g opportunities. Thus, the development of basic scientists who understand the osteopathic profession is a two-way street. Although much has been acco mplished in this area, the cadre of train ed clini cal and bas ic science investigators must be expanded to those who understand the principles and clinical experi ences of osteopathy so that they can frame their research questions in the light of osteopathic clinical experience and theory. Without this understanding, data will not be examined from the perspective of osteopathic treatment and insight.

ETHICAL CONSIDERATIONS IN OSTEOPATHIC RESEARCH

Human Subjects Protection Since the end of World War II, th ere has been a growing understanding of the problems associated with the ethical considerations of research on both human and animal subjects. The horrible experiments performed by phys icians on prisoners in the Nazi co ncentration camps sparked reforms and regulations to control human medical experimentation. Coming out of the Nuremberg Trials and codified in th e 1964 D eclaration of Helsinki , these regulations h ave been the subject of continuing review, refinem ent, and discussion since then (18-20). The researcher who co ntemplates doing research in osteopathic topics must be aware of and abide by the current human subject regulations. Not only is this the law, but it is the moral and just thing to do. In fact, no reputabl e journal will publish results of a human study without evid ence that applicable human subject guidelines have been scrupulou sly fo llowed.

The novice investigator must be familiar with not only the principles of ethical treatment of subjects, but also with the procedures in effect in the institution where rl1e research will be done. In the event that a private physician wishes to co nduct human subject research in a private office, the research must first be approved by an appropriate human subjects review board , usuall y known as the institutional revi ew board (IRB). The TRB is a governmentally sanctioned body whose members are appointed by the institutional executive in charge of research and the President or CEO of the institution , and must include individuals with specific interests, including a person who has no other affi liation with the institution .

INSTITUTIONAL REVIEW BOARD AUTH ORITY The IRB has the authority to deny or approve any research proposal involving human subjects. The main purpose of the IRB is to protect th e safety of th e subjects. It can stop ongoing research if it deems protection not suffi cient or un covers problems in the research . When applications for research are submitted to the IRB , the application can receive expedited review if certain conditions are met, such as that th e research uses only data collected in the normal course of office practice and that are not identified with a patient. However, it is not up to the investigator to determin e whether the research is exempt, can have expedited review, or must und ergo full review. Case reports and retrospective revi ews of cases (see discussion below) see n in the routine office practice do not gene rally need IRB approval unless the patient is identified or if written permission is given prior to release of any inform ation.

MAJOR INSTITUTIONAL REVIEW BOARD CONSIDERATIONS The major factors in human subj ect resea rch include: Informed consent Confidentiality Risk Absence of coercion One of the cornerstones of human subject protection is the principle of informed consent. This idea holds that the subject be informed of the study fully and co mpletely and be ab le to give free consent to participation. If the subject be a minor, incapable of giving consent due to mental or other disabili ty, or a prisoner, special and specific protections are specified. The principle of subject confidentiality is another viral concern. The subject's confidentiality is to be protected and not divulged without the subject's written consent. Thus, medi cal and research data are considered private matters when lin ked to an identifiable subject. Data are usually coded in such a way that they cannot be linked to a particular pati ent and great care must be taken that no such link can be inferred. Risk to the patient is another factor in human research. Risk to a patient runs from essentia.lly nonexistent to grave. If the risk is anything but incidental , the subject must be fully informed of that risk and have every option to decline parti cipation. The

74. Foundations for Osteopathic Medical Research

risk must also be justified by potential gain, perhaps not to the individual subject, but to the field. This assessment is difficult to make,. and the investigator must therefore justify the study well. Absence of coercion is a complex topic that is often debated in study design. Is providing a monetary incentive to a subject for time taken by the study coercion? Is the investigator using force of personality or doctor-patient relationship to coerce the subject to enter the study? These questions are difficult to quantify, and the committee and investigator must consider them carefully. IRBs are usually in existence in osteopathic medical schools and in many hospitals. Each IRB is allowed operating discretion within established NIH guidelines as to how it reviews protocols. Some IRBs meet on a regular basis and others are on call. The potential investigator is responsible for finding the protocols used by the appropriate IRB and fully following these regulations. It cannot be overemphasized how important it is to be cognizant of current guidelines for human subject protection and to fully adhere to them . For current and full information, including downloadable human subjects research guidelines, go the NIH web site at: http://ohsr.od.nih.gov.

Ani mal Protection No less important in research on human subjects is the protection of subjects in animal research . As is evident from the media, animal rights have become a volatile issue in much of the world. Some of the emotion surrounding animal rights obviously stems from the fact that animals cannot give informed consent or judge risk in a study. In addition, by its nature, animal research often ends in the subject's death. For these and other reasons, some groups use violence to attempt to stop animal research. Not unlike human subject protection, a well-defined, protective structure has been implemented by the NIH and other groups, such as the American Association for Assessment and Accreditation of Laboratory Animal Care (AAALAC), have promulgated guidelines and rules for the proper use of animals in research studies. The Animal Care and Use Committee (ACUC), a governmentally mandated body enforces these rules at research institutions. Like the IRB, the ACUC has the authority to shut down research not in compliance with applicable regulations and must approve all animal research prior to its start. The osteopathic researcher who wishes to use animals in research must first successfully seekACUC approval. As with the IRB, each ACUC has latitude in its procedures about which the investigator must be informed. Again, as with human research, the investigator must be meticulous in following animal care and use guidelines: first and foremost, for moral and ethical reasons but also because humanely treated and well cared for animal subjects provide more reliable information. For more information on animal care and use guidelines, visit the NIH Office of Animal Care and Use site at http://oacu.od. nih.gov/. Another useful site is the American Association for Laboratory Animal Science site at www.aalas.orgor the AAALAC site at www.aaalac.org.

Applying for Institutional Review Board or An imal Care and Use Committee Approval The process for applying for research approval for either human or animal research is determined by each committee. Some commit-

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tees meet monthly or more often; others meet on call. However, at the least, each protocol submitted for IRB or ACUC approval will have to contain the following elements: Background literature review Justification for the project Hypothesis to be tested Complete description of the methods to be used For human research: • Informed consent form • Confidentiality statements • How subjects will be obtained and paid for service For animal research: • Evidence that animals will be legally obtained and humanely housed • Evidence that precautions will be taken to minimize any necessary pain or suffering • Evidence that other alternatives to animal use are not available Data to be collected Statistical methods for analysis Any pilot data available These items represent a fair amount of work that must be done prior to submitting a protocol for review. It also means that the investigator will find it necessary to think through the studies prior to getting approval. The appropriate approvals are also necessary before funds are awarded for the proposed research from government agencies.

TYPES OF RESEARCH IN OSTEOPATHIC MEDICINE Basic Science Within the purview of osteopathic research, there are several valid types of studies. Perhaps the most basic is research that flows from basic science studies. This research includes studies designed to define the basic functions of the body and mind, and explain how they interact with the environment. These studies are mainstream biomedical research. An increased understanding of the human organism and its function is invaluable in validating osteopathic practice. The osteopathic profession must therefore nurture the basic sciences.

Basic Research in Other Institutions and Professions Basic science has been performed for many years in most biomedical facilities and research institutes. Most basic research relevant to the osteopathic profession is done not in the educational institutions of the profession but in other biomedical settings. The amount of research that can be supported directly by the profession is small compared with the amount of such research performed around the world. The total amount of funding available from within the osteopathic profession for support of its research programs is less per year than the annual budgets of many individual laboratories outside the profession. This suggests two things. First, maximal use must be made of data from laboratories outside the profession. Osteopathic researchers and clinicians

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V/!1. Basic and Clinical Research for Osteopathic Theory and Practice

must cultivate interactions with biochemical researchers at other institutio ns who can supply data and interpretations. Second , the limited resources of the profess ion must be put into research endeavors rhar provide the greatest rerum in explaining osteopathic experience and theory. This req uires, as stated above, that investigators within the osteopathic profession understand the uniqu e and defi ning concepts of osteopathy within which to interpret their findings. Without this understanding, the investigato r is un ab le to interpret the findin gs in ways that are useful to rhe profession, and a large parr of the research investment is lost. T he use of data from laborato ries outside the profession is certai nl y a ve ry useful and fruitful endeavor. We have made use of this mechanism in proposing mechanisms for the facilitated segment (2 1). However, care must be taken in using data generated in studi es not specifically designed to answer the question to which the d ata are now being applied . Unless the limitations and specifi cs of the data are well known , implications can easily be made that are beyond the scope of the data and hence potentially mi sleading. It is important to realize these limitations, but to use d ata an d sources from outside the profession whenever possible. Such was the case when the AAO commissioned two internatio nal symposia held in 1989 and 1992, which resulted in proceedings publications (1 7,22) that have been very useful in info rmin g the profess ion of possible mechanisms for clinical phenomena and the results of manipulati ve treatment.

Integrative Model Building Integrating Basic Science and Clinica l Observation A seco nd type of research activity necessary within rhe professio n is the integration of basic science knowledge and clinical observatio n. This endeavor is extremely valuable and potentially dangerous. A recent article by Van Buskirk (23) illustrates such research. Tn this article, Van Buskirk builds a theoretical model of somatic dysfunction based on nociceptive input. He marshals an impressive array of basic science data and synthesizes it in a unique way from his clinical understand ings and observations. T he res ult is a well-grounded look at one of the central concepts of rhe osteopathic philosophy of health and disease. This is rhe valuable aspect of the article. T he dangerous part is that the model will be taken as fact. Van Buskirk goes to great lengths to point out that the model seems to be expl anatory but still needs to be subjected to rigoro us research verification and clinical observation before ir can be accepted as proven. Unfortunately, the pioneering models rhar came o ur of rhe resea rch ofKorr and Denslow (11,24) suffered from being taken as factual expl anation rather than as models in need of experimental verification. Once a model has been accepted as truth, the perceived need for further research or theory is impeded o r stopped , and the model beco mes accepted as truth. T hi s ca n be disastrous if the model is then shown to be erroneous o r incompl ete because there are then no alternatives to take irs place. Integrative model building provides much needed direction for both bas ic and clinical research but must not be taken at face val ue without verification and experimental testing. T hus, the osteopathic professio n must continually examine irs theo ri es and subject its ex pl anatio ns to close scrutiny. The vast

body of clinical evidence demonstrates that the precepts of the osteopathic profession are sound. However, often the profession embraces explanations that are not solidly research based. T he result is theory taken for fact with further exploration of alternative theory or factual bas is effectively stymied.

Synthesis and Meta-Analysis Research Two types of scholarly activities that can be of immense benefit to any area are rhe synthesis review and the meta-analys is. Synthesis papers are efforts to rev iew and critical ly analyze an area or field of study. In this type of work, the author wo uld select a top ic area for analysis and review aU ava ilab le work in that area. Although the review is in itself important, a synthes is then analyzes the work that has been done and attempts to find common th emes, areas of agreement or disagreement, and then builds a hypothesis as to what the accumulated knowledge of the area is saying. T his type of paper can often point to why seeming co ntradi cti ons between studies exist, what studies should be done to fin alize questions in the field, and so forth . Early in my career, we did such a synthes is for the fi eld of spinal · cord learnin g (25). T he insights from that activity directed spinal cord plasticity research for many yearsnor only in our laboratories, but in other labo rato ries (26). Often, a good synthesis of an area will o pen rhe area for mo re intensive study and can be an impetus for real advances in an area that was seemingly uninteresting or filled with co nflicting data. The meta-analysis is another useful tool for research. T his analysis attempts to accumu late all studies in a field rhar are deemed sufficiently ri goro us and determin e the combined power of the res ults. In this way, by statistically combin ing smal ler studies that are not particularl y convincing by themselves, it is often possible to achieve sufficient statistical or analytical power to have confidence in the phenomenon being in ves tigated. Such an analys is was done on the area of spinal manipulation for low back pain and resulted in acceptance of that modali ty as effective treatment for acute low back pain (27). An analys is of spi nal palpatory procedure validity and reliability is currentl y under way at the Center for Compl imentary and Altern ative Medi cine at the Un iversity of California Irvine College of Medi cin e, and is sponsored by the trust fund acquired by that school when the Cal iforni a Coll ege of Osteopathic Medicine beca me rhe University of California Irvine College of Medicine in 1962. More info rm ation on procedures of meta-analysis ca n be found in many statistical texts (28).

Qualitative Studies in Osteopathy Valuable information can often be ga thered by means of surveys and interviews. Such studies, although nor experimental, are often the on ly way to find trends in po pulations, practice distributions, or to gather the collected thought of experts in a field. Often , surveys seem simple and easy to perform. T he investigator must only write down a few questions o n a topic and send them our to some selected individuals and wait for the returns. Such simplicity is illusory. Good surveys must be well planned and executed. The topic must be carefully framed and the questions prepared with precision . Pitfalls in rhe use of surveys include poorly Framed questions, problems in determining to whom the survey shou ld be sent, poor return rates, and o thers (28). Prior to instituting a

74. Foundations for Osteopathic Medical Research su rvey, an invest igato r must co nsult texts and/or experts in survey des ign and procedure. Within the osteopathic profession , Johnso n and Kurtz have performed several surveys addressing such i~s u es as srudent interests and the use of manipulative treatment (29-3 1). These studies have provided a baseline for the use of osteopathic manipu lation in the profession and are invaluab le in charting future direction within th e profession . T hese surveys are excellent examples of well-done and analyzed survey srudies. Another instrument rhat can provide valuable information is the collection and analys is of ex pert interviews or wrirings of often long-departed authors. T hese methods also often seem deceptively imple. ln fact, as with surveys, interviews with experts require extensive preparation and careful planning. Both directed and open-en ded questions may be asked and answers recorded for late r transcription , or the expert may be asked to write on predetermined topics. In any event, the answers must be carefull y anal yzed for content and other information. The analysis of writings by departed authors ca n be valuab le in translating what may now seem to be arcane jargon into rerms understandable in today's terminology. For example, why d id Andrew Taylor Srill pur so much emphasis on rh e fasciae of the body? What did he mean by such re rms as "fluids of life?" To understand rhese ideas in rh e way in which Srill did, ir would be necessary to find rhe meaning of those terms in the late 1800s, as well as to look at rhe conrext in which he used them . Various means of content an alys is are ava ilable to help in such a task (32). Both interview analysis and writing analysis can be of grea t value to osteopathic understandin g.

Epidemiology and Outcomes Studies Ep idem iologic studies have nor been widely used in the osteopathic profession. It should be noted , however, that there are some ve ry important epidemiologic topics awaiting study. Because epidem iology refers to the study of patterns of health and disease and what influences these patterns, those influences on hea lth and loss of health that are of particular interest to osteopathic medi ci ne sho uld be subjected to such studies. One of the most important such study would be the incidence and natural history of so matic dysfun ction in normal populations and various subpopulations with defined illn ess. As with most studies, epidemiologic studies of rhis entity would require careful planning and executio n. Howeve r, ir could reveal very important informatio n on rhe poremial uses for manipulati ve rrearment modalities. T he in te rested investigato r can find more inform atio n in such references as Medical Epidemiology (33). O utco me studies are a very important type of research that bridges borh ep idemiology and at times, experimemal studies. In the usual such study, outcome measures are taken or reviewed for patient populations, and the outcomes of one type of treatment outco me, cost, patiem satisfaction , and so on are reported. O utcome studies usuall y require large patient popu lations to gain sufficient data to be meaningful.

Research on Manipulation As one of the key elements of osteopathic care, m an ipulative treatment should be the subj ect of increas ing an1ounts of research in

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the profession. In research aimed at investigating the usefulness of man ipulati ve treatment, there is much confusion abo ut proper research methodology. However, the researcher app roaching osteo pathic manipulatio n as an indepe ndem variable musr decide which of rh e following is to be evaluated: A rrearment or manipulative technique Osteopathic manipulative treatment (OMT) Osteopathic health care Depending on the aspect of manipulation to be studied, different experimental designs will be employed. Too often, investigators fail to distin guish berween these three entities and hence have difficul ty d etermining the co rrect experimental design for their study.

MANIPULATIVE TECHNIQUES One of the most illustrative studies of manipulative technique is the Irvine study, performed by Buerger and colleagues ar rhe School of Medicine at the Uni ve rsity of Califo rnia, Irvine, in the late 1970s and early 1980s (34,35). T hey wished to determine the effects of a single late ral recumbent roll (high-velocity/ lowamplitude thrust) on low back pain. T he stud y was elegantl y designed and executed , with a result that showed an immediate effect of the lateral recumbent roll on certa in measured variab les; simply positioning the patient for a lateral recumbent ro ll and omitting the thrust did not provide the same changes. After a few weeks, however, no differences berween the experi mental and control gro ups remain ed , probably the result of the nature of the presenting complaint, which has a natural history of relief in a few weeks. Nonetheless, an immedi ate effect of the thrust was seen. T he point missed by many readers was that rhe investigation was not of OMT bur of a treatment technique.

THE IRVINE STUDY COMPARED WITH CLINICAL TRIALS OF MEDICAL INTERVENTIONS In many ways, the Irvine study was similar to drug studi es. One specifi c manipulative technique was used on each parienr in the experimenral grou p (and nor in rhe conrrol group), rhe parienrs we re blinded to whether rhey received manipulation, and measurab le variables were used. In rhe ty pical drug erial, the specifi c effects of a certain chemi cal compou nd on rhe course of a specific ser of symptoms are srudied . T he des ign of the study co ntrols for orher facto rs rhar might cause a change in the outcome. Th is is a legitimate model for the study of a specifi c technique within manipu lative treatment. If the intent of the study is to determine rhe effect of a specific and repeatable manipulation, the research design shou ld emulate the design of a drug rrial, including attempts to blind th e patient to whether the technique was delivered . Such studies are useful in instances where there may be reaso n to suspect thar a specific manipulative technique would change a particular cond ition . Great care must be taken to control for: T he actual presenting comp laint Whether the patiem has knowledge of manipulation

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The actual delivery of the technique to make certain that it is given in the same way to each patient Such studies can be useful as long as it is recognized that the study's purpose is to evaluate the effect of a specific, single, or small group of physical manipulations on a specific condition. Another recent example of this design was published by Wells and colleagues (36), who looked at the effects of a set of standard manipulative techniques on gait parameters of patients with Parkinson disease. They found that the standardized techniques produced increased performance in various aspects of gait in these individuals. Such designs, performed correctly, give information on the effects of a technique on some aspect of patient function.

STUDIES OF MANIPULATIVE TREATMENT This type of research is used to study the effects of OMT on one or more measurable patient parameters. The research design and the goals are somewhat different from those used in technique studies. Korr (37) has elegantly reviewed these differences . Osteopathic theory and practice holds that the full treatment of an individual by an osteopathic physician entails an interaction berween the physician and the patient that is not static but dynamic, changing from treatment to treatment and instant to instant as the treatment progresses. The physician responds to the dynamic changes in the patient's function; the patient responds to the attitudes and touch of the physician. The treatment is not a prearranged set of movements and thrusts given to each patient, but an ongoing stimulus/response synergism berween the physician and patient, with the patient's response guiding the actions of the physician. In this case, the manipulation cannot be predetermined or prescribed by the research protocol but must "go with the flow" in response to the reactions of both physician and patient. The manipulative treatment is properly a "black box." The physician/patient interaction determines what manipulative treatment is performed. The physician is free to do what is deemed best for the interaction. Because one of the basic axioms of osteopathy is that each person responds differently to stress and treatment, this freedom of interaction cannot be removed from the physician without changing the research to a technique investigation. To investigate manipulative treatment rather than a manipulative technique, manipulative treatment must be used. The recent study on the effects of osteopathic treatment on low back pain by Andersson and colleagues (38), comparing manipulation with standard of care is a case in point. In this study, treating osteopathic physicians were allowed to use any manipulative techniques necessary for the patient. The study found that there were no differences in outcomes, but that the group treated with manipulation required less medication and physical therapy. In this study, unlike in a technique study, the physician chose the treatment that was indicated for the patient.

Technique Versus Manipulative Treatment Once the difference berween these rwo basic types of research on manipulation is realized, many of the other problems associated with investigating manipulation can be much more easily

resolved. Both types of research are valuable and valid. Research on techniques gives information on specific techniques; research on treatment gives information on what the osteopathic physician does in practice. Both are necessary and essential for the future of the profession . Their differences must be recognized and appreciated for appropriate studies to be designed.

Subtypes of Manipulative Treatment Within the general types of research on manipulative treatment, there can be several subtypes. One aims at the effect of manipulative treatment in general on some aspect of a disease or body function. This could be called the. nonspecific design. It is done to improve body function without identifying specific somatic dysfunction in patients with some clinical presenting complaint. The treating physician provides a general manipulative treatment without specifying areas of somatic dysfunction or specific areas to be addressed. By contrast, in specific treatment designs, the physician applies manipulative treatment to specific somatic dysfunction as defined by palpatory diagnosis and documented with such signs as asymmetric motion, tissue texture changes, and so forth. This type of treatment is designed to restore function or ameliorate functional difficulties and may or may not be related to actual presenting complaints (the patient may not be aware of some somatic dysfunction). In each of these study types, appropriate data on what is done must be collected, and specific measures of outcome must be made.

Effectiveness Studies A third type of study incorporates either of the first rwo: the effectiveness study, in which manipulative treatment is given to alleviate a specific presenting complaint. The patient is selected for a particular complaint, such as low back pain; the treating physician gives appropriate manipulative treatment. The effect of the treatment on the complaint (e.g., low back pain) is measured. This study type may or may not require the delineation of somatic dysfunction during treatment. Efficacy studies are the most usual in the literature because the measure of results is the most straightforward.

Functional Outcomes of Manipulative Treatment In the fourth design subtype, the functional outcome design, the effect of manipulative treatment on general physiologic function is assessed. In the philosophy of the osteopathic profession, the origin of disease is believed to be some loss of normal function in the body that then allows for the development of clinical symptoms. This type of study is accomplished on clinically disease-free subjects with somatic dysfunction who are addressed with specific treatment. Measures of outcome are such things as: Immune system function Tolerance to stress General activities of daily living assessments (in older subjects) Other measures of normal function that assess general health and function

74. Foundations for Osteopathic MedicaL Research Presumably, such studies would find increases in the funct ional abi li ty or capacity of treated subj ects.

TOTAL OSTEOPATHIC CARE STUDIES Another ge neral study design takes into acco unt the total care give n by the osteopathic phys ician ; it is not limited to manipulative treatment. T his study type assesses th e health statlls of patients given care by osteopathic physicians and presumably, but not necessaril y, includes manipulative treatment over the cou rse of ca re. Such smdies are longi tudinal or cross-sectional in nature and include as data such things as disease episodes and measures of total body function and activities of daily living. If the osteopathic philosophy of health is taken seriously, there is a heavy com po nent of preventive care that would include periodic manipul ative treatment to co rrect so matic dysfunction as it occurs. Such ca re should prevent a least some of the acute disease episodes seen in non manipulated subjects. A smdy of this kind wo uld be ex pensive and long-term, and could be approached in various ways. Research of this type could show whether the application of osteopathic principles to health care is differentiated from disease care. Practitioners applying total osteo pathic care to their patients wo uld be used to determin e if their outcomes in terms of patient health were different from physicians nor using osteopathic care. Obviously, there would be many potentially confoundin g facto rs that would have to be analyzed. Interesting results, such as cost/ benefit ratios, quality oflife issues, and others, could be ad dressed.

DES IGNING AND CONDUCTING OSTEOPATHIC RESEARCH Understanding the bas ics of what type of study is to be done is an important step in beginning osteopathic research. Realizing the importa nce of ethical co nsiderations and d ata confidentiality is vital. T he next steps in a research proj ect are also vital. These steps ca n be charac teri zed as follows: Observation Literature search Hypothesis building Stud y Design Data Collection Data Analysis Discussion of res ults Publication These steps are all necessary and important in the conduct of research in any field. We will briefly discuss each.

Observati on Virtually all biomedical research stems from clinical observation. T he clinician observes patients and their response to illness and treatment. He or she often conducts impromptu "experiments" to see if there is any effect o n a patient's outcome. Such observations are valuable, but rarely co nclusive. Observations are usually subj ect to roo man y un certainties, called biases, to lead to

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definitive co nclusions about w hat actuall y occurred or whether there was reall y an effect of a certain treatment on a condition. The real ization over many years that observation by itself was rarely useful in establishing reliable cause and effect relatio nships in fact led to the art of resea rch design. H owever, observation is the beginning point for inves tigation. The investigato r should begin with observation of his o r her practi ce. What is of special interest to the investigator? One of the most important aspects of doing research is to pick a topic that piques the interest. Once that is accomplished, the basis of a research project is laid . A prime example of observation being the basis for a lifetime of research is that of Larry Jones (39). He made the observatio n of a patient with severe muscle spasm that was relieved by placing the patient into an extremely awkwa rd position to alleviate the pain. Instead of dismissing the res ult as spurious o r in consequential , Jones pursued the observation and developed the area of strain/counterstrain.

Literature Search The next step in developing a research project is the literature search. This is a very important step and o ne that is often either slighted or done without sufficient diligence. T he first steps in a literature search are to examine texts and other reference works easily available. Do they show that the problem interesting the investigator has already been thorou ghl y researched? Is there an abundance of literature already available? Or does a preliminary search reveal little or no information ? Texts and reference books are called secondary literature because they repo rt seco nd hand on research articles (primary literature). Hopefull y, so methin g will easil y be found in th e secondary literature that will lead to primary research articles or even reviews of the topic. The search for information will almost inva riably lead to the primary literature; to journals in whi ch research findings are presented. The search for primary literature can be greatl y simplified by using one of the many computer resources now ava il ab le. T he National Library of Medicine (NLM ) has the largest co mpilation of medical literature in the world. This reso urce is avai labl e to anyone with World Wide Web access. T he "search engin es" for the NLM database may be accessed free throu gh servi ces like PUBMED or by fee-for-service engines, such as PaperChase. These search engines make searching the many millio ns of articles in MEDLINE and its associated databases easy and fast. However, the search must be done with some ski ll in selecti ng appropriate search terms or author names, or the res ult may be a return of thousands of often irrelevant articles. H o pefull y, the search will be productive in producing several articles and papers on the topic at hand. The investigator m ay then proceed to acquire the articles through libraries or by ordering them o n-lin e, and begin to read about what is known about his or her topic. The search can be both a time-co nsumin g and strenuous task. In osteopathic medicine, there is o nly one journal included in the NLM databanks: the journaLofthe American Osteopathic Association (JAOA). Because the NLM Medline data base o nl y goes back to 1966, it is also important to review articles in earlier iss ues of the JAOA (as it often is for other journals). T hus, the investi gator may have to acmally go to a library with ho ldings of the journal and search back issues, or as k the librar ian to review an index of the journal for relevant topics. In addition, other osteopathic

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VII! Basic and Clinical Research for Osteopathic Theory and Practice

source materials sho uld be searched. The AAO has an important coll ection of osteopathic articles in its Yearbook collection and has now released a CD-ROM with its bibliography in searchable form . This listing should be included in any search. Other osteopathic collections, such as the Osteopathic Annals (no longer published) , are also valuable sources of information. Many of the on-line databases available to the investigator are listed in Table 7 4. 1. We are grateful to Willard and Swartzlander (40) for granting permission to use this table. When using any database, it is advisable to keep careful records of articles read and what was in each. A computer database program, such as Reference M anage r or Endnote (www.isiresearchsoft.com), is excellent

for this purpose, and such programs also allow easy co nstruction of bibliographies when writing papers. What should be looked for during a literature search? Obviously, the primary goal is to find articles and information on the topic of interest. What has been found abo ut the topic? Wh at research or observations have already been made? It is also important to find how others have looked at the area. If research has been done, how was it done, and what measures did the investigators use in the studies? What techniques and research designs were used? If other research has been done, it is best to find how it was done, what pitfalls we re encountered, and how they were overcome.

TABLE 74.1. MAJOR REFERENCE SOURCES FOR THE MEDICAL AND LIFE SCIENCESa Print

CD-ROM

Online

Index Medicus (1879 + )

Medline (1966+ ) OVID Cambridge Scientific Abstract DIALOG SilverPiatter

Medline (1966+ ) OVID NLM DIALOG Data Star

Excerpta Medica (1946+ )

EMBASE (1974+ ) OVID SilverPiatter

EMBASE (1974+ ) OVID DIALOG

Biological Abstracts (1926+ )

Biological Abstracts (1985 + ) OVID SilverPiatter

BIOSIS Previews (1969 + ) OVID DIALOG DataStar

Cumulative Index to Nursing a Allied Health (1960+ )

CINAHL (1983 + ) OVID SilverPiatter Cambridge Scientific Abstracts

CINAHL (1983 + ) OVID DataStar

Chemical Abstracts (1907 + )

CA Search (1967 + ) OVID DIALOG Data Star ORBIT

Science Citation Index (1961 + )

SCISEARCH Institute for Scientific Information (lSI)

SCISEARCH (1974+ ) DIALOG Data Star

Hospital Literature Index (1945+ )

Health Planning and Administration OVID

Healthline (1975+ ) NLM Health Planning and Administration {1975 + ) OVID DIALOG

Current Contents-Clinical Medicine (1973 + ) Current Contents-Life Sciences (1958+ )

Current Contents on Diskette Institute for Scientific Information (lSI)

Current Contents OVID DIALOG

Psychological Abstracts (1894+ )

PsycLIT (1974+ ) OVID Si lverPiatter

PsyciNFO (1967+) OVID DIALOG

Nutrition Abstracts (1931 + )

CAB Abstracts Si lverPiatter

CAB Abstracts (1972 + ) OVID DIALOG CHIROLARS (1900+ ) OVID

Physician's Desk Reference (PDR) Merck Manual

Physician's Desk Reference Medical Economics with or without Merck Manual (continued)


1 177

TABLE 74.1. (continued) Print

CD-ROM

Martindale: The Extra pharmacopoeia

Martindale CD-ROM Microindex

Online Martindale Online DIALOG DataStar Comprehensive Core Medical Library (CCML) (1982+ ) OVID (full text) National Library of Medicine (NLM) MEDLINE AIDSLINE AIDSDRUGS AIDSTRIALS BIOETHICSLINE CATLINE AVLINE CHEMLINE HEALTH CANCERLIT TOXLINE TOXLIT DIRLINE SERLINE HSTAR SPACE LINE PDQ

•The underlined terms represent specific databases; non underlined terms represent the vendors carrying the databases. MEDLIN£, produced by the U.S. National Library of Medicine (NLM), is one of the premier sources of biomedical literature. MEDLINE corresponds to three print indexes: Index Medicus, Index to Dental Literature, and International Nursing Index. More than 3,700 journals are indexed and more than 70 % of the records contain author abstracts. EMBASE, the Excerpta Medica database, is a leading source for biomedical and pharmaceutical literature. It contains citations and abstracts to more than 3,500 international journals. 810515 Previews is one of the world's most comprehensive databases in the life sciences. More than 6,500 serials, 2,000 international meetings as well as books and monographs are monitored for inclusion. CINAHL provides bibliographic access to important nursing and allied health journals in the fields of cardiopulmonary technology, emergency services, laboratory technology, medical assistants, occupational therapy, physica l therapy, physician's assistants, radiologic technology, respiratory therapy, and surgical technology. CA SEARCH database includes more than 10 million citations to the literature of chemistry and its applications. SCISEARCH is a multidisciplinary index to the literature of science and technology prepared by the Institute for Scientific Information (lSI). Cited reference searches are possible in this database. Health Planning and Administration contains references to nonclinical literature on all aspects of health care planning and facilities, health insurance, the aspects of financial management, personnel administration, manpower planning, and licensure and accreditation that apply to the delivery of health care. Current contents is a weekly service that reproduces the tables of contents from current issues of leading journals in clinical medicine and life sciences and five other subsets. PsyciNFO database provides access to the international literature in psychology and related behaviora l and social sciences, including psychiatry, sociology, anthropology, education, pharmacology, and linguistics. CAB Abstracts is a comprehensive file of agricultural and biologic information and contains all records in the 26 main abstract journals published by CAB International. CHIROLARS is a health care database that emphasizes health promotion, prevention, and conservation care. More than 700 periodicals are included from medical, osteopathic, physical therapy, chiropractic, and other disciplines. National Library of Medicine computer files contain approximately 15 million records covering its holdings of books, journal articles, and more. W ith GRATEFUL MED software, health professionals in even the most rural areas can access the files listed in this table.

Thus, the literature review is a vital and often very poorly done parr of any study. Careful literature review will often save the investigator much work and even embarrassment. It is not good to find, after doing a study, that someone else has already done it or one sim ilar. The literature search allows the investigator to go to the next step of research design: the formation of the research hypothesis.

be clear and concise. It must state exactly what the research is to investigate. Most beginning researchers try to make the hypothesis too complex or design a hypothesis that is simply not testable. For example, the hypothesis "osteopathic treatment is good for headaches" is not a good hypothesis. Although we would like to think that the statement is true, can we test it? T he answer is no. What is "osteopathic treatment?" What does "good" mean? What type of headache is to be studied? A good experimental hypothesis is simple, precise, and well defined.

The Hypothesis One of the most important aspects of designing any research project, be it quantitative or qualitative, experimental or observational, is forming the hypothesis. The hypothesis is the statement of the question being asked by the study. The hypothesis must

The Hypothesis Dictates the Study Design The hypothesis also will dictate the design of the study to be done. Too often, an investigator produces an imprecise hypothesis and

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then has diffi culty designing the appropriate study because the actual question and its implications are no t clear. If the hypothesis is clear and simpl e, the des ign of the study will not only be much mo re evident, but it will be defensible to others. For example, in the lrvine study referenced above (4 1), the hypothesis was simple and straightfo rward: "What is the effect of a lateral recumbent ro ll thrust on measures of well-defin ed , acute low back pain?" This hypothes is defin ed the study as a technique study on a well-defined probl em, acute low back pain (which was very precisely specified). T hus, the hypo thesis, not a preco nceived notion of design, must di ctate the study design. Too o ften, it is assumed that one type of study design is the only one appropriate for some type of resea rch, such as manipulative medi cine, when in actuality, the design Aows fro m th e question being as ked. If the in vestigator has the questio n clearly in mind , the research design can be chosen and refin ed to reAect th at questio n, no t some other question that is not being asked . Once the hypothesis is determined , it is usually converted to the "nul l hypothes is." Th e null hypothesis simply states th e negative of the experimental hypo thes is. T hus, if the experimental hypo thesis was that "a lateral recumbent thrust will have an effect o n acute low back pain," the null hypoth es is would be that "a lateral recumbent thrust will have no effec t on acure low back pain ." T he null hypo thesis can be disproved by a study showing an effect, but a study showing no effect does not necessarily prove th at no effect exists. Rather, it shows only that an effect was not observed in th e present study. Thus, the null hypothesis is the preferred statement with the intent of th e study to disprove it. In fact, many study designs provide bo th null and experimental hypo th eses.

Study Design T he design o f a research project is vital to the success and value o f th at project. In osteopathi c resea rch, there are many types o f studies that ca n be don e, as o utlin ed above in this chapter. Once the investi ga to r has chosen the topic of the study and has at leas t stated th e hypothes is, if not completely refined it, the choice of resea rch designs must be made. Is the research to be: Observat io nal Epidemiologic Descriptive Ex peri men tal Each of these types of research has particular requirement for design co mpo nents (28,32,42). The investigator must consult with ex peri enced clinical research designers fo r appropriate help. In th e area of research o n manipulati ve techniques or treatment, the most usual type of study is either a descriptive or experimental study. In descriptive studies, patients are simply treated, and the res ults of th e treatm ent are reported.

is given, the treatment is described , and the res ults are reported. T he case study was the staple fo r medical research many years ago, but is now only infrequently used. Many medi cal journals will no lo nger publish case studies except under the most strin gent circumstances. Case studies are useful as observations leadin g to more complete studies, but rarely stand on their own. T he limitations of case studies include poor recording of findin gs, incomplete history and physical reporting, and in many cases, un confirmed diagnosis. If the inves tiga tor beli eves th at a case is sufficiently unique to warrant publica tion, a very co mplete literature review must be do ne prior to artempted publication to ass ure that no such findin gs have been previously reported. Kaprow and Sandho use recentl y repo rted o n the treatment of a case by osteopathic manipul atio n, an exampl e of a relati vely unique treatment of an un comm on compl aint (43).

Case Series: Retrospective Case series are of two types. T he first is the retros pecti ve case se ries. In this design , the inves tigator searches the offi ce fil es fo r al l cases of a similar type and attempts, through reviewing th e cases, to find co mmonalities in symptoms, trea tment, o r o utco mes th at warrant publication. T he retrospective case series brings together similar cases to add credibili ty to a unique o r new cl inical enti ty or treatment regime. The retrospecti ve case series may add weight to an argument th at a new o r unrecognized clinical syndrome is emerging, or that a new treatment technique is effecti ve, but suffers the sam e probl ems as the single case study; the data are usuall y not uniform and diagnoses may be lackin g. In additio n, there is little assurance in a retrospective case seri es that all patients of th e targe ted type have been included; it is possible that o nly selected cases have been repo rted, makin g the results seem more benefi cial than is actu all y the case.

Case Series: Prospective Prospective case series studies are usuall y done after the realization that some treatm ent has a greater impact th an th ought or can be used on some unique condition. In this study type, nothin g new is introduced, but on ly usual and standard practices may be used in a different manner. H owever, the means of identify ing prospective patients, the data to be co llected, and the methods of treatment are clearl y specified in advance. All patients that meet the predefined criteria are treated and th e data recorded unifo rmly. Thus, there is some ass urance that the patients actually had the specified condition and the data ga thered are uniform . In most cases, case series do not have to be approved by an IRB unl ess a new treatment is being tried or data not usually coll ected in the course of practice are being collected. Although so mewhat more indicative of effect, the prospective case series fall short of providing convincing arguments fo r effecti ve ness, because there is no comparison with other treatments o r subj ects.

CASE STUDIES Case Report A case study is the report of a single, supposedly unique case, or o f a unique treatment of a case. In case studies, a patient's history

OTHER OBSERVATIONAL STUDY DESIGNS As mentioned above, vari ous other types of designs, such as in terview, epidemiologic, survey, and outcomes designs, are useful

74. Foundations for Osteopathic Medical Research for many aspects of osteopathic research and can bring powerful and useful data ro bear on such questions as: How do the attitudes of osteopathic students toward the profession change over their training? How satisfied are the patients of osteopathic physicians? What did statements of pioneers in the profession mean? How do patients of osteopathic physicians choose their doctors? What is the incidence of somatic dysfunction in the normal population? These and many other questions are awaiti ng well-planned studies and would produce information valuable for planning the future of the profession.

Experimental Design The proof of cause and effect relationships is very difficult. Humans are very good ar recognizing what seem to be correlations between two events, a trait that has undoubtedly been honed over thousands of years. The rustle of grass on a dark night correlates well with rhe approach of a tiger intent on finding a meal, and quickly becomes a signal for retreat to a safe cave. However, rhe rustle does nor cause rhe cat ro eat the unwary human. The human (and other animal) nervous systems are well adapted to recognizing correlation, bur poorly designed to establish cause and effect. The art (and some would say, science) of experimental design has been developed to fi nd ways to be able to assign cause and effect relationships in all areas of science. Medical science is one of the most difficult areas in which to assign cause and effect relationships . The human organism is very complex, and what may seem like cause and effect relationships may be nothing more than random variation in function or disease stare, or even the patient's own perception of how they are feeling. For example, the drug Laetrile was for years thought to produce good results for advanced cancer patients, but was finally shown to be useless and perhaps harmful (44). Patients and doctors alike thought that there was a cause-effect relationship between cancer outcomes and Laetrile therapy (that Laetrile cured cancer); in fact, there was neither a cause-effect relationship, nor even a decenr correlation. In experimental studies, a treatment group of some sort is compared with a control group. Ideally, rhe experimental and control groups differ in only one way; the treatment is given to rhe experimental group and not to the control group. Although this seems a simple task at first, in reality it is very difficult, especially in medical areas. As the complexity of this task unfolds, remember that when designing a research project, there is no such thing as the perfect design . Research designs always mean making compromises and cho ices that open the results to other interpretations. The problem is not that the design is not perfect; rhe problem is in not recognizing the imperfections and dealing with them.

Types of Experimental Designs Experimenral designs for osteopathic research can take several forms, depending on the question being asked . These include:

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Between-subject designs Within-subject designs Crossover designs Variations The hallmark of an experimental design is rhe comparison of the treated or experimental group of patients with a group receiving no, or some other, treatment. The experimental study is always prospective, that is, ir is planned in advance and must always be approved by an IRB.

BETWEEN-SUBJECT DESIGNS The simplest experimental design is that comparing a treated group with a histOrical control. Hisrorical controls would be patients from rhe practice or from other practices that had received some other form of treatment than the one being investigated. This design is considered robe weak in irs ability to define causeeffect relationsh ips. It is only one step above the prospective case series design, because the control subjects may or may not be comparable ro the experimental subjects. However, in some cases, such as very severe disease stares or when it is considered unethical ro withhold a putative treatment, ir may be the only way ro attempt tO determine the effect of a new or altered treatment regimen . The most usual of the experimental designs is the two or more group direct comparison design. In this study design , patients fitting the criteria for inclusion in the study are random ly assigned ro one group or the other. If the design is an experimental and control group design, the subjects in rhe experimental group receive the treatment and the subjects in the conrrol group receive either no treatment o r some alternative (perhaps community standard) treatment. The results of the two groups are then compared on one or more measures.

Independent and Dependent Variables The rrearmenr given to the experimental group is the "independent variable," and the measures taken tO judge results in both groups are the "dependenr variables." Thus, in a study comparing the lateral recumbent thrust, such as the Irvine study, the independent variable was the thrust given to the experimental group, but nor the control group. The dependent variables included straight leg raising and judgmenr of pain before and after the treatment. One of the hardest aspects of research on osteopathic manipulative trearmenr is finding good dependenr variables or measures of results .

Random Assignment to Groups In experimental studies, it is very important that the two groups of patients be as much alike as possible. For example, if some systematic difference between the groups existed at the beginning of the study, such as the mean age of the experimental group being 24 and the control group being 56, a better result in the experimenral group may well be due nor to the rreatmenr provided, bur to the superior health of the younger patients. The comparability of the groups is usually achieved by "random assignment" of rhe

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Vllf Basic and Clinical Research for Osteopathic Theory and Practice

pati ents to the gro ups. T he patients are assigned to the groups co mpletel y at random , so that neither the investigator's bias nor o ther fac to rs will result in patients in one group being different in any systematic way from the other group. There are many ways to do rando m assignment (44), but it is vital that it be don e; how it is to be do ne must be specified prio r to the study. Randomizatio n can be as simple as flipping a coin to determine the group a patient is ass igned to, but mo re reliable means are available, such as rando m number tables in books o r o n co mputers.

Blinding O ne of the most impo rtant as pects of experimental research is the principle of blinding. It is well kn own th at even the most honest in ves tigato r can unwittingly affect the results of a stud y by judging the results of a treated patient as better than an untreated patient. T his often slight and unco nscious bias o r systematic error has often res ulted in faul ty and unreliable results from an o therwise well -designed study. To preclude this ty pe of error, it is almost always necessary to make sure that the person measuring the outco me of a treatment does no t kn ow whether the patient received the ex perimental treatment (independent variable) o r not. lf the observer is blind to the patient's gro up, the study is call ed a sin gle blind study. If the patient is also blinded to the treatment give n, the study is a double-blind study. At times, it is also des irable to have o thers in the stud y blind to patient group. H owever, at the absolute least, the observer must be blind to the patient's treatment status. If blinding of this sort cannot be show n o r is not feasible, the study has a very serious problem that alm ost always will make the results suspect. T his subj ect will be fur ther discussed in the secti o n o n Special C onsiderations o n Osteopathic C lini cal Research , below.

WITHIN-SUBJECT AND CROSSOVER DESIGNS T he research types reviewed above include mainly those that use plann ed co mpariso ns between experimental and control groups, or lo ng- term de terminations of health status that are then compared with the ge neral population . M any vari ations on these stud y types exist. Another group of study types should receive careful attentio n when the effects of manipulati ve techniques or treatment are studied. T hese designs are within-subject des igns; they essentiall y use the same subject as bo th the control and experimental gro up. Keating et al. (45) have summarized this type of design in so me detai l. T he within-subj ect study usually involves fo llowing a patient for a period of tim e to determine the baselin e symptoms and wh ether they are fa irly stable o r changin g in some fairly predi ctabl e fas hio n. After the baseline measurement, treatment is introduced and the measurements co ntinued. The measured variables can be co mpared befo re and after treatment to see if the treatment had an effect. T he baseline measurement period will va ry amo ng several subj ects, allowing the treatm ent to be introduced at different times, assuring that th ere was no peculiar effect of tim e o n treatment interventio n. T his is known as the variable baselin e, within-subject study des ign. Frym ann (46) used this design type in her study of th e effects of osteopathic care of children with neurologic and develo pmental defi cits.

C rossover designs usually use experimental and control groups, but after the control group has fini shed, these patients are "crossed over" to receive the experim ental trea tment. Crossing over sometimes meets obj ections that th e control group will not get the benefit of a supposedl y effective treatment. T hi s design is useful if the illness or disease being studied is no t particularly severe and can wait to receive the experimental treatmen t. C rossover and within-subj ect studies are not es pecially effecti ve if the measurements and symp to ms are not fa irly stable fo r a period of time that can be used as the control condi tio n. [n addition , there is some problem with establishing whether the manipulative intervention actuall y d id cause any change in the symptoms being measured . H owever, these d es igns allow treatment for every subject in the stud y, whereas the co ntro l gro up does no t receive treatment in traditi onal ex perim ental and contro l gro up studies. Th e study designs considered here have many va riations that must be considered before final design elements are determined. So me of the m ajor issues in design of osteopathic research are considered below in the Special Considerations section of th is chapter. T he investigator is also urged to co nsult design experts and /o r reference texts (28,32) .

Data Collection The actual work of do ing the study co mes onl y after ca reful planning, written statement of the study, and IRB approval. It is absolutely necessary to do th e preliminary steps carefull y and compl etely, or the study will almost certainly be useless d ue to prob lems of design, executio n, o r data collectio n. T he entire procedure of the study design must be written o ut so that al l those in volved in the study will full y understand every step. W hen writing o r reviewing a clinical study protocol, [ do not consider the design to be complete until the info rmed reader of the protocol will know from readin g the document what happens to the patient all the way through the study. Data collection is the actual perform ance of the study. The patients are recruited, assigned to gro ups, n·eated (o r not), and measurements performed. T he data are coll ected by the app rop ri ate study participant, including measures of somatic dysfun ctio n, fun ctional tests, labo ratory results, and so forth. All data must be kept confidential until the study is over (unless it is agreed to look at preliminary data earlier). T he study grou p sho uld meet frequentl y durin g the study itsel f to discuss any problems or con cerns. D ata analysis is the next step.

Data Analysis On ce data collection has been completed, th e tas k of data analysis begins. Data from most studies must be subj ected to som e for m of statistical analysis as a help in decisio n making. At most, statistical analysis is a way to help the investigato r make inform ed decisions abo ut the meaning of the data. Statistical tests are of three basic types: D escriptive statistics N onparametric statistics Parametric statistics

74. Foundations for Osteopathic MedicaL Research Descriptive statistics give information about the basic attributes of the collected data, such as the mean, median, and stanqard deviation . T hese numbers tell the investigator how each group performed on the dependent variables used . However, to obtain information about whether there might be a difference between the performance means of the experimental and control groups, some form of non parametric or parametric statistical tests are used. The decisions about whether the independent variable caused a change in the experimental group's responses (dependent variables) rely on the results of tests of significance. Statistical tests to determine differences between group data rely on the assumption that the experimental or independent variable caused a change in the experimental group that resulted in an actual difference being created between the groups, as measured by the dependent variable(s). According to this view, if the measure was the distance moved by the leg in a straight leg raisi ng test, both groups would have the same average movement prior to treatment, but the treated group would have more movement after treatment. Thus, the treated group would now be a different gro up or population, as measured by straight leg raising tests. T he treatment changed them from what they were before to a group able to perfo rm straight leg raising to a greater level. SeveraJ things determine how well the statistical test is able to indicate this difference. Two of the most powerful of these are the amount of variability in the initial measurements of the groups, and the number of subjects in each group (subject numbers are discussed below, under Power). If all subjects initially had exactly the same movement distances, then a very small increase in all the treated subjects would be detected by the statistical test as a significant effect. However, if there was a great deal of variability amo ng the subjects, then a much larger average increase due to the treatment would be necessary before the statistical test could predict that the treatment had produced an effect. Thus, variability is best kept as small as possible between subjects in any swdy. Parametric statistical tests, such as the t test or analysis of variance (AN OVA), make some assumptions about the distributions of the data and the population of subjects, in effect relying on the data to have a "normal" or bell-shaped distribution. If the data do not have roughly such a distribution, it is best to use non para metric statistics, such at the Mann-Whitney rest, to determine whether the results of the swdy show a difference due to the independent variable (47). Many fairly simple computer programs are now available to help with statistical analysis. Such programs as KaleidaG raph (www.synergy.com), Instat {www.graphpad. com), GB Stat (www.gbstat.com), the SPSS packages (such as SYSTAT at www.spssscience.com/SYSTAT), and others are available for both Apple and IBM-compatible computers (see also, for example, http://ebook.stat. ucla. edul) . However, statistical assistance should be sought to avoid mistakes in analysis.

STATISTICAL SIGNIFICANCE Tests for differences between groups provide an estimate of whether differences in the dependent measures seen between the groups after the study can be relied on to have acwally been produced by the independent variable, or whether the differences are

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more likely to have been the result of random or chance Auctllations. The reliability of the difference is called the significance of the test, or the level of statistical significance. By tradition, and some logic, the usual standard value that must be reached for a difference between the experimental and control groups to be considered significant is p = 0 .05. T his is the so-called p val ue, and is a measure that takes into account the variability of the data and the numbers of subjects in the study, among other things. The p value is essentially an estimate of the probability that the study would show a difference as great as or greater than the observed difference purely by chance. T hus, a pvalue equal to 0.05 means that on ly one time in 20 or five in I 00 would a difference as great or greater than that observed happen by chance alone, if the experimental variable actually had no effect. Thus, p values greater than 0.05 are considered probably due to chance fluctuations in measurement o r to weak effects of the experimental variable. If the p value is 0.05 or less, it is assumed that the chances o f finding the observed differences by chance are so small that the differences can be accepted as due to the experimental variable. It is a mistake, however, to assume that if the data show a p value "approaching" 0.05 (p = 0.056, for example), that the data are "almost" significant. In many cases, the addition of additio nal subjects or other refinements of the study produce no more significant results. If the d ata are close to significance, consider ways to redo the study with less variable data or stronger treatment. The investigator must generally consult with a biostaristician before fin alizing a study d esign. The statistician will give advice on what data can be successfully analyzed and how the data can best be collected. In addition, due to the number of different statistical tests available, the methods of analysis should be specified before the swdy is undertaken.

Discussion Once the data are analyzed, the investigator can undertake a discussion of the results and the study. The results must be considered in light of the background of the swdy, the resul ts themselves, and the interpretation of those results by the investigato r. Data are o nly data; they are nothing until interpreted. The results of any swdy can be looked at in vario us ways. Consider what happened in the Irvine study. Osteopathic physicians looked at the data and basically said that the study was not impo rtant because the independent variable, the thrust, was not osteopathic treatment or spinal manipulatio n, but only a thrust. Allopathic physicians viewed the results as insigni ficant because the thrust and nonrh rust groups showed no differences 3 weeks later. However, immediately after the technique, there was a significant difference. Presumably, the thrust patienrs would have been able to return to work sooner, an important difference to an insurance company paying for rime off work. Thus, if the study had been correctly interpreted as a technique study and the immediate effects recognized as important, the study would have made more of an impact. The discussion or interpretation of the data is where the investigator can state his o r her opinion of the outcomes, link them to other data, and interpret them for the osteopathic profession. The discussion should not be too grandiose, claiming that the

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study had proven everything in the universe (unless it really has), but the investigator should legitimately link the study to the areas of interest and suggest to the reader how the data are important. T his is another reason that a good literature review is necessary; without that background, the investigator will not be able to properly interpret the results.

Writing and Publication If it is not documented, it did not happen. This statement is true for data gatherin g, observations during a study, orders given for participants of a study, and for publication of the results of a study. If a study is done but not published, it did not happen. It is viral to write a report of a study and publish it in some format. There are numerous books available for the novice scientific writer (48). However, the investigator can follow basically the same format as that given above in the design of a study for writing a scientific paper. T he parts of a research paper, although varying to some extent, are basically: Abstract In rroductio n Methods Results Discussion Conclusions (sometimes nor included) References T he abstract of any paper should present a concise and informative overview of the paper. Where the idea came from should be stared; this can be an overview of the literature review or observatio ns that led to the idea for the study. T he major methods sho uld be give n along with the major findings. The import of these findin gs finishes the abs tract. Such statements as "The results are found below" or "The results will be discussed" are inappropriate. T he abstract is the on ly thing that many people will read, so it must immediately tell the reader why they should look at the rest of the paper. Seeing it as unimportant, many writers das h off an abstract although it is a very imporrant parr of the paper. T he introductio n is basically the background of the study. It gives an overview of the literature and other information about why the study was conceived. It provides the reader with the rational for the hypothes is of the study. In fact, the introduction can be conceived of as a funnel with the hypothesis being at the bottom, small end. T he introductio n starts from the big picture overview and comes down to the hypothesis. T he reader can see immediately why the hypothesis makes sense, given the background. Of course, so me reports, such as case histories, have no hypothesis, but nonetheless, should have the background presented in the introduction . The methods section is a fully derailed report of the procedures, rests, manipulative procedures, subject selection criteria, and so forth of the study. The methods section should allow a reader knowledgeable in the field to reproduce the study. The methods secti on should present sufficient detail that the reader can make judgments about the validity and usefulness of the study results.

The results section presents the actual data from the study and the analyses of the data. It gives tab les and graphics to clearly show the reader the outcomes of rhe study. Graphs should be presented in formats that clearly show differences, data trends, and group data descriptions. Most graphs showing group data should show error bars so cl1at the reader can see the amount of variability within the data (28,48). As with statistical analysis programs, there are several computer programs available to help with graphic presentations, such as KaleidaGraph (www.synergy.com), GraphPad (www.graphpad.com), GB Star (www.gbstat.com), and Microsoft Excel. One of the most common errors in presenting data in a paper is to have graphics that are misleading, confusing, or not readily interpretable. As stated earlier, the discussion section is where the autho r can express his or her opi nio ns on the outcomes of the study. It is often helpful to begin the discussion sectio n with a bullet recap of the major results. This helps both the writer and the reader to focus on the important aspects of th e data. T he discussion allows the author a place to express op inions abo ut the meaning of the data and interpret it for the reader. Of course, the reader does not have to agree with the writer's interpretations. The reference section should list the so urces consulted by the author. All references that are cited in the text or that contributed to the ideas in the article should be ci ted. It is a se rious ethical problem to use the material of others and not give att ribution to them. Plagiarism is poorly looked o n. It is a good idea to be inclusive rather than excl usive in referenci ng others' work. T he beginning and even the seasoned author can get help in writing articles by co nsulting the instructions for autho rs given in most meclical journals. T he only osteopathic journal fu lly indexed in the Index Medicus library is the journal ofthe American Osteopathic Association OAOA). It publishes instructions to authors in each issue, and these can be viewed on the internet at the AOA web site, www.aoa-net.org. Another invaluable source of information on writing style is the Publication Manual ofthe American Psychological Association (49). T his invaluable book gives not only style guidelines but also informatio n on presenting graphics, writing theses, plagiarism, and much m o re. When considering a journal for publication of an article, first choice should be give n to journals indexed in the Index Medicus or similar worldwide listings . The target audience should be identified and the chosen journal should target that aud ience. The journal should be peer-reviewed to insu re quality of the articles published. If the study is not sufficient for stand-alo ne publication, the author should consider presenting the data at a medical or scientific meeting from which abstracts are published. T his .provides a public reference of the work. T he AOA research conference held each year in conj unction with the AOA convention is such a venue. The abstracts of the scientific presentations are published in the JAOA and indexed in the world literatu re.

SPECIAL CONSIDERATIONS IN OSTEOPATHIC CLINICAL RESEARCH In the sectio ns on research design, several ideas were introduced that require discussion in terms of osteopath ic research questions.

74. Foundations for Osteopathic Medical Research The areas that are of special interest to the design of osteopathic studies are: The "gold standard" for medical research The question being asked Blinding Contro l gro ups Patient populations Pilot studies and statistical power Inclusion/exclusion criteria Dependent variables

The "Gold Standard" for Clinical Research The randomized, double-blind. placebo-controlled study (RDBPC) has evolved as the "gold standard" for clinical research studies. T his design was developed in the 1940s and 1950s as the appropriate design to rest the effects of drug treatments. The major elements of this particular design are: Randomi zation of subjects in to the treatm ent gro ups (or arms) Blinding of subj ects, drug givers, and data collectors as to treatment given Provision to the co ntrol subjects of a "placebo" o r inactive substance that is indistinguishable from the active drug T his design was developed to answer a very specific question in drug therapy. For practical purposes, the question or experimental hypothesis to be answered is, "What is the effect of this drug on the natural co urse of a disease process in the human unaware of what drug is given?" The random ass ignment of subj ects to the experimental or control group hopefull y assures that the experimental and co ntrol gro ups (o r more groups if, for example, a gro up give n neither drug nor placebo is used) have the sa me characteristics to begin the stud y. The blinding of the patient to what is being received (active drug or inactive substance) will hopefully assure that the patients in the experim ental gro up do not feel better simply because rh ey are getting an active drug. In other words, the psychological aspects of the trea tment shou ld be equal for the two groups. Blinding the drug giver and ca regivers as to which group the patient is in hopefully insures that the treated patients do not get subtle cues that they are being given an active substance; blinding the data gatherers ass ures that bias is not introduced by knowing the patients receiving the active drug. T hus, for the question being asked, this design is a good one. U nfortunately, studies of manipulative treatment are not always amenable to this design, and may often ask different questions. T hus, we must exami ne briefly what affects the interpretation of clinical trials.

Validity and Bias The validi ty of a study is si mply how strongly we can believe th at the results are a reflection of what is actual ly the case. Did the manipulative technique really cause the observed change or was some other mechanism at work? Will the technique wo rk with other patients, or was the result limited to the patients being studied? M any factors can influence how results can be interpreted, and these factors are cal led biases.

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T he definition of bias in a research study is basical ly anything that could interfere with the correct interpretation of the results of the study. If the study asks about the effect of a technique on low back pain, then measuring the pain differently in experimenral and co nrrol groups would co nstitute a bias that would in val idate th e results. There are many forms of bias that affect the validity of a study.

External Validity Simply put, an external bias is somethin g that interferes with the gene ralization of the results of a study from the patients in the study to other patients (32) . If an experimenter wanted to have an extern all y valid study of the effects of a manipulative technique on asthma in the general population , the study group would be chosen not from a hospitalized population but from the whole group of peo ple with asthma. If the as thma study patients were all hospitalized , the effects of a manipulative technique might well be different than if the technique were performed o n patients with a less severe form of the disease. The study would not be externally valid because it would not be generalizable to the whole population of asthma sufferers. Of course, if the intent of the study were to study the effects of manipulative interventions o n as thma in hospitalized patients, it would be externally valid. Thus, it is very imponanr to frame the hypothesis with knowledge of whom the subjects will be and to whom the data will be generalized . Many things can affect external validity, including: Lack of proper control procedures Improper selection of pati ents Simple length of tim e th e pati enr is in the study (symptoms may change over time even without treatment) Biases that threaten the extern al validi ty of a study are often fairly eas ily seen and recognized. For the example above, th e bias of using only hospitalized patients as subjects obviously limits the res ults to that population of patients . Other problems of ge neralizability are not so obvious. For this reaso n, the investigator must keep records of the patients and be ab le to d efine at least the demographics of the patients so that th e reader will be able to judge which population the results are most likely to be app licable to.

Internal Validity Much more serious are the threats to internal validity. T hese biases are often very subtle and can make statements abo ut the actual meaning of results difficult if not imposs ible. A non blinded observer who takes data in a study and who knows whether or not the subj ect was treated is an obvious source of bias that wi ll almost surely make interpretation of between-group differences impossible. Other sources of biases threatening internal valid ity include (32): Inappro priate control groups Measures that do not accurately determine the response being studied Objectivity in the measures being used Small numbers of patients in the groups Initial differences between experimental and control gro ups

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Random fluctuations in the course of a disease process Regression of symptoms to the m ean M any others T hus, the investigato r must pay close attention to issues affecting the internal validity of the study design and would be well advised to consult an experienced clinical trials designer on the issue.

DESIGN OF OSTEOPATHIC CLINICAL TRIALS

Blinding As noted above, the design of clinical trials of osteopathic manipulation is more complex and may ask different questions than drug trials. Obviously, the person providing the treatment cannot be blinded to whether manipulation is given or not. In some cases, the patient can be blinded to treatment condition, as in the Irvine study. None of the patients included in the study had any experience with manipulative treatment, an d results showed that there was no difference between the groups as to their recognition of whether m anipulation had been given or not. Blinding was done for the data gatherers, so the study can be considered a blinded trial with the exception of the treating physician. Although patient blinding is poss ible in cases of technique studies li ke the Irvine study, it is not as likely in studies of full treatment effects. In addition, it is difficult to find large numbers of patients in most osteopathic practices that are completely na·ive to manipulation. Thus, the question of patient blinding is one that must be examined for each study and dealt with as the study and situation allow. The co nsequences of not blinding the patients to treatment are co nsidered under the section on control groups, below. In any event, it is imperative to have the data collectors blinded as to gro up assignment.

Population Selection In most cases, studies of manipulative treatment will use patients from the investigators' practices. The study design should include recording the demographics of the patients so that there will be a basis to generalize from the study population to other patients. It is obvious th at the patients coming to an osteopathic practice are not a random sample of the general population, bur a highly self-selected group that may be motivated to seek osteopathic care. T hus, caution must be taken when generalizing results of manipulative trials to the general population, and this bias must be taken into acco unt.

Control Groups One of the most contentious issues in osteopathic research design is the issue of appropriate control groups. T he idea of the control group stems from the necessity of having some way to compare the active treatment with some baseline. As mentioned above, historical controls are sometimes used, bur are far from ideal. Historical controls may differ widely from the contempo rary study group in many as pects, so give only an impression of effects . Historical controls are used only as a last resort.

The "gold standard" control is the placebo control. Defined above, the placebo control is designed to mask from the patient the knowledge of whether the active drug or the inactive substance is being given. Such a control is meant to rake the psychological effects of the patient's knowledge on the interaction between drug and disease natural history out of the therapeutic picture. It has been widely assumed that the simple knowledge of treatment had about a 30% effect on the patients response to the treatment (the "placebo effect") (50). Thus, according to the com monl y held view, the simple psychological effect of knowing that a treatment was being given could alleviate symptoms by a large amount. Thus, the placebo control is designed to keep the placebo effect from entering into the difference a drug would make in the course of a disease. Significant questions are being raised about the placebo as an effective control condition (51-54). For example, is the "placebo effect" really as robust as has been assumed? Is factoring out the psychological effect giving a true picture of the actual effect of a drug or treatment on the course of a disease, or is the placebo control consistently causing an underestimation of the total effect of drug plus knowledge? It is now well known that an individual's psychological status has real and measurable effects on their physiologic processes (see Willard, Chapter 8). Is the placebo the best control for treatment studies? The placebo's sister control group, the sham control, is often used in studies of manipulative treatments and techniques. With a sham control, some type of "hands-on" experience is given to the patient so that the physiologic and psychological effects of placing the hands on the patient are equal in the treatment and control groups. The Irvine study is a good example of a sham treatment control. Because the question being asked was regarding the effectiveness of the thrust alone, a sham was appropriate. However, what if the question being asked is of the effect of the osteopathic treatment as a total treatment effect? Is it then not appropriate to rest the total treatment, including the effect of hands-on and patient knowledge, against giving the patient no treatment? The question being asked determines the control group. If the question is to test the totality of the treatment effect against no treatment, and treatment includes the effect of putting hands on the patient, then the approp riate control is a patient receiving only rest during the treatment rime. It may also be appropriate to use the musculoskeletal examination as the "sham" in such cases. Here, both groups would receive the structural exami nation, bur the control group would then rest while the manipulative treatment was given to experimental group. Blinding of the subjects to treatment group in many cases is simply impossible, thus leaving the co ncept of a "placebo" group as a moot point. Another control often used in manipulation studies is the "community standard" control in which, for example, low back pain is treated manipulatively in the experim ental group, but by drugs, physical therapy, and counseling in the contro l group. This type of active control group is aski ng yet another question : Is the effect of manipulation equal to or better than standard care? T he recent Andersson study (38) on manipulative treatment for low back pain is a good example of this type of control group. Because of the ethical considerations of giving no care to a patient in a "do nothing" control group, the active or commun ity standard


of care control may be the only way some conditions can be examined. Thus, the osteopathic researcher must carefully determine the actual intent of the experimental question prior to determining the appropriate control gro up. The myth of the "gold standard" must not be forced onto research designs for manipulation. If the question of the study is whether the manipulative treatment is better than nothing, a rest or nothing control is appropriate. If the question is whether the manipulation is better than community standard care, the appropriate control is the active community standard treatment. If the question is whether the manipulation is better than simply placing hands on the patient, probably the best control is the examination-only control. Thus, careful consideration of what is being asked will determine the appropriate control group, nor a preconceived notion of what a control should be.

Study Size and Power Studies on the effects of manipulative treatment are in their infancy. It is difficult for an individual investigator to procure sufficient subjects for a large study. In fact, it is now becoming increasingly evident that many studies have not been sufficiently large for their results to be reliable. The term for the probability that a study comains sufficient subjects for an effect to be accurately found if, in fact, there is an effect of the independent variable, is called "power." The measure of the power of a study is called power analysis (55). The probability that the statistical analysis of a clinical trial will show a significant p value is remarkably large if the number of subjects in the study is small. In a study with few subjects, one subject's large change in findings may result in a significant effect, although the effect is not general. In this case, a "type I" error will result; the experimental hypothesis that there is a treatment effect will be accepted although no such effect is present. Thus, power analysis gives an estimate of the number of subjects required in a study to be reasonably sure that if there is an effect it will be found. Power calculations can be made with relatively simple formulas found in standard books (55) or on the internet (http://ebook.stat. ucla. edulcalculatorlpowercalc/, for example).

Pilot Versus Full Studies Thus, the Andersson study, although well done with about 178 patients, is most likely sti ll lacking sufficienr patient numbers to fulfill power requirements (38). Studies nor meeting standard power requirements must be termed "p ilot studies," and their results shoLJd be viewed with caution. Pilot studies are very useful in giving indications of what effects may be valuable to further study and in providing data on the amount of variability inherent in outcome measures; therefore, they are very valuable. Studies that meet the required numbers of subjects indicated by power calculations are considered full-scale studies and, other things equal, are more reliable than studies with fewer subjects.

Drop-Outs The problem of drop-outs can be acute in any clinical study. In studies of manipulation, the investigator must account for

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patients not finishing the study. This is important because of the potential for causing imbalances between the experimental and control groups. For example, if all the patients with more severe disease dropped our of rhe experimental group bur stayed in the control group, the results would be inaccurate or biased towa rd a larger effect in the experimental group. The usual practice is to try to determine the cause of the patient's failure to finish the study and to carefully examine rhe drop-ours for commonalities that could affect study results.

Inclusion/Exclusion Criteria The issue of inclusion/exclusion criteria is also difficult in many studies of manipulative treatment. The inclusion criteria are those things that make the patient eligible for the study, such as low back pain. However, the inclusion criteria must be well specified and measurable prior to the study. In the example oflow back pain, the type, duration , and other factors should be carefully delineated. An area that needs special attention in inclusion criteria is that of a well-defined diagnosis. Often, studies of manipulation do not have well-defined structural diagnoses that can be justified and defended to the greater medical community, which results in poor acceptance of the study. Exclusion criteria are those factors that exclude a patient from a study. These can be age, pregnancy, drug use, and so forth. Exclusion criteria must also be clearly specified in the study design . It had been standard practice to excl ude women from many drug studies because of the danger of pregnancy. This practice resulted in a lack of information on the effects of drugs on females (poor external validity), and the effects were often different than the effects on males. It is now unacceptable to simply exclude females; if a study does so, explicit reasons must be given.

Dependent Variables Selecting Appropriate Measures The best measures to determine if a manipulative procedure had an effect are often difficult to decide. These measures are known as the dependent variables because their values are supposedly dependent on the experimental treatment. In studies of the efficacy of a manipulative technique or a manipulative treatment on the outcome of a specific disease process, the measures are presumably some aspect of the disease process or of the natural course of the symptoms. In assessing the contributions of manipulative treatment to resolution of somatic dysfunction or to the maintenance of health, the task of defining sensitive dependent variables becomes more difficult. Some dependent measures include: Measures of immune system function Studies of the activities of daily living Episodes ofloss of health (for long-term stud ies) Other measures ofbody funct ion, including reports offeelings of well-being and comfort One of the problems in many studies of manipulative treatment is the use of purely subjective, dependent variables in the study. Typically in these cases, an examiner performs a musculoskeletal examination of a patient and records the somatic

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dysfunction found. The treating physician typically repeats the examination and treats the findings for experimental subjects and simply does nothing for control subjects. The blinded examiner then performs a second examination and reporrs differences between the two examinations. The problems inherent in this design are mainly a lack of any knowledge of the reliability of the examiner. How much do the findings vary between examinations (repeat reliability) and how do the examinations of the two examiners correlate (interexaminer reliability)? These are significant issues that must be acknowledged in such a study. The answer to such issues is to use dependent variables that are not dependent on the subjective examination of either a blinded examiner or the treating physcian. Such measures can be instrumented measures, such as Doppler blood flow, respiratory volumes, and so on. Whatever the dependent variable or variables, the measures of manipulative treatment results should include an evaluation of whether the treating physician determined that the treatment given actually did what it was designed to do. Sometimes the manipulation fails ro accomplish the desired immediate outcome in restoring range of motion or proper muscle relaxation. These facts must be recorded and used in analysis of the outcome of the treannenr so that unsuccessful treatments can be looked at separately from those judged to achieve the desired end points. This will help reduce the variability of the data. Another problem in choosing dependenr variables is the temptation to simply measure everything available and hope to find a few that change. This may be a good strategy for a preliminary exploration of a treatment technique, bur holds many pitfalls. In fact, this is sometimes called "oh heck" research design : Oh heck, let's do this and see what happens! Given enough measures, the probability that one or a few will show significant changes is very high . In fact, if 20 dependent measures are chosen for measurement, expect that one will show a significant outcome by chance (when no effect actually exists). Thus, special statistical tests must be used when several measures are studied to guard against chance significant results. It is best to design a study with a few dependent variables that have either been shown to be affected by rhe independenr variable, or to have good reason for suspecting that they may be so affected.

Characteristics of Well-Designed and Pitfalls of Poorly Designed Osteopath ic Research Good osteopathic research will have the characteristics of any well-designed clinical study. These characteristics include: A complete and well-documented literature search A well-defined working hypothesis Research design is logical and fits the hypothesis Complete and well-documented methodology Statistical methods and data processing procedures defined in advance Power calculations completed Well-defined inclusion and exclusion criteria Both objective and subjective dependent variables Adequate statistic and logistic supporr IRB approval obtained

These characteristics of a well-designed osteopathic trial should lead to reliable and believable data. On the other hand, some of the pitfalls, especially for novice investigators, include the converse of the above, but also some perhaps less-obvious points when planning and conducting research: Planning is incomplete and not well documented Protocols are nor rigorously followed Record keeping is not complete Time for study completion is underestimated Patients cannot be recruited in sufficient numbers Study is too complex Too many dependent variables Many of these areas have been covered earlier in the chapter. However some deserve brief mention here. As a study is carried out, it is very imporranr for the investigator to make sure the protocols are followed at every step. If a mistake is made, ir must be noted and any problem corrected. Mistakes will be made in any prorocol; difficulties arise if the mistakes are not acknowledged. Many investigators underestimate rhe time needed to complete a study. At times, parienrs cannot be recruited readily or replacement patienrs must be sought. These things can add significantly to rhe time required for study completion. A careful invesrigaror plans extra time inro the study design. It is good to offer a bonus to key personnel for subject recruitment and for help with the protocol. As stated in the hypothesis section, a simple study is often the best one. A study with roo many hypotheses ro be rested or roo many dependent variables or measures can become uncontrollable and even impossible to analyze. lt is ofren better to perform several small, well-designed studies that together paint a picture, than one large, complex study that is nor interpretable.

CONCLUSION Clinical research in osteopathic medicine is at the cutting edge of research design technology. The uncertainties surrounding controls, dependent variable measures, and interpretation of results makes it a difficult and challenging field. Well-designed studies that make a small contribution to understanding the mechanisms and efficacy of manipulative treatment, such as are now coming out in the osteopathic literature, will eventually paint a compelling and fascinating picture of this treatment modality. The profession must take full advantage of the fourth osteopathic period of research to strengthen its foundation in rhe coming years.

REFERENCES 1. Smith WA. Skiagraphy and the circulation.] Osteopath. 1899;5(8):365384. 2. Northup GW, ed. Osteopathic Research: Growth and Development. Chicago, IL: American Osteopathic Association; 1987. 3. Burns L. The Nerve Centers, vol ll. Cincinnati , OH: Monfort and Company; 1911. 4. Burns L. Basic Principles, voll. Los Angeles, CA: The Occident Printery;

1907.

74. Foundations for Osteopathic Medical Research 5. Burns L. The Physiology ofConsciousness, vollll. C in cinnati , OH: Monfo rt and Company; 19 1 I. 6. Burns L. Cells ofthe Blood, vo iiV. A. T. Sri ll Research lnsrirure; 1931. 7. Burns L, ed. Pathogenesis of Visceral Disease Following Vertebral Lesions. C hicago, .I L: Ameri can Osteopathic Association; 1948. 8. Kelso AF, Townsend AA. T he srarus and future of os teo pathic research. In: Northup GW, ed. Osteopathic Research: Growth and Development. C hi cago, IL: American Osteopathi c Association; 1987:93- 11 7. 9. Denslow JS. The Early Years of Research at the Kirksville College of Osteopathic Medicine. Kirksville, MO: Kirksvi lle Coll ege of Osreoparhic Medicine Press; 1982. I 0. Denslow JS, Korr IM , Krems AD. Quantitative studies of chronic faci litation in human moroneuron pools. Am j Physiol. 1947; 105(2):229238. 11 . Ko rr IM . The neural basis of rhe osteopathic les ion. jAm Osteopath Assoc. 1947: 19 1- 198. 12. Korr IM. The emerging co ncept of rhe osteopathi c lesion. jAm Osteopath Assoc. 1948;Nov:l -8. 13. Beckwith G. T horacic verteb ral mechani cs. jAm Osteopath Assoc. 1944;43:436-439. 14. Sri II AT. Autobiography ofA. T. Still. Ki rksville, MO: A. T. Sri II ; 1897. 15. Sti ll AT. Osteopathy Research and Practice. Kirksvill e, MO : The P ioneer Press; 19 10. I G. Non hup GW. Osteopathic Medicine: An American Reformation. C hicago, LL: American Osreoparhic Association; 1966. 17. Patterson MM, Howell JN , eds. The Central Connection: Somatovisceral Viscerosomatic Interaction. Indianapolis, IN: American Academy of Osteopathy; 1992. 18. Enserink M. Helsinki 's new clin ica l rules: Fewer placebos, more disclosure. Science. 2000;290(20 Ocrober):4 18-4 19. 19. Eman uel EJ , Wend ler D , Grady C. What makes cl ini cal research ethical? }AM.A. 2000;283(20):270 1-27 11. 20. Taylo r T E. Increased Supervision of C lini ca l Research ar Home and Abroad. jAm Osteopath Assoc. 200 1; I 01 (I 2):696-698. 21. Parrerso n MM , Steinmetz J E. Lo ng- lasring altera tions of spinal refl exes: A porenrial basis for so ma ric dysfun ction. jAm Osteopath Assoc. 1986;2:38-42. 22. Willard FW, Patterson MM , eds. Nociception and the NeuroendocrineImmune Connection. Indianapolis, IN: American Academy of Osteopathy; 1994. 23. Van Buskirk RL. Nociceptive reflexes and the so matic dysfunction: A model.} Am Osteopath Assoc. 1990;90(9):792-794. 24. Denslow JS, Korr IM , Krems AD . Q uantitative studies of chronic facil itation in human moroneuron pools. Am} Physiol. 1947:229-238 . 25. Patterso n, MM. Mechanisms of class ica l conditioning and fixation in spinal mammals. Adv Psychobiol. 1976;3:38 1-436. 26. Patterson MM , GrauJW, eds. Spinal Cord PLasticity. Bosro n, MA: Kluwer Academic Publishers; 200 I. 27. Shekelle PG , Adams AH , Chassin MR, et al. Sp inal manipulation for low-back pain. Ann Intern Med. 1992; 11 7(7):590-598. 28. Dawson B, Trapp RG. Basic and Clinical Biostatistics, 3 rd ed. New York, NY: L-Ing Medical Books/McG raw- Hill; 200 I. 29. Johnso n SM, Bordinar D. Professiona l idenriry: key ro the furure of d1e osteopathic medical profession in the United Sta tes. j .Am Osteopath Assoc. I 998;98(6):325-331. 30. Johnso n SM, Kunz ME. Diminished use of osteopath ic manipulative treatme nt and irs impacr on the uniqueness of the osteopathic professio n. A cad Med. 20 0 I ;76(8):82 1-828. 3 1. John son SM, Kurtz ME, Kurtz JC. Va riables influencing th e use of

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osteopathi c manipulati ve treatment in fam il y. jAm Osteopath Assoc. 1997;97(2):80-87. Trochim WMK. The Research Methods Knowledge Base, 2 nd ed. C ir1cinnati, OH: Aromic Dog Pub lishin g; 200 I. G ree nberg RS. Medical Epidemiology, 2 nd ed. New Yo rk, NY: App leton & Lange; 1966. Buerger AA. A controlled trial of rotation al manipul ation in low back pain. Man Med. 1980;2: 17-26. Hoehler F, Tobis J, Buerger AA. Sp in al man ipul atio n for low back pain. }AMA. 1981 ;245(18): 1835-1838. Wells MR, Giantinoro S, D 'Agare D, et al. Sta ndard osteopathic manipulative treatmenr acutely improves ga it performance in patients wirh Parkinson's disease. jAm Osteopath Assoc. 1999;99(2) :92- 98. Korr IM. Osteopathic medicine: the profess ion's rol e in society. j Am Osteopath .Assoc. 1990;90(9) :824-832. Andersson GBJ , Lucente T, Davis A, er al. A co mpariso n of osteopathic spin al manipulation wirh standard ca re for pati ents with low back pain. N Eng/] Med. 1999;34 1(19): 1426- 143 1. Jo nes LH. jones Strain-Counterstrain. Boise, ID: Jo nes Stra in Co unterstrain; 1995 . (Avai lable from the Ameri can Academy of Osteopathy, Indianapolis, lN.) W illard FH , Swartzlander B. Basic Research and Osteopathi c Medi cin e. In : Ward RC, ed. Foundationsfor Osteopathic Medicine. Baltimore, MD: Wi lliams & Wilkins; 1997; 1107- 1 11 4. Hoehler FK, Tobis JK, Buerger AA. Spinal manipulation for low back pain. }AMA. I 981 ;245(1 8) : 1835-1838 . Hulley SB, C ummings SR. Designing Clinical Research: An Epidemiologic Approach. Baltimore, MD: Wi lliams & W ilkins; 1988. Kaprow MG, Sandhouse M. Refracro ry ron ico llis after a fall. j Am Osteopath Assoc. 2000; 100(3): I 48-150. Pocock SJ. Clinical Trials: A Practical Approach. New York, NY: John Wi ley and Sons; 1983. Keating JC, Sevi lle J , Meeder WC, et al. lntrasubj ect experim ental designs in osteopathic medicine: Appli catio ns in clini cal practice. j Arn Osteopath Assoc. 1985;85: 192-203. Frymann VM, Carney RE, Sprin gall P. Effect of osteopathic medical management on neurologic development in children. JAm Osteopath Assoc. I 992;92(6) :729-744. Daniel WW Biostatistics: A Foundation for Analysis in the Health Sciences. New York, NY: John Wi ley and Sons; 1999. Byrne DW. Publishing Your Medical Research Paper: What They Don't Teach You in Medical School, 2nd ed. Baltimore, MD: Williams & Wi lkins; I 998. Publication Manual of the American Psychological Association, 5rh ed. Washington , DC: American Psychologi cal Associatio n; 200 I. Beecher HK. T he powerful placebo. }AMA. I 955; 159( 17): 1602- 1606. H robjarrsson A, Go tzsche PC. ls the placebo powerl ess? An analysis of clini cal trials comparing pl acebo with no treatment. N Eng/} Med. 200 I ;344(21): 1594-1602. Kiene H . A critique of the double- blind clinical trial. Altern Ther Health Med. 1996;2(1):74-80. AI- Khatib SM , KaliffRM , Hassel blad V, et al . Placebo co ntrols in shortterm clinical trials of hypertension. Science. 200 I ;292(15 June):201 320 15. Kien le GS, Kiene H. Pl acebo effect and placebo co ncept: A critical methodological and co nceptual analysis of reports on me magnitude of d1 e placebo effect. Altern Ther Health Med. 1996;2(6):39-54. Murphy KR, Myors B. Statistical Power Analysis. Mahwah, NJ: Lawrence Erlba um Associates; 1998.

THE RESEARCH STATUS OF SOMATIC DYSFUNCTION DEBORAH M . HEATH NORMAN GEVITZ

KEY CONCEPTS • • • • •

History and definition of somatic dysfunction Inrerexaminer agreement of palpatory findings Instrumentation and identification of somatic dysfunction Clinical correlations of somatic dysfunction Current challenges of clinical research

HISTORY One of the many challenges facing osteopathic clinical research is to simulate the clinical encounter as closely as possible. Another is to capture the distinctiveness of the operating osteopathic principles while studying the influences of the practical application of these principles (1) . Although individual osteopathic clinicians have claimed positive clinical results, systematic and controlled research has been progressing slowly. Historically, scientific inquiry ar osteopathic colleges and hospitals has not had a high priority in a profession where rhe major emphasis has been placed on the laudable service goal of producing primary care physicians (2). Consequently, osteopathic researchers have often struggled to find the resources and the time to conduct scientific studies on the distinctive diagnostic and therapeutic aspects of osteopathic principles and practices. External sources of funding have been difficult to secure. Through its Bureau of Research, the American Osteopathic Association has annually devoted a small pool of funds to support mostly pilot studies. It has, however, committed several hundreds of thousands of dollars to underwrite Andersson and associates' (3) large outcome study comparing the management of back pain by MDs and DOs, which was recently published in the New England journal ofMedicine. A distinctive aspect of osteopathic practice is the identification of the presence of "somatic dysfunction" and its relevance to health. The particular role of somatic dysfunction, once referred to as "the osteopathic lesion," in health and illness has irs roots in studies initially conducted at the A. T. Still Research Institute in Chicago by John Deason early in the century, later

by Louisa Burns on the Pacific Coast, and then by J. Stedman Denslow and Irwin Korr and their associates at Kirksville in the 1940s and beyond (4). Although basic science research on rhe phenomenon that became known as somatic dysfunction made considerable strides in decades pas t, din ical research has been difficult to conduct due to several methodological and resourcebased factors . Ideally, an instrument that could objectively identifY somatic dysfunction and irs relationship to physiologic and pathologic processes would expedite the understanding of palpatory findings and simplifY some of rhe unique challenges in osteopathic clinical research. To dare, objective measurement of somatic dysfunction remains elusive. The term somatic dysfunction is of relatively recent origin. As early as 1863, the English anatomist and surgeon, John Hilton, identified what he called "sore spots" along the spinal column, which he associated with pathology at segmentally related viscera (5). Andrew Taylor Still used several descriptive terms to denote the meaning of his palpatory findings (6) . The term "osteopathic or bony lesion" gained currency with the work of Lo•1isa Burns (7); however, the term "osteopathic lesion" gradually declined as a physiologic understanding of the phenomenon gained favor over the conception of an anatomic displacement. D enslow and Korr's work led to the concept of the "facilitated segment," which helped explain certain patterns of spinal findings that were not necessarily segmentally related to pathology elsewhere (8). In recent decades, the Educational Council on Osteopathic Principles (ECOP), using consensus-based discussions, fleshed our the concept of somatic dysfunction. Somatic dysfunction is currently described as an "impaired or altered function of related components of the somatic (body framework) system: skeletal, arthrodial, and myofascial structures, and related vascular, lymphatic, and neural elements ... The positional and motion aspects of rhe somatic dysfunction may be described using at least one of three parameters: a) the position of the element as determined by palpation and referenced to its adjacent structure, b) the directions in which motion is freer, and c) the directions in which motion is restricted" (9). The early 1980s marked a transition for several forms of osteopathic clinical research. Increased attention was devo ted to understanding the distinctive diagnostic procedures osteopathic physicians employed to identifY somatic dysfunction. For

75. The Research Status of Somatic Dysfunction example, Dinnar, Beal and associates (1 O) videotaped 15 actual doctor-patient encounters and categorized five classes of musculoske.Jetal diagnostic procedures. Three classes of diagnostic tests (i.e., general impression, regional motion testing, and position of landmarks) were not considered unique to osteopathic diagnosis. However, in two classes of procedures, involving vertebral segment location and motion characteristics, the authors concluded that these constituted distinctly osteopathic procedures. They noted that tests in these two latter classes required high levels of sensory skill, precise anatomic knowledge, and were subject to considerable individuality in their application by different physician·s. Knowing more about these distinctive osteopathic diagnos tic procedures was fundamental in steering the direction and amplifying the quality of osteopathic clinical research. By incorporating these unique diagnostic procedures into osteopathic clinical research, it was believed that the somatic component of health and disease could be more precisely identified, and its role in health and disease could be elucidated. The nature of the somatic component and how it is exhibited in health and disease continues to be a crucial question for the osteopathic profession. This chapter on somatic dysfunction will focus on clinically oriented research that has been published in the journal of the American Osteopathic Association (JAOA) since 1980. Research studies involving certain forms of osteopathic diagnosis not focused on the spine will not be discussed here nor will research on general physiologic benefits of osteopathic manipulative treatment (0 MT). Rather, we will consider three categories of somatic dysfunction-oriented clinical research over the last 2 decades. The first category is interexaminer agreement and somatic dysfunction. The second category is the use of instrumentation and somatic dysfunction. The third category is the clinical correlations of somatic dysfunction.

INTEREXAMINER AGREEMENT AND SOMATIC DYSFUNCTION Throughout much of the osteopathic profession's history, clinicians have reported the presence of"lesions" or somatic dysfunction based on their own understandings. These findings were generally nonstandardized and lacked independent verificationeither through other examiners or through instrumentation. Nevertheless, over the years, there have been studies where multiple examiners, blinded from each other's evaluation, have tried to determin e whether there existed a high correlation of their palpatory findings. Beal reported on nine such studies completed from 1951 to 1985 that looked at patterns of somatic dysfunction throughout the spinal column (11 ). Beal graphed the distribution of somatic dysfunction findings of these researchers and concluded that the incidence of somatic dysfunction was not uniform throughout the spine. He noted there were peaks and valleys, with the peaks occurring at the transitional areas of the spine (i.e., the occipital area, the cervicothoracic area, the thoracolumbar area, and the lumbosacral area). Nevertheless, Beal noted great variation in reported findings between studies. He attributed these discrepancies to observer influence, differences in testing procedures and their interpretation, and different subject populations. He noted that osteopathic researchers did not share

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a broadly accepted protocol of tests for the evaluation of spinal somatic dysfunction other than general categories of tissue texture, asymmetry of bony landmarks, and segmental joint motion. Experience in doing structural examinations was also a critical variable. In 1980, Kappler reviewed the results of 837 examinations performed on the same patients by experienced osteopathic physicians and students in a hospital setting between 1969 and 1972 (12). He found that student examiners tended to record more findings and that the findings of experienced examiners were more localized in groups than specific areas. He concluded that the experienced examiner tends to discard "insignificant" findings prior to their possible entry onto the medical record. McConnell, Beal, and associates (13) noted the problem of low interexaminer agreement in a study published in 1980. Six osteopathic physicians each examined upward of 15 of 21 volunteer patients with acute spinal complaints. They reco rded their findings numerically on a scale ofzero to three with respect to clinical significance. lnterexaminer agreement on segmental location was low. Of25 area-by-area comparisons, only four demonstrated significant agreement. The authors concluded that if high levels of interexaminer agreement were to be achieved, the examiners must first agree on the areas to be examined, the test procedures to be used, the method of quantifying the intensity of the findings, and the method of recording. The effort to standardize diagnostic procedures among multiple examiners in research on spinal somatic dysfunction has been led by William Johnston and his associates. In their 1981 study of interexaminer agreement, Johnston and co-workers focused on passive gross motion characteristics along the vertebral columns of human subjects using a series of selected palpatory tests (14). Six gross motion tests were used on 161 subjects . Each of three examiners performed a test three times on the same subject and recorded three findings. Criteria were established for agreement among examiners and for subjects with inconsistent findings among examiners. Data from two tests revealed better than random agreement with a high confidence level for cervical rotation (less than 0.00 1). Subjects with inconsistent findings contributed greater than 25% of disagreement for each of the six tests. In their next study, Johnston and associates (15) hypothesized that a high level of interexaminer agreement could be obtained on passive motion testing of selected subjects with "stable" (i.e. , persistent) findings of regional motion asymmetry. They noted that because transient findings are more likely to change during the multiple examinations needed ro rest interexaminer agreement, subjects with major findings that were stable needed ro be identified. The agreement o.f two examiners on the direction and the intensity of asymmetrical response ro cervical rotation was used ro identify 14 subjects with stable palpable findings from a total sample of70 subjects. Data from examination of all 14 subjects by a second set of examiners revealed a high level of agreement on subjects with stable findings. Using a numerical scale to substitute for directions of findings, permutation testing revealed a confidence level of less than 0.01. In a third study, Johnston and associates (16) selected procedures of palpatoryexamination and established criteria for finding segmental dysfunction in the thoracic spinal region. Five trained individuals examined 30 subjects for deep tissue tension about a bony segment. The intensity of findings was graded on a scale

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of zero (least) to three (most). For each of the five examiners, agreement levels exceeded 79% in distinguishing between two marked segments, one with relatively normal tension (less than one) and one with increased deep tissue tension (greater than two). Statistical analysis rejected the hypothesis that the distribution of agreements could have been reached by chance (chi square calculated 91.3 versus 3.84).

INSTRUMENTATION AND SOMATIC DYSFUNCTION The validity of palpatory findings has been advanced through interexaminer studies. However, even if two or more examiners have a high degree of agreement as to the presence or absence of somatic dysfunction, it is highly desirable to have subjective findings documented through objective instrumentation. Indeed, while working with electromyography in the 1940s, Denslow and associates (17) wrote the first articles on what became known as somatic dysfunction for basic science research journals. Beginning in 1985, Johnston, Vorro, and Hubbard (18) wrote the first of four papers on employing instrumentation in somatic dysfunction research. In the first study, 16 subjects were placed in groups according to their symmetry or asymmetry, as determined by a palpatory test for passive side-bending of the cervical region. Using kinematic analysis, the authors assessed both active and passive movement responses. Head orientation was measured at the end of range after six primary rotations. Two secondary deviations from each primary rotation were also observed. Data revealed a significant decrease in all six primary ranges in the combined asymmetric groups as compared with the symmetric group. A similar relationship was observed for secondary deviations. There was no significant difference in these motions between the right and left asymmetric subgroups. The authors concluded that the palpable clinical sign of asymmetry in response to passive cervical side-bending appears to be an early indicator of a measurable impairment of cervical function . In the second publication of this series, Vorro and Johnston ( 19) reported myoelectric data collected simultaneously with their kinemetric study. Three specific muscle sites and three spinal sires on the paravertebral musculature were each monitored bilaterally. A profile analysis was used to examine relationships among subject groups, head motion, muscles, and side of recording for the time elapsed prior to the beginning of electrical activity. When all movements were considered and analyzed, a significant interaction between symmetry and side resulted (p :::0 0.03). This indicated that in regard to muscular activity at each of the six sites, symmetric subjects differed from asymmetric subjects when right- and left-side measures were considered. Asymmetric subjects were slower to initiate action, and the action was reduced in time and strength of contraction. The third paper addressed additional kinematic data collected regarding three-dimensional orientations of the head accumulated throughout the paths of movement (not just at their end points, as in their previous reports) (20). The fourth paper evaluated 34 asymptomatic subjects categorized to symmetry group based on initial palpatory rests comparing regional motion responses of the head and neck to right and left side-bending (21).

Electromyographic techniques were used to study muscular activity, indicating contraction frequency for each muscle monitored during active and passive motions. Subjects diagnosed with regional motion asymmetry exhibited a significantly altered organization of electrically active and electrically silent muscles. This pattern of muscle contraction was compromised just as frequently in the passive as in the active phases of motion. In addition to kinematic and electromyographic studies, a few osteopathic researchers have experimented with thermography as a means of correlating palpatory findings of somatic dysfunction with instrumental methods. Kelso, Grant, and Johnston (22) evaluated thermographic measurement of skin temperature of the back to determine the feasibility for its use on osteopathic examination and manipulative treatment. In 35 subjects, they found variation in skin temperature of2° to 3° Celsius. Although they found no uniform pattern of variation, warm and cool areas could be identified. In another pilot study, Walko and Janouschek (23) employed thermography to provide information on how cervicothoracic pain responds to OMT. Of five women subjects receiving OMT, all demonstrated a decrease in skin temperature of the cervicothoracic region after treatment. To date, however, it would appear that thermographic findings do not offer sufficient specificity for research purposes on somatic dysfunction.

CLINICAL CORRELATIONS The identification and location of somatic dysfunction, whether through interexaminer reliability studies or through the correlation of palpatory findings with instrumental measures, has particular meaning if somatic dysfunction can be associated with specific clinical entities for the purpose of diagnosis and treatment. In 1980, Kelso, Larson, and Kappler (24) reported general findings of a study conducted a decade earlier on more than 6,000 hospital patients who received a structural exc.mination. The authors concluded that there was an increased frequency of findings in somatic tissues segmentally related to diseased viscera. However, they also noted that it was evident from the results that the frequency of any one somatic fjnding in a region or segment did not predict the health status of a patient and that there was no specific segmental relationship that will signal probable presence of visceral disease. In the 1970s, Johnston and associates (25) looked at the relationship between spinal findings through palpation and hypertension. They reported somatic findings on normotensive and hypertensive patients, providing evidence of a consiste11cy in location of specific palpatory findings arranged in a pattern within the cervicothoracic region of some hypertensive patients. In 1980, they reported a preliminary interexami ner reliability study of 132 subjects (26). Three trained examiners ascertained the presence or absence of three components of the somatic pattern that had been described. Twenty-seven agreements were possible based on three motion tests used to examine each of nine vertebral segment levels in the cervicorhoracic region. There was a high frequency of agreement among the three examiners on the presence of pattern components in hypertensive subjects (77%), and low frequency of agreement on the presence of pattern

75. The Research Status of Somatic Dysfunction components in normotensive patients (25%). Although the absolute level of inrerexaminer agreement in this study was only 40%, the difference berween the value and the value predicted on the basis of a random distribution of agreemenrs was highly significan r. In a third srudy, Johnsron and associates (27) looked at 307 normotensive and hyperrensive volunteers. In this srudy, they used agreemenr on findings of three independenr trained examiners during three consecutive examinations of the spinal region CS ro T7 as the criteria for persistence of palparory cues . Distribution of agreements on presence of stable findings was bimodal, with the values in the lower range of agreement fitting closely ro the frequency predicted by a random model. Within this lower agreemenr range of 216 subjects with unstable findings, there were 48 hypertensive patients (22.2%). Within the group of 91 subjects with stable findings, there were 48 hyperrensive patients (52.7%) The researchers concluded that a relationship exists berween the hypertensive condition and a reproducible somatic component. More recently, Johnsron, Kelso, and associates (28) extended this general line of research. A standardized palparory examination determined whether there were specific motion asymmetries cenrered at spinal segments C6, T2, and T6 in 253 normotensive and hyperrensive subjects. The examiner was blinded as ro whether a subject was hypertensive. Of 193 volunteers independently diagnosed as hypertensive, borderline, and graded, 113 (56%) were found by the researchers ro have the C6T2T6 partern. Of 61 normotensive patients, 24 (39%) were found with this pattern. Of these subjects, 184 (73%) agreed ro return for follow-up examination 4 ro 8 months later. Of the 132 rerurning hypertensive and normotensive patients with the C6T2T6 pattern on initial visit, this pattern persisted in 118 (89%) individuals. Johnsron and Kelso (29) later completed a longirudinal study that demonstrated, among other findings, that the C6T2T6 pattern persisted from 3 ro 10 years in 16 of 16 subjects with a grade rwo or greater hyperrension. Inrerestingly, several additional studies have focused on the role of somatic dysfunction in cardiovascular disease. Beal (30) looked for somatic dysfunction in 108 patients already diagnosed with a variety of cardiovascular problems, including coronary arrery disease, ischemic heart disease, angina, myocardial infarction, hyperrension, hypertensive cardiovascular disease, congestive heart failure, valvular disease, arrhythmia, and pericarditis. Of all the patients in his study, Beal found 94 (87%) had segmental dysfunction of rwo or more adjacenr vertebrae from T 1 roTS on the left side. Somatic dysfunction at C2 on the left was also present in 69 (63%) patients. Beal recognized certain biases in his study. As patients were examined from the cardiac service, there was an expectation on the parr of the examiner that a pattern of somatic dysfunction would be observed. Cox and associates (31) studied a series of 97 consecutive patients who had cardiac catheterization. Within 1 week of angiography, patients underwenr a musculoskeletal examination consisting of segmenral evaluation of pain, range of motion, soft tissue texture, and "red reflex" by a blinded examiner. Univariate and multivariate analysis revealed a high correlation berween coronary atherosclerosis and abnormalities of range of motion and soft tissue texture at T4.

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In a study that was somewhat similar ro rhar of Cox et al., Beal and Kleiber (32) looked for somatic dysfunction in 99 patients scheduled for cardiac catheterization on the day preceding angiography. Somatic dysfunction was found on the left side from T1-5 in 85 patients. In 70 patients, diagnosed somatic dysfunction correlated with evidence of coronary artery disease, although in 15 cases, somatic dysfunction was associated with the cardiologist's diagnosis of normal or subclinical disease. The authors considered the issues of"sensitivity" and "specificity" of their testing. The sensitivity of rhe test for left-sided somatic dysfunction in the T1-5 region as a predicror of the incidence of true positive results for the diagnosis of coronary artery disease in this study was 92%. However, the specificity of the test for left-sided somatic dysfunction in the same region as a predictor of the incidence of true negative results (i.e., patients who did not have coronary artery disease) was only 30%. Thus, the authors concluded that the palpatory test should not be used as a specific test for coronary artery disease. A paper by Nicholas and associates (33), first published in the British Medical journal and later reprinted in ]AOA, looked at patterns of somatic dysfunction related ro myocardial infarction (MI). Sixty-rwo parienrs were randomized for the purpose of being seen by DOs for palpation of segments T1-8. Twentyfive patients had clinically confirmed acute MI. Twenty-rwo patients without known cardiovascular disease served as controls, and 15 were excluded because of diagnosed cardiovascular disease other than MI. The control group was found to have a low incidence of palpable changes throughout the thoracic region uniformly distributed from T1-8. The MI group evidenced a significantly higher incidence of soft tissue changes confined almost entirely to the upper four thoracic levels. The authors concluded that their data suggest that myocardial infarction is accompanied by characteristic soft tissue changes that are readily detected by palpation. In addition ro cardiovascular studies, rwo other articles from the 1980s considered the relationship berween somatic dysfunction and other organ systems. In reviewing hisroricallirerarure, Beal and Morlock (34) determined that the majority of previously published palpatory findings of somatic dysfunction and pulmonary disease occurred within the spinal area ofT2-7. To rest these findings, rhe authors recruited 40 patients with diagnosed pulmonary disease. On examination, they found that all patients showed evidence of somatic dysfunction in the pulmonary reflex area ofT2-7. In a controlled clinical trial, Johnston, Kelso, and associates (35) examined three groups of patients to rest the assumption that somatic manifestations of renal disease would be present in the spinal region of T9-12. One group had advanced renal disease; rhe rwo control groups consisted of normotensive and hypertensive patients without signs of renal disease. Recorded findings of both palpatory examination and thermography of the thoracic spinal region revealed a significantly higher frequency of segmental dysfunction and areas of elevated skin temperature in the region ofT9-12 for the renal group. More recently, as parr of a broader study, Reeves and associates (36) found that the average gross number of somatic dysfunctions in 14 patients abstaining from caffeine increased from 3.57 at point of withdrawal to 7.78 on day four after withdrawal.

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VIII Basic and Clinical Research fo r Osteopathic Theory and Practice

However, the specific locations of the somatic dysfunction were neither identified nor correlated. The positive findings of some of these aforementioned clinical studies were subjected to serious methodological challenge by Tarr and associates (37). In this study, the researchers attempted to ascertain whether experienced DOs could diagnose disease states using palpatory findings as their source of diagnostic clues . Five examiners saw a total of 100 subjects. Two of the examiners were allowed to palpate the subject; the other three were not. None of the five examiners had any knowledge of the subject's medical history, and none were allowed to talk to the subjects. Nonpalpating examiners had only visual clues to aid in diagnosis while the palpating examiners had both vis ual and palpatory clues. Of the 100 subjects, 22 had documented gastrointestinal disease, 31 individuals were demonstrated to have asthma, and 47 control subjects had a negative history for either gastrointestinal pathology or asthma. The results showed that neither the palpating nor the nonpalpating physicians could correctly categorize the subjects as gastrointestinal patients, asthma patients, or controls. The authors noted that in some previous studies correlating palpatory findings with pathologic states, the researchers already knew their subjects were ill or even that they suffered from some specific condition. This knowledge could bias results. Tarr and associates concluded that reports of specific palpatory findings being associated with pathologic states required further studies on the accuracy of palpatory findings be conducted. The design of such studies, they maintained, should include an analysis of both total correct and incorrect observations. In addition, they argued that a well-designed investigation of the accuracy of palpatory diagnostic techniques required some control for nonpalpatory clues. The arguments ofTarr and associates with respect to the adequacy of prior clinical correlation studies, the results they obtained in their study, as well as the greater controls they recommended to be built in to this type of research, may have unintentionally contributed to a decline in conducting further clinical correlation projects. Some clinical researchers have instead turned their attention to conducting studies that look at various effects of osteopathic manipulation but do not directly tie the treatment given to the specific locations where spinal somatic dysfunction is located. Indeed, aside from the work of Johnston and Kelso on hypertension, it would be 10 years before another clinical correlation study by different authors would appear in the ]AOA. In 1997, Iwata, Rodas, and associates (38) obtained permission to perform a musculoskeletal structural examination on each of the subjects in a study of 60 hospitalized patients with psychotic and affective disorders. The results of this study indicated that psychotic and affective disorders each tend to affect a different portion of the musculoskeletal system. Psychotic patients exhibited increased musculoskeletal dysfunction in the lower extremities. Patients with affective disorders were found to exhibit increased cervical and thoracic dysfunction. The authors suggested that at the clinical level, the structural examination may be used to correlate psychiatric disorders with dysfunctional regions of the musculoskeletal system. Given Tarr and associates' aforementioned conclusions, it was perhaps not surprising that the author of a letter to the]AOAeditor (39) critiquing this article observed that it suffered for not comparing psychiatric patients with appropriate control subjects.

CONCLUSION Clinical research on somatic dysfunction is sti ll in its formative stage. Despite a greater number of articles after 1980, inquiry into the nature of somatic dysfunctio n and its clinical significance remains modest. Nevertheless, research under osteopathic auspices has demonstrated that if appropriate training is provided, several examiners can achieve a high degree of agreement on the presence or absence of somatic dysfunction at specific spinal locations. Research has also demonstrated that some instrumentation , most notably electromyography, can provide objective instrument-based evidence confirming palpatory findings. Although several investigators have associated patterns of somatic dysfunction with specific pathologic states, methodological issues of researcher bias have been raised, and future studies will need ro address these concerns. In addition, many of the studies reviewed here are notable for their small sample size. Importantly, none of the studies cited above test whether somatic dysfunction as specifically identified in subjects can be eliminated through the use of osteopathic manipulation, and that such treatments are correlated in any way with demonstrable physiologic changes elsewhere. Osteopathic research on somatic dysfunction is currently at a crossroads. Many of the more productive contributors in the 1980s are now at or past the usual retirement age. In the last 10 years, research on somatic dysfunctio n has appeared to slow. There are currently few full-time faculty members in osteopathic colleges who devote a significant portion of their time to clinical research. A new generation of such researchers needs to be developed from today's students. Arguably, the osteopathic profession has a social and ethical obligation to support research on its distinctive diagnostic, prognostic, and therapeutic aspects. This research must take place to a considerable extent in and be supported by osteopathic colleges and hospitals. Expansion of resources to facilitate institutional research in the osteopathic profession is essential. The methodological difficulties and expense of conducting controlled clinical studies should not prevent increased investment in the ongoing obligation of determining the relative value of distinctive osteopathic app roaches in maintaining or improving the health of patients and building on the body of osteopathic clinical resea rch conducted during recent decades.

REFERENCES I. Korr IM. Osteopathic research: The needed paradi gm shift. jAm Osteopath Assoc. 1991 ;9 1: 156- 171. 2. Gevitz N . "Resea rched and demonstrated: " inquiry and infrastructure in osteopathic institu tions. jAm Osteopath Assoc. 2001 ;10 1:1 74-179. 3. Andersso n G, Lucente T, Davis A, et al. A co mparison of osteopathic spinal manipulatio n with standard ca re for pati ents with low back pain. N Eng!} Med. 1999;34 1:1426- 1432. 4. Gevitz N. The DO's: Osteopathic Medicine in America. Baltimore, MD: Johns Hopkins Un iversity Press; 1982:53-55, 90- 93. 5. Hilton J. On Rest and Pain, 2 nd ed. New York, NY: W. Wood; 1879. 6. Still AT. Osteopathy: Research and Practice. Kirksvi ll e, MO : Pub li ~ h ed by the author; 1910. 7. Burns L. Pathogenesis of Visceral Disease following Vertebral Lesions. Chicago, IL: American Osteopathic Associatio n; 1948.

75. The Research Status of Somatic Dysfunction 8. Denslow JS, Korr IM . Quantitative studies of chronic facilitation in human motoneuron pools. Am] Physiol. 1947:150:229-238. 9. Glossary of O steopathic Terminology. In: Foundations for Osteopathic Medicine. Baltimore, MD: Williams & Wilkins; 1997. I 0. Dinnar U, Beal M, Goodridge J, et al. Classification of diagnostic tests used with osteopathic manipulation.) Am OsteopathAssoc.1980;79:451-

455. 11. Beal M. Incidence of spinal palpatory findings: a review. JAm Osteopath Assoc. 1989;89: I 027- 1035. 12. Kappler R. A comparison of structural examination findings obtained by experienced physician examiners and student examiners on hospitalized patients. JAm Osteopath Assoc. 1980:79:468-471. 13. McConnell D, Beal M, Dinnar U, et al. Low agreement of findings in neuromusculoskeletal examinations by a group of osteopathic physicians using their own procedures. JAm Osteopath Assoc. 1980;79:441-

450. 14. Johnston W, Elkins M , Marino R, et al. Passive gross motion testing: Part II. A study of interexaminer agreement. JAm Osteopath Assoc. 1982;81 :304- 308. 15. Johnston W, Beal M, Blum G, et al. Passive gross motion testing: Part III. Examiner agreement on selected subjects. JAm Osteopath Assoc. 1982;81 :309-313. 16. Johnston W, Allan B, Hendra J, et al. Interexaminer study of palpation in detecting location of spinal segmemal dysfunction. JAm Osteopath Assoc. 1983;82:839- 845. 17. D enslow J. Pathophysiological evidence for the osteopathic lesion. In: Goldstein M, ed. The Research Status of Spinal Manipulative Therapy. Bethesda, MD: U. S. Dept. of Health, Education, and Welfare; 1975:227-234. 18. Johnston W, Vorro J, Hubbard R. Clinical/biomechanical correlates for cervical function: Part l. A kinematic study. JAm Osteopath Assoc. 1985;85:429--437. 19. Vorro J, Johnston W. Clinical biomechanic correlates for cervical function: Parr II. A myoelectric study. JAm Osteopath Assoc. 1987;87:353367. 20. Vorro J, Johnston W, Hubbard R. Clinica l biomechanic correlates for cervical function: Part Ill. lntermittem secondary movements. JAm Osteopath Assoc. 1991;91: 145- 155. 21. Vorro J, Johnston W. C linical biomechanic correlates of cervical dysfunction: Parr 4. Altered regional motor behavior. JAm Osteopath Assoc. 1998;98:317-323. 22. Kelso A, Gram R, Johnston W. Use of thermograms to support assessment of somatic dysfunction or effects of osteopathic manipulative treatment. JAm Osteopath Assoc. 1982;82: 182- 188.

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23 . Walko E, Janouschek C. Effects of osteopath ic manipu lative rreatmem in patients with cervicothoracic pain: Pilar study using thermography.

JAm OsteopathAssoc. 1994;94:135-141. 24. Kelso A, Larson N, Kappler R. A clinical investigation of the osteo pathic exam ination. JAm Osteopath Assoc. 1980;79:460--467. 25. Johnston W. lnrerexaminer reliabiliry studies: spanning a gap in medical research. JAm Osteopath Assoc. 1982;81 :819- 829. 26. Johnston W, et al. Palpatory findings in the cerv icothoracic region. Variations in normotensive and hypertensive subjects. A preliminary report.

JAm Osteopath Assoc. 1980;79:300- 308. 27. Johnsron W, Hill J , Elkiss M, et al. Identification of stab le somatic

28.

29.

30. 31.

findings in hypertensive subjects by rrained exam in ers using palpatory examination. JAm Osteopath Assoc. 1982;81 :830- 836. Johnston W, Kelso A, Babcock H. Changes in presence of a segmenta l dysfunction pattern associated with hypertension: Parr 1. A short-term longitudinal study. JAm Osteopath Assoc. 1995;95:243- 255 . Johnston W, Kelso A. Cha nges in presence of a segmental dysfunction pattern associated w ith hypertension: Parr 2. A long-term lon giwd in al study. jAm OsteopathAssoc. 1995;95:3 15- 318. Beal M. Palpatory testing for somatic dysfunction in patients with ca rdiovascular disease. JAm Osteopath Assoc. 1983;82:822-83 1. Cox J, Garbis S, Dick L, et al. Palpable musculoskeletal findings in coronary artery disease: Results of a double-blind study. jAm Osteopath

Assoc. 1983;82:832-836. 32. Beal M, Kleiber G. Somatic dysfunction as a predicror of coro nary arrery disease JAm Osteopath Assoc. 1985;85:302- 307. 33. Nicholas A, DeBias D, Ehrenfeuchter W, et al. A somatic co mpo nem to myocardial infarction. JAm Osteopath Assoc. 1987;87:123-129. 34. Beal M, Morlock J. Somatic dysfunction associated with pulmonary disease. JAm Osteopath Assoc. 1984;84: 179-183. 35 . Johnsron W, Kelso A, Hollandsworth D, et al. Somatic manifestations in renal disease: A clinical research study. JAm Osteopath Assoc. 1987;87 :2235. 36. Reeves R, Struve F, Parrick G. Somatic dysfunction increase during caffeine withdrawal) Am Osteopath Assoc. 1997 ;97 :4 54--456. 37. Tarr R, Feely R, Richardson D , et al. A co nrrolled study of palpatory diagnostic procedures: Assessment of sensitiviry and specificity. JAm Osteopath Assoc. 1987;87:296-30 1. 38. Iwata J, Rodas J, G lonek T, et al. Comparin g psychotic and affective disorders by musculoskeletal srructural exam ination . ) Am Osteopath Assoc. 1997;97:715-720. 39. McPartland J. C lari fying inaccuracies made regarding neuropsychiarric disorders and musculoskeletal exami nations. jAm Osteopath Assoc. 1998;98:477--478 (letter).

OUTCOMES RESEARCH AND DESIGN RICHARD J. SNOW JOHN C. LICCIARDONE RUSSELL G. GAMBER

The various diagnostic and therapeutic interventions available to health care providers have grown exponenrially over the last 3 decades. Although the efficacy (how well these intervenrions perform in a conrrolled setting) of many of these interventions is often demonstrated in randomized clinical trials, their effectiveness in larger populations is often unknown. For example, a surgical procedure that removes plaque from the carotid artery, caro tid endarterectomy, had been used for 20 years before two large, randomized clinical trials, the North American Symptomatic Carotid Endarterectomy Trial (NASCET) (1) and the Asymptomatic Carotid Atherosclerosis Study (2) defined the procedure's efficacy in stroke reduction . These randomized clinical trials enrolled patients into surgical programs with low perioperative stroke and mortality rates. Thus, the actual results obtained in the general community may vary widely from those obtained in the co ntrolled studies (3). This is one example of the importance of traclcing outcomes in clinical practice. Understanding the principles of outcomes research, including irs biostarisrical and epidemiologic underpinnings, provides clinicians with the knowledge necessary to evaluate the strengths and weaknesses of various research designs and to better assess the therapeutic value of a given intervention. Also, as clinicians function under increased expectations of practicing evidence-based medicine, they will need to evaluate the biomedical literature and understand the ration ale behind clinical practice guidelines.

EVALUATION OF OSTEOPATHIC HEALTH DELIVERY A framework originally attributed to Donabedian (4) describes health care delivery systems in terms of structure, process, and outcomes. Structure can be defined as the physical plant, equipment, human resources, and governance of the health care delivery system. Process is best described as the interaction between rhe parienr and the health care delivery system. Examples can range from the prescription of an antibiotic or diagnostic test to open-heart surgery. Outcomes, rhe results of such clinical interacrions, are frequently used to make judgments about the quality of health ca re. Thus, it is important that osteopathic physicians become engaged as active participants in the evolution of outcomes measurement and management in health care (5) .

Outcomes may be generally measured along four axes. First, clinical outcomes include such events as morbidity, disease complications, and mortality. Second, functional outcomes include measures of physical or mental functioning and may use generic instruments, such as the Medical Outcomes Study Shorr Form-36 (SF-36) or the health status survey (6), or may use condition-specific outcomes tools, such as the srroke impact scale (7), the Roland-Morris disability questionnaire, and the Oswestry disability index for low back pain (8-1 0), and the WOMAC osteoarthritis index for knee or hip osteoarthritis (11) . Third, patients' perceived outcomes focus on parienr satisfaction and use such tools as the patient satisfaction ques tionnaire (PSQ) ( 12) or the Press-Caney instrument (13). Finally, finan cial outcomes are measured by costs, charges, or by surrogates, such as length of stay. The term "outcomes research" broadly encompasses the evaluation of health care delivery using the framework described above. The plethora of medical procedures brought about by advances in biotechnology, combined with increased demands on health care delivery systems because of an aging population , will increase the need for information about the most efficient treatment protocols. Outcomes research will help supply this information. In the realm of osteopathic medicine, outcomes research will help meet increasing demands to quantify the effects that osteopathic treatment, particularly osteopathic manipulative treatment (OMT), has on health (14). The recent des ignation of rhe Texas College of Osteopathic Medicine as the home of the national Osteopathic Research Center represents a response to demands for research on the efficacy of OMT. The implications for osteopathic medicine are obvious as the profession continues to strive to demonstrate irs unique contributions to health care delivery. Recently, as described below, the body of literature addressing the impact of osteopathic medicine on clinical outcomes has been growing. In part, the future of osteopathic medicine relies on continuing and expanding such efforts to empirically demonstrate the unique role that osteopathic physician play in health care delivery. Demands for improved and standardized health care are becoming more apparent to those involved in health care delivery. Administrators of hospitals and health care plans need information to understand the financial impact of evolving technologies for managing health care organizations. Physicians need to

76. Outcomes Research and Design assimilate and understand the mulrirude of diagnostic and therapeutic options ro determine rhe best ways ro treat patients. The sensitivity (abili ty of a rest ro correctly idenrifY patienrs with a disease) and specificity (ability of a rest ro correcrly idenrifY parienrs without a disease) of tests and the expected and observed outcomes of patients will become important aspects of communicating with and managing the health care of patients. The need ro develop methods ro practice evidence-based medicine and ro better understand the outcomes of patients was recenrly reinforced by the Institute of Medicine (15). Their report en tided Crossing the Quality Chasm cited deficiencies of current health care delivery in providing evidence-based medicine in a consistent manner. This latter approach has the potential ro improve the health of patients under the care of osteopathic physicians. This chapter will describe, in a general manner, the rools and methods available ro conduct clinical outcomes research. It will rouch on hypothesis testing, srudy design, and related methodological issues. The chapter provides an overview of the field, with the intent of encouraging those interested in becoming more avid consumers of outcomes research information, as well as those wishing ro add ro the body of knowledge regarding osteopathic medicine. Examples of outcomes research are provided ro demonstrate various approaches ro assessing the impact of osteopathic medicine.

HYPOTHESIS TESTING The foundations of outcomes research are similar ro and largely overlap those of clinical research. The basic rools include epidemiology and biostatistics, a field of statistics concentrating on the unique aspects of statistical resting in biomedical settings. Epidemiology has been defined as the study of the distribution of health-related events in specified populations and the application of such studies ro control health problems (16). Initially, as a basic science for public health, epidemiology was used ro describe diseases according ro person, place, and rime, and to identifY the determinants of disease. Over time, however, epidemiologic methods were used for hypothesis generation and testing in rhe clinical arena. Biostatistics serves ro complement epidemiology by providing the analytical framework for testing hypotheses. A clinical outcomes study begins with the hypothesis. It is essential to develop rational and testable hypotheses by thoroughly reviewing prior research in the field of srudy. Classically, hypothesis development involves framing the fundamental question as a statement indicating that there is no difference in effect or outcomes between treatment and control groups. This so-called "null hypothesis" is then tested in a structured manner. As an example, the null hypothesis in a randomized clinical trial testing a new anticoagulant's effect on deep vein thrombosis would be stated as: "There is no difference between the rates of deep vein thrombosis in patients treated with the new anticoagulant and those treated by conventional methods. " An example of the null hypothesis in an observational srudy examining the effectiveness of carotid endarterecromy in high- and low-volume hospitals would be stared as: "There is no difference in the clinical outcome of patients

1195

H0 False

Study Decision

H0 True

Do not Reject H0

Correct

Type II Error

Type I Error

Correct

Reject H0

FIGURE 76.1. Schemat ic representation of the four possible, mutually exclusive, outcomes of hypothesis testing. Ho denotes the null hypothesis.

receiving carotid endarterectomy in high-volume cenrers versus low-volume centers." Clinical outcomes may be measured by a variety of methods along the four axes previously described. When testing the null hypothesis, two murually exclusive types of errors may occur (Fig. 76.1). If, in the clinical trial of anricoagulation described above, it is erroneously concluded that there is a difference in the rates of deep vein thrombosis between the treatment and conrrol groups, then a type I error is committed. The type I error, caused by rejecting the null hypothesis when it is in fact true, is considered the most important threat in hypothesis testing. Because this type of error results in the erroneous conclusion that a treatment improves parienr care when, in fact, it is no better than placebo or convenrional treatment, tolerance of a type I error is set at a low level. Scientific convention defines the acceptable risk of this event as a and sets irs limit at one rime our of twenty, or 0.05. The p value denotes the actual probability that a type I error was committed in a particular srudy. The other type of hypothesis testing error that may occur in the anricoagularion trial example is to conclude that there is no difference in the rates of deep vein thrombosis between the treatment and conrrol groups when a difference truly exists. This is known as a type II error and irs acceptable risk is defined as {3. Although scientific standards for an acceptable f3 are not as well established as for a, 0.20 is often used. Type II errors are attributed ro insufficient numbers of research subjects for adequately performing hypothesis testing. The number of subjects in a srudy, or sample size, is a measure of rhe statistical power of a study. The relationship between risk, or probabili ty, of a type II error and statistical power is given by the expressiOn: (Probability of type II error)

=

1 - (Power)

Thus, all other things being equal, the probability of committing a type II error can be decreased by increasing the number of subjects in a study. A common pitfall in inrerpreting the biomedical literature involves subgroup analyses, which consider only a subset of subjects in a srudy. Subgroup analyses that fai l to demonstrate a significant difference in clinical outcomes between subgroups may be associated with high probabilities of type II errors because oflimited numbers of subjects. Thus, such subgroup analyses must be

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adequately powered co address the research question or hypothesis at hand; otherwise rype II errors will be likely. This concept has been summarized by the phrase, "the absence of proof is not the proof of absence." An adequate sample size for randomized clinical crials, or subgroup analyses, may be compuced by using four faccors: the minimal difference berween scudy groups char the invesrigacor considers imporcanc enough co detect, the anticipated event rate in the control population, and the acceptable probabilities of committing rype I and rype II errors, a and {3, respectively. Type I and rype II errors in clinical scudies need co be underscood when incerpreting the biomedicalliteracure. Because of the potential for these errors, several randomized clinical crials are needed co rest the same hypothesis before statistical inferences can be comfortably applied in a clinical setting. For example, there were live randomized clinical trials examining the reduccion of stroke risk afforded by the use of warfarin (an ancicoagulant) in individuals with atrial fibrillation. The sixth scudy was scopped when evidence from the preceding scudies was published, as it became unethical co withhold the drug from individuals based on the published informacion. By this account, it cook five studies to define the use of warfarin in atrial fibrillation as the standard of care. The exercise of computing the needed number of subjects for various hypothesis tests increases awareness of the cost of executing clinical studies. Testing a hypothesis that seeks to detect small differences berween study groups, involving a lowfrequency event or end point, can require several thousand subjects. The costs of subject recruiting, acquiring informed consent, collecting data, and tracking participants in such a large group can run in co millions of dollars. Thus, it is important co estimate sample size co avoid embarking on a research project char cannot be realistically implemenced within the available budget and scheduled time frame.

STUDY DESIGN Experimental studies are best exemplified by randomized clinical trials. Such trials, with specific inclusion and exclusion criteria, enroll pari ems and randomly allocate them co treatment and control anns. The external generalizabiliry of a randomized clinical erial is determined by how well the scudy subjects reflect the general population. This is determined, in part, by the selection of subjects through the applicable inclusion and exclusion criteria. In the previously cited NASCET randomized clinical erial, patients aged 80 years and greater were excluded. Because of this, the erial results cannot be adequately extrapolated to determine the effect of carotid endarterecwmy on stroke risk reduction in individuals 80 years of age or older. A rationale for exclusion of older subjects is that the demonstration of a potentially beneficial surgery effect (carotid endartereccomy) over medical treatmenc requires the patient co be observed (i.e., co survive) long enough co offset the 2% risk of stroke or mortaliry associated with surgery. The method of allocating subjects w the treatment or control arms in a randomized clinical trial involves random numbers or other statistical methods to ensure that no bias exists when patients are assigned to one arm or another (Fig. 76.2). This ex-

All individual s Exclu ion criteria

Time

FIGURE 76.2. Selection of subjects for a randomized clinical trial.

peri mental design provides the most valid approach w hypothesis testing. Theoretically, by randomizing the patients to either arm, the investigator removes any patient factors char might bias or confound the results of the scudy. As an example, if investigators resting the hypothesis chat a new anracid reduces the incidence of ulcers sampled subjects in a way that resulted in higher numbers of subjects taking aspirin in the control group, they would likely find a lower rate of ulcers in the creatmenr group. The investigators may erroneously atcribute the lower rate of ulcers to the antacid, when in realiry it may be related co the confounding influence of greater aspirin use among controls compared with those in the treatment group. In this example, aspirin use is considered a confounder because it is associated with both the group assignment and the study outcome. A cruly randomized study would eliminate the threat to validity posed by this confounder by apportioning comparable percentages of aspirin users co each arm of the scudy. Inspection of the baseline characteristics of scudy groups in a randomized clinical trial is useful to assess the adequacy of the randomization process, particularly by checking for potential selection bias and by comparing the frequencies of potential confounders in each group. Similar characteristics in the treatment and control groups provide evidence char randomization has been properly executed. In such cases, randomized clinical trials provide the most accurate assessmenc of the effect of an intervention on patients who are included in the scudy. This represencs high internal validiry. When a comparison of treatment and control groups indicates a subsrancial imbalance in a baseline study variable or important confounder, potencially serious threats to validiry are found. To maincain internal validity, more sophisticated multivariate statistical techniques maybe needed to adjust for such confounder imbalances. Selection biases may be more subtle and difficult, if not impossible, to correct. They may seriously hamper the abiliry to excrapolare study results to other populations, resulting in poor external validiry. Experimental scudies represent the most valid mechanism for hypothesis resting and are the standard of evidence required by the Food and Drug Administration when considering new drug approvals. Experimental studies generally are expensive because they require substantial resources to recruit, randomize, and follow patients over rime. Because of these financial barriers, many interventions commonly used in health care delivery have nor been tested by randomized clinical crials.

76. Outcomes Research and Design O ther obstacles to conductin g randomi zed clinical trials exist, includin g ethical issues. All scientific evidence linking tobacco use to lung cancer is based o n no nrandomized swdies. These are also known as pseudo-ex perimental , qu as i-experimental, or observational sw d ies. Because very ea rl y observatio nal studies suggested there was a stro ng association between lung cancer and tobacco use, a rando mi zed clinical trial res ting the association became unethical because it would require randomi zing individuals to a study arm exposin g them to a cancer-causing age nt. Observatio nal studies can test hypotheses wirhour randomiza tio n of subjects to treatment and co ntrol groups. Although there are several di ffe rent types of observa t ional studies, two rypes are most com mo nl y seen: case-co ntrol , o r retrospective, studies (Fig. 76.3) and cohort, o r prospecti ve, studies (Fig. 76.4). Such stud ies o fte n wo rk well in situations when randomi zed clinical tr ials are no t feasible or possible. T he ability to detect statistical associatio ns between naturally occurrin g events and outcomes cann ot always be do ne using randomized clinical trials. An examp le of this involves ex posure to electro magneti c fields and risk of leukem ia. T he association between the two has been h ypothesized fo r the las t several decades. Tes ting th e hypothesis using a ra ndom ized cl inical trial would be impracti cal for several reasons. First, the ethical issues regardin g human research subjects are obvio us when setting up an experiment that would be exposing indi vid uals to a po tential carcinogen. Seco nd, because of the relative infreq uency of the outcome (leukemia), the number of subjects in the treatment and co ntrol gro ups would have to be very large to ensure adequate statistical power and to maintain an accepta bl e risk of type II error. Fin all y, follow-up on a large nu mbe r of subjects for 20 years or longer to determin e if they develop leuke mia wo uld be very expensive. Under such circumstances, the hypothesis wo uld be rested much more efficiently us ing a case-co ntrol study. Despi te co ncerns abo ut po tential biases and under- or overestimation of treatment effects in observational studies, there is li ttle evide nce fo r such problems in well-designed studies over the

Exposed to intervention or risk factor

Not exposed to intervention or risk factor

Exposed to intervention or risk factor

Not exposed to intervention or risk factor

Time

FIGURE 76.3. Design of a case-control, or retrospective, study.

[_Al l indi viduals

Exclusi

Time

1197

I

n criLcria

I Study popul ati on I

~dom~nI Ex posed to intervention I Not exposed to interventio n or

l

or risk fac wr

ri sk fac tor

/~ Has outcome or develops disease

D oes not have outcom e or

develop disease

I

/~ H as outcome

or develops di sease

D oes not have outco me or

develop disease

FIGURE 76.4. Design of a cohort, or prospective, study.

last two decades ( 17, I 8). Regardl ess of th ese co ncerns, obse rvational studies provide an opportuni ty to rest hypo th eses th at may otherwise not be testable using randomi zed clinical trials. T hei r use will continue to grow in clinical research and public health. lr is incumbent on osteopathic phys icians examining such studi es and their res ults to understand the strengths and weaknesses of the study designs and the potential threats th at such weaknesses and biases can pose to applying resea rch findin gs in the clinical arena (Table 76.1). In a case-control study, subj ects are initi ally class ifi ed o n the bas is of whether they have (cases) or do not have (co ntrols) the disease of interest. To avoid selectio n bias, co ntro ls should be representative of the sam e populatio n that generated the cases. As an example, it is h ypo thesized that the use of as pirin is associated with an increased risk o f developing ulcer disease. A case-contro l study would select subj ects with diagnosed ulcer disease fro m a defin ed population and also identi fy a set of controls witho ut ulcer disease from that same population . Sometimes contro ls may be marched to the cases on attributes that are related to disease occurrence, such as age, sex, caffeine use, tobacco use, no nstero idal anriinBammatory use, and diet in this case. After selection o f cases and controls, the past history and frequency of as pirin use is asce rtained for subj ects in each group. Statistical analys is o f rh e amount and frequency of aspirin use in the cases and controls determin es if any association between as pirin use and ulcer disease exists. One advantage of the case-co ntro l stud y design is irs ability to demonstrate an associatio n using relati vely small numbers of subj ects. T his advantage is most evident when exam ining diseases that occur infrequently. A good example o f this is the above-mentioned relationship between electromagneti c fo rces and leukemi a. Because leukemia is a rare di sease, occurrin g in the range of one to five cases per I 00,000 persons, it would be necessary to follow a large number of individuals exposed to electromagnetic forces to determine any relatio nship usin g a cohort, or prospective, study. The case-control study design dramaticall y decreases the number of subj ects need ed because o f irs retrospecti ve nature. A case-control study starts wirh subjects known to have leukemia and identifies suitable co ntrols. T hus, the total number of cases and controls numbers is in the hundreds compared to the hundreds of tho usa nds using any o th er study design.

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VIII. Basic and Clinical Research for Osteopathic Theory and Practice TABLE 76.1. COMPARISON OF CASE-CONTROL AND COHORT STUDIES Factor

Study group Comparison group Outcome measures Measures of risk

Length of study Cost of study Population size needed Potential bias Best when

Problems

Case-Cont rol Stud ies (Retrospect ive)

Persons w ith disease Persons without the disease Proportion of cases exposed and proportion of controls exposed Odds ratio Attributable risk Relatively short Relatively inexpensive Relat ively small Assessment of exposure Disease is rare Exposure is common among the diseased Selection of appropriate controls often d ifficult Incomplete information on exposure

Limitations of case-control studies result from potential biases that can be introduced when implementing the study. Recall bias, a problem introduced when asking subjects about exposures that may have occurred years before, can become a threat if there are long periods between exposure and manifestations of the disease. In the above example, there can be a long lag period between the exposure to electromagnetic forces and development ofleukemia. Responses to questions about exposure to high-tension wires during childhood may be inaccurate. More importantly, subjects with leukemia, when compared with controls, may differentially recall (either inflate or deflate) their exposure to high-tension wires near their house as a child. Other limitations of this type of study design include the potential bias introduced by improper selection of controls. A study that suggested an association between pancreatic cancer and coffee consumption was biased by the fact that potential controls were excluded if they had any previous gastrointestinal complaints. Because coffee is known to produce dyspepsia, eliminating subjects from the control group because of dyspepsia inappropriately reduced the number of coffee drinkers among the controls relative to the cases and made it appear that there was an association between coffee use and pancreatic cancer. The results were already published in a prestigious peer-reviewed journal before the bias was discovered and the association discounted (19,20). The other type of observational study design is the cohort study, also known as a prospective study (Fig. 76.4). This type of study is commonly used in clinical research. Using a cohort study to test a hypothesis requires following subjects over a period of time to demonstrate an association between exposure to a risk factor or intervention and a specified outcome. The ongoing Framingham study is an excellent example of a cohort study. The Framingham study has provided the groundwork for many of the associations between risk factors and heart disease that are used for clinical decision making in primary and secondary prevention of heart disease. The Framingham study also identified the link between atrial fibrillation, a chaotic atrial rhythm, and stroke. By following subjects over a long period of time, investigators were

Cohort Studies (Prospective)

Exposed persons Non-exposed persons Incidence in exposed versus incidence in non-exposed Absolute risk Relative risk Attributable risk Generally long Generally expensive Relatively large Assessment of outcomes Exposure is rare Disease is frequent among exposed Selection of non-exposed comparison group often difficult Loss to follow-up

able to identifY a link between frequency of stroke and atrial fibrillation, even after adjusting for other factors that may be linked to stroke, including hypertension and age. The Framingham study was set up as a cohort study by measuring the baseline characteristics of a community of people and then following them over time for the occurrence of disease events. Analysis of the disease events includes a comparison of antecedent risk factors in those individuals experiencing the events and those not experiencing the events. The recruitment and follow-up of offspring of the early Framingham study subjects also affords a unique opportunity to study the effects of hereditary factors on heart disease. Another example of a cohort study is the carotid endarterectomy outcome study mentioned previously (3) . This study compared stroke morbidity and mortality rates in patients receiving carotid endarterectomy in high-volume versus low-volume centers. Patients entered the study when they received the surgery at either a high- or low-volume hospital. They were then tracked for 30 days to determine the occurrence of stroke or death, and statistical tests were used to compare the frequency of the end points in each of the two groups. Potential selection bias is an important factor to consider in interpreting the results of such studies. High-volume centers may serve as a referral site for complicated or high-risk cases, thereby attenuating the effects of technical expertise that may have been acquired by frequently performing carotid endarterectomy. Classification of patients' disease status may be used to control for this phenomenon when seeking to assess the surgical proficiency of high- and low-volume centers.

OUTCOMES RESEARCH IN THE REALM OF OSTEOPATHIC MEDICINE Over the last 2 decades, there have been increasing efforts aimed at quantifYing clinical outcomes associated with various aspects of osteopathic health care, particularly 0 MT. Perhaps most notably, there have been several randomized clinical trials to assess the

76. Outcomes Research and Design efficacy of OMT in patients with low back pain . The first, a randomized clinical tri al involving patients referred to a universitybased ~ack clinic in Cal ifornia from 1973 to 1979, found significant benefits with the first manipulative treatment when cornpared with a combined treatment involving soft-tissue massage and a sham manipulation technique (21). However, no significant benefits were attributed to m anipulation at discharge, which, on average, occurred 30 days after the initial treatment. This trial has been criticized on the basis that it studied the effects of a particular manipulation technique rather than of OMT in general (22) . Anothet' randomized clinical trial was performed at two medical offices of an Illinois-based health maintenance organization from 1992 to 1994 and involved patients with "subac ute" low back pain lasti ng at least 3 weeks but less than 6 months (23). This trial compared OMT using a variety of techniques (each at the discretion of the treating provider) with standard care for low back pain . T here were no significant differences in primary clinical outcomes between the OMT gro up and the standard-care group at 12 weeks. However, the OMT group used significantly less medication and physical therapy. A recently completed randomized clinical trial examined the efficacy of OMT as a co-treatment in subjects with chronic low back pain of at least 3 months' duration (24). Subjects were randomized to either OMT, sham manipulation, or a nointervention control group. OMT and sham manipulation subjects received interventions of comparable duration at the same intervals over 6 months. T he main outcome measures included the SF-36 health status survey, the Roland-Morris disability questionnaire, a vis ual analog scale for back pain , and satisfaction with back care. Compared with no-intervention controls, OMT subjects reported less back pain and greater satisfaction with their back care throughout the trial, better physical functioning and mental health at 1 month, and fewe r co-treatments at 6 months. Although there were no significant benefits associated with OMT when compared with sham manipulation, the trial was sufficiently powered to detect only moderate to large differences in treatment effects . The most comprehensive evaluatio n of spinal manipulation for low back pain, including non-osteopathic approaches, was undertaken by the Agency for Healthcare Research and Quality, fo rmerly known as the Agency for H ealth Care Policy and Research (25). A total of 112 articles were screened, and more extensive reviews of random ized clinical trials, meta-analyses, and cost analyses were cond ucted . The two highest-quality, randomized cli nical trials that evaluated manipulation in patients with acute low back pain found significant improvements in pain and functio n in the manipulation gro ups compared with the control groups (26,27). Two meta-analyses, one based on 29 controlled trials (28) and another based on 23 randomized clinical trials (29), both attrib uted significant short-term benefits to manipulation for low back problems. T he recommendation of the Agency for Healthcare Research and Quality concerning spinal manipulation is that manipulation can be helpful for patients with acute low back problems without radiculopathy when used within the first month of sym ptoms (25) . The strength of evidence fo r this recommendation is graded as "B," indicating that moderate, research-based evidence was available from a relevant,

11 99

high-quality scientific study or multiple adeq uate scientifi c studies. A recent review of the continued validity of this clinical practice guideline found that only minor updating is needed, mostly involving the recommendations for back schools, lumbar corsets, and epidural steroid inj ections (30). OMT has also been shown to be useful in ambulatory patients with other musculoskeletal conditions. A pilot study randomized female fibromyalgia patients to four groups that received various interventions in addition to their current medications (3 1). T hose patients randomized to an OMT group were treated weekly with a combination of] ones strain/countersrrain techniques and other osteopathic modalities applied to troublesome tender poi nts identified by rhe patient. Over 6 monrhs, th e patients receivin g OMT reported significant benefits involving their perceived pain, attitudes toward treatment, activities of dai ly living, and perceived functional ability. Another srudy randomi zed geriatric patients with chro nic shoulder problems, such as tendonitis, bursitis, and os reoarrhritis, to receive either OMT or sham manipulation in addition to their usual treatments (32). OMT included o nly the sevenstep Spencer technique performed twice during each sess ion. Sham manipulation consisted of the seven pos itions of the Spencer technique without administration of the actual corrective forces. Patients were initially treated biweekly and then monthly. Over the 14-week course of treatm ent, both gro ups experienced significantly increased range of motion and decreased pain compared to baseline; however, after treatment, the OMT group continued to demonstrate improved range of motion while th e sham manipulation gro up experienced decreased mobility. OMT has also been found to reduce hospital length of stay in several studies involving a variety of diseases. A small , randomized clinical trial compared patients who received a daily, standardized OMT protocol involving myofascial release, soft tissue, and strain-counterstrain techniques during their hospitalization for pancreatitis with those who received only conventional hospital care for pancreatitis (33). T he OMT patients experienced a mean reduction of 3.5 days in their hospita l stays. Another randomized clinical trial studied the efficacy of OMT in older patients hospitalized with acute pneumonia (34). In addition to convenrional medical trearmenr for pneumonia, OMT patients received osteopathic manipulation and co ntrol patients received light touch sham treatments-each twice daily based on a standardized protocol to ensure comparable patient co ntact time. OMT patients experienced a sho rter duration of antibiotic use and a mean reduction of 2.0 days in their hospital stays. In the field of rehabilitation, two OMT studies in patients with knee or hip osteoarthritis who had recently undergo ne arthroplasty have yielded conflicting results . The first study, described as a "prospective, single-blinded, two-group, march-controlled outcome study," assessed the benefits of OMT as a complement to usual postsurgical care after knee or hip arthroplasty (35). OMT patients performed better than controls by negotiating stairs earlier and ambulating farther during their in-hospital rehabilitation. The study was limited, however, by lack of double blinding and sham treatments to control for anticipated therapeutic effect. A more recent study examin ed similar research questions using

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VIII Basic and CLinicaL Research for Osteopathic Theory and Practice

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Foundations for Osteopathic Medicine

Foundations of Osteopathic Medicine

Osteopathic Medicine Recall

Careers in osteopathic medicine

Counterstrain Approaches in Osteopathic Manipulative Medicine

Pediatric Manual Medicine: An Osteopathic Approach

The DOs: Osteopathic Medicine in America

Somatic Dysfunction in Osteopathic Family Medicine

Osteopathic Diagnosis

Foundations of Psychiatric Sleep Medicine

Myofascial and Fascial-Ligamentous Approaches in Osteopathic Manipulative Medicine

Foundations for Integrative Musculoskeletal Medicine: An East-West Approach

Manual of Osteopathic Technique

Atlas of Osteopathic Techniques

Foundations for Programming Languages (Foundations of Computing)

Cranial Osteopathic Biomechanics, Pathomechanics and Diagnostics for Practitioners

Foundations for Programming Languages (Foundations of Computing)

Foundations for programming languages

Foundations for Financial Economics

Foundations for Microwave Engineering

Foundations for programming languages

New Foundations For Logic

Foundations for financial economics

Essential biochemistry for medicine

A Medicine for Melancholy

A Medicine for Melancholy

Computational Biomechanics for Medicine

Polymers For Regenerative Medicine

Computational biomechanics for medicine

Complementary Medicine for Dummies

Polymers for Regenerative Medicine

Foundations for Osteopathic Medicine

Foundations of Osteopathic Medicine

Osteopathic Medicine Recall

Careers in osteopathic medicine

Counterstrain Approaches in Osteopathic Manipulative Medicine

Pediatric Manual Medicine: An Osteopathic Approach

The DOs: Osteopathic Medicine in America

Somatic Dysfunction in Osteopathic Family Medicine

Osteopathic Diagnosis

Foundations of Psychiatric Sleep Medicine

Myofascial and Fascial-Ligamentous Approaches in Osteopathic Manipulative Medicine

Foundations for Integrative Musculoskeletal Medicine: An East-West Approach

Manual of Osteopathic Technique

Atlas of Osteopathic Techniques

Foundations for Programming Languages (Foundations of Computing)

Cranial Osteopathic Biomechanics, Pathomechanics and Diagnostics for Practitioners

Foundations for Programming Languages (Foundations of Computing)

Foundations for programming languages

Foundations for Financial Economics

Foundations for Microwave Engineering

Foundations for programming languages

New Foundations For Logic

Foundations for financial economics

Essential biochemistry for medicine

A Medicine for Melancholy

A Medicine for Melancholy

Computational Biomechanics for Medicine

Polymers For Regenerative Medicine

Computational biomechanics for medicine

Complementary Medicine for Dummies

Polymers for Regenerative Medicine

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